A . 



TEXT-BOOK 



OF 



PRACTICAL MEDICINE 



DESIGNED FOR THE USE OF 



STUDENTS AND PRACTITIONERS OF MEDICINE 



ALFRED L. LOOMIS, M.D , LL.D, 

Professor op Pathology and Practical Medicine in the Medical Department op the UniveR' 
sity op the City op New York ; Visiting Physician to Belleyue Hospital, Etc. 



EIGHTH EDITION 



REVISED AND ENLARGED 
WITH TWO HUNDRED AND FIFTEEN ILLUSTRATIONS 




NEW YORK 

WILLIAM WOOD AND COMPANY 
1889 



COPYRIGHT, 1389, 

By WILLIAM WOOD & COMPANY. 



Press of J. J. Little & Co., 
Astor Place, New York. 



PEEFACE TO FIRST EDITION. 



In the preparation of a Text-book of Practical Medicine, my experience 
as a medical teacher has led me to employ, quite extensively, plates illus- 
trating the morbid changes and objective symptoms of disease. 

The present work, both in text and illustration, is practically a revision 
and an elaboration of lectures given during the past eighteen years in the 
Medical Department of the University of the City of New York. 

I have avoided, as far as possible, the discussion of unsettled questions, 
and in order to economize space have made reference to many of these only 
in brief foot-notes. 

The Classification adopted is that which it has been my custom to fol- 
low in teaching, and is based on our present knowledge of the etiology of 
disease. 

It is well known that many diseases present very different types in differ- 
ent countries, and I have selected for description those types commonly 
observed by the American physician. 

I have considered only those diseases which come strictly within the 
province of Practical Medicine, and have endeavored to indicate the 
treatment usually followed in this country. 

The illustrations, with but few exceptions, have been made by my assist- 
ant, Dr. Maurice K. Miller (Instructor in the Laboratory of Normal and 
Pathological Histology, University Medical College). The microscopical 
drawings were, in most instances, made from sections prepared in the Lab- 
oratory by Dr. Miller, especially for this work, and they will, I believe, 
aid in the appreciation of the actual morbid processes and conditions. 

In the consultation of Authorities, particularly the German and French, 
in the reading of the proof, and in the preparation of the Index, I have 
been assisted by Dr. Leigh Hunt, Assistant Instructor in the Pathological 
Laboratory of the University. 

If I have failed to give credit — either in the text or in foot-notes — to 
those from whom many of the facts stated have been drawn, it has been 
an unintentional omission. 

19 West 34th Street, New York City, 
July, 1884. 



PREFACE TO THE EIGHTH EDITION. 



In the progress of medical sciences during the four years since the 
third edition of this treatise was published, many unsettled questions 
have received definite answers, and numerous theories have crystallized 
into definite forms of fact or fancy. The author has always sought to 
maintain a conservative yet liberal attitude in his consideration of any 
statements emanating from recognized authorities. The contributions of 
intelligent observers, both in this country and Europe, have been care- 
fully studied, and it is believed that the present edition, much of which 
has been rewritten, and all of which has undergone careful revision, will 
be found abreast with the present position of conservative scientific medi- 
cine ;. that its dogmatic affirmations will be found reliable, and its state- 
ments of still debatable questions will prove unbiassed and just to both 
sides, although intended to be conservative rather than radical. 

Such changes as are at variance with former editions have been made 
as the result of more exact knowledge of the etiology and pathology 
of disease, and from a more extended experience in its treatment. The 
important additions include brief descriptions of the more frequent path- 
ological processes, and a detailed statement of the methods employed in 
bacteriological study, with an enumeration of the distinguishing charac- 
teristics of those micro-organisms which at the present time are regarded 
as pathogenic. Several additions also have been made to the list of dis- 
eases considered. In the revision, Phthisis has been classed as an infec- 
tious disease, although retained among pulmonary diseases for description, 
and its pathology and etiology rewritten in conformity with its bacillary 
nature, adopting the name pulmonary tuberculosis. 

The pathological term nephritis has been substituted for the indefinite 
one Brightfs disease, with a view of making a more exact classification 
of renal diseases. 

The methods advised to be pursued in bacteriological studies are those 
now employed in the " Loomis' Laboratory," the details of which have 
been furnished by J. D. Byron, M.D., Instructor in the Bacteriological 
Department of the Laboratory. 

The changes and additions which have been made in the plates have 
been furnished by H. P. Loomis, M.D., Director of the Pathological 
Department of the Loomis Laboratory. C. E. Quimby, M.D., Assistant 
Professor of Practice in the Medical Department of the University of 
the City of New York, has rendered me valuable assistance in the prep- 
aration of this edition. 

A. L. L. 

19 West 34th Street, 
New York, August, 1889. 



CONTENTS. 



INTRODUCTION. 



GENERAL PATHOLOGY. 



INFLAMMATION. 



1. — Inflammation of Serous Surfaces. 

2. — Inflammation of Mucous Surfaces. 

(a) Croupous Inflammation of Mucous Surfaces. 

(b) Diphtheritic Inflammation of Mucous Surfaces. 

(c) Ulceration of Mucous Surfaces. 

3. — Parenchymatous Inflammation. 

4. — Interstitial Inflammation. 

5. — Fate of Pus Pages 1-8 



1. — Parenchymatous Degeneration. 

2. — Fatty Infiltration. 

3. — Fatty Degeneration. 

4. — Colloid Degeneration. 

5. — Mucoid Degeneration. 

6. — Calcareous Degeneration. 

7. — Pigmentation. 

8. — Amyloid Degeneration. 

9. — Necrosis 11-20 



HYPERTROPHY. — ATROPHY 



9-10 



DEGENERATIONS. 



TUBERCLE.— TUBERCULOSIS 



21-23 



BACTERIOLOGY. 



1. — Technology. 

2. — Examination and Staining. 

3. — Biology. 

4. — Classification 



24-34 



SECTION I. 



DISEASES OF THE BESPIBATORY ORGANS. 



DISEASES OF THE NASAL PASSAGES. 



Acute Coryza. — Chronic Coryza. — Hypertrophic Nasal Catarrh. — Atrophic 
Nasal Catarrh. — Oz^na 35-42 



Vlll CONTENTS. 

DISEASES OF THE LARYNX. 

Acute Catarrhal Laryngitis. — Chronic Catarrhal Laryngitis. — Chronic 
Laryngitis of Phthisis. — Chronic Laryngitis of Syphilis. — (Edema Glot- 
tidis. — Croupous Laryngitis. — Laryngeal Ulcers. — Neuroses of the Lar- 
ynx. — Tumors of the Larynx Pages 43-67 



BRONCHITIS. 

Acute Catarrhal Bronchitis. — Acute Capillary Bronchitis. — Chronic Catar- 
rhal Bronchitis. — Bronchiectasis. — Croupous or Plastic Bronchitis. — 
Bronchial Asthma. — Bronchial Hemorrhage. — Haemoptysis 67-95 



DISEASES OF THE LUNGS AND PLEURA. 

Acute Lobar Pneumonia. — Lobular Pneumonia. — Interstitial Pneumonia. — 
Pneumonokoniosis. — Pulmonary Hyperaemia. — Pulmonary (Edema.— Pulmo- 
nary Infarction. — Pulmonary Apoplexy. — Pulmonary Gangrene. — Pulmo- 
nary Anaemia. — Pulmonary Collapse. — Pulmonary Emphysema. — Cancer of 
the Lungs. — Non-Malignant Growths in the Lung and Pleura. — Syphi- 
litic Disease of the Lung. — Atrophy of the Lung.— Parasitic Diseases. 
— Pleurisy, (a) Plastic. — (b) Serofibrinous. — (c) Suppurative. — (d) Interstitial. 
Cancer of the Pleura. — Pyopneumothorax. — Hydrothorax. — Hemothorax. 
— Pulmonary Tuberculosis, (a) Acute Tuberculosis.— (b) Chronic Tubercu- 

96-235 



SECTION II. 

DISEASES OF THE DIGESTIVE SYSTEM, INCLUDING DIS- 
EASES OF THE LIVEK, SPLEEN, AND PANCKEAS. 

DISEASES OF THE MOUTH. 

Stomatitis, (a) Catarrhal. — (b) Follicular. — (c) Gangrenous. — (d) Ulcerative. — 
Thrush. — Diseases of the Tongue, (a) Glossitis.— (b) Cancer. — Paro- 
titis 236-246 



DISEASES OF THE PHARYNX. 
Tonsilitis. — Inflammations. — Retropharyngeal Abscess 247-251 

DISEASES OF THE (ESOPHAGUS. 
Inflammations. — Cancer 252-255 

DISEASES OF THE STOMACH. 



Inflammations, (a) Acute.— (b) Sub-acute. — (c) Chronic. — (d) Phlegmonous. — Dys- 
pepsia. — Cancer and Ulcer. — Neuroses. — Haematemesis.— Dilatation. . 256-286 



CONTENTS. 



DISEASES OF THE INTESTINES. 

Enteritis. — Diarrhcea. — Cholera Morbus. — Cholera Infantum, — Intestinal 
Dyspepsia. — Dysentery. — Typhlitis. — Appendicitis. — Perityphlitis. — Intes- 
tinal Ulcers. — Intestinal Hemorrhage. — Intestinal Obstruction. — Waxy 
Degeneration. — Cancer. — Rectitis. — Periproctitis. — Hemorrhoids. — 
Intestinal Parasites. — Intestinal Colic. — Constipation. — Peritonitis. — 
Ascites Pages 287-368 



DISEASES OF THE LIVER. 

Hyperemia, (a) Active. — (b) Passive. — Inflammations, (a) Interstitial Hepatitis 
or Cirrhosis. — (6) Circumscribed Hepatitis or Abscess. — (c) Diffused Hepatitis 
or Acute Yellow Atrophy. — Perihepatitis. — Pylephlebitis. — Degenerations. 
(a) Amyloid. — (b) Fatty. — (c) Pigmentary. — (d) Atrophic. — New Growths. 
(a) Cancer. — (b) Gummata. — (c) Hydatids. — (d) Tubercle. — Jaundice 369-428 

DISEASES OF THE GALL BLADDER AND DUCTS. 

Inflammations, (a) Catarrhal. — (b) Exudative. — Cancer. — Enlargement. — Gall 
Stones. — Functional Derangements 429-443 



DISEASES OF THE PANCREAS. 

Acute Diseases. — Degenerations, (a) Fatty. — (b) Waxy. — Morbid Growths 
(Cancer, Tubercle, etc.) — Cysts. — Calculi 444-446 

DISEASES OF THE SPLEEN. 

Hyperemia. — Inflammation, including Embolism and Infarction. — Hypertro- 
phy. — Degenerations.— Morbid Growths. — Parasites 447-453 



SECTION III. 

DISEASES OF THE HEABT, BLOOD-VESSELS, AND 

KIDNEYS. 

DISEASES OF THE HEART. 

Pericarditis. — Endocarditis. — Valvular Lesions. — Hypertrophy. — Dilata- 
tion. — Myocarditis. — Degenerations. — Atrophy.— Rupture. — Thrombosis. 
— Aneurism. — Morbid Growths and Parasites. — Tuberculosis of the Peri- 
cardium. — Neuroses. — Hydropericardium. — Pneumohydropericardium. — 
Syphilitic Disease of the Heart.— Basedow's Disease 454-546 



DISEASES OF THE BLOOD- VESSELS. 

DISEASES OF THE ARTERIES. 



Acute Endarteritis. — Chronic Endarteritis. — Periarteritis. — Degenera- 
tions, (a) Fatty. — (b) Waxy. — (c) Calcareous. — Syphilis. — Hypertrophy, 
Atrophy, and Narrowing. — Arteriocapillary Fibrosis 547-558 



X 



CONTENTS. 



DISEASES OF THE VEINS. 

Acute Phlebitis. — Chronic Phlebitis. — Varix. — Thrombosis. — Embolism. — 

Thoracic Aneurism. — Abdominal Aneurism. — Mediastinal Tumors 

Pages 554-568 



DISEASES OF THE KIDNEYS. 

THE URINE. 

Normal Constituents. — Urinary Sediments. — Uremia 569-582 

THE KIDNEYS. 

Renal Hyperemia. — Renal Hemorrhage. — Nephritis, (a) Acute Nephritis, 
Parenchymatous and Interstitial. — (b) Chronic Nephritis, Parenchymatous and 
Interstitial. — (c) Amyloid Degeneration. — Pyelitis. — Hydronephrosis. — 
Cystic Kidney. — Renal Calculi. — New Growths (Cancer, etc.). — Parasites. 
— Perinephritic Abscess. — Floating Kidney. — Hematuria. — Chyluria. — 
Cystitis 583-646 

SECTION IV. 
ACUTE GENERAL DISEASES. 

MIASMATIC CONTAGIOUS DISEASES. 

Fever. — Typhoid Fever. — Yellow Fever. — Cholera. — Cerebro-spinal Menin- 
gitis. — Septicemia. — Pyemia 647-728 

ACUTE CONTAGIOUS DISEASES. 

Diphtheria. — Erysipelas. — Acute Miliary Tuberculosis. — Typhus Fever. — 
Relapsing Fever. — Small-pox. — Inoculation and Vaccination. — Varicella. 
— Scarlet Fever. — Measles. — German Measles. — Miliary Fever. — Influ- 
enza. — Whooping-cough. — Hydrophobia 729-845 



MALARIAL DISEASES. 

Intermittent Fever. — Remittent Fever. — Continued Malarial Fever.— Per- 
nicious Fever. — Dengue Fever. — Chronic Malarial Infection 846-894 



SECTION V. 
CHRONIC GENEEAL DISEASES. 

Rheumatism. — Gout. — Lithemia. — Diabetes. — Anaemia. — Chlorosis. — Progres- 
sive Pernicious Anaemia. — Leucocythemia. — Pseudo-Leukemia. — Addison's 
Disease. — Ammonemia. — Hemophilia. — Scurvy. — Purpura. — Myxcedema. — 
Scrofula.— Rickets.— Alcoholism.— Trichinosis.— Syphilis 895-964 



CONTEXTS. 



xi 



SECTION VI. 

DISEASES OF THE NEEYOUS SYSTEM, INCLUDING DIS- 
EASES OF THE BRAIN, SPINAL COED, AND FUNC- 
TIONAL NEEYOUS DISEASES. 

GENERAL SYMPTOMATOLOGY. 
Of Nervous Diseases Pages 965-971 

DISEASES OF THE BRAIN. 

Cerebral Hyper^3iia {Active or Passive). — Cerebral Anaemia. — Meningitis. — 
Cerebral Thrombosis and- Embolism. — Cerebral Softening. — Cerebral 
Apoplexy. — Abscess of the Brain. — Cerebral Tumors. — Sclerosis of the 
Brain. — Hypertrophy of the Brain. — Atrophy of the Brain 972-1031 



DISEASES OF THE SPINAL CORD AND ITS MENINGES. 

Spinal Hyperemia. — Spinal Meningitis. — Acute Myelitis. — Chronic Myelitis. 
— Non-inflammatory Softening. — Acute Bulbar Paralysis. — Progressive 
Bulbar Paralysis. — Infantile Spinal Paralysis. — Acute Spinal Paralysis 
of Adults. — Chronic Anterior Myelitis. — Progressive Muscular Atrophy. 
— Cerebro-spinal Sclerosis. — Locomotor Ataxia. — Spasmodic Tabes Dorsa- 
lis. — Amyotrophic Lateral Sclerosis. — Pseudo-Hypertrophic Paralysis. — 
Acute Ascending Paralysis. — Spinal Apoplexy. — Tumors of Spinal Cord. — 
Spina-Bifida and Hydrorachis 1032-1075 



DISEASES OF THE PERIPHERAL NERVES. 

Peripheral Neuritis. — Localized Spasm and Paralysis. — Chronic Lead Poi- 
soning. — Chronic Mercurialism. — Paralysis Agitans. — Facial Paraly- 
sis. — Eclampsia and Infantile Convulsions. — Tetanus. — Neuralgia. — 
Megrim 1076-1095 

FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM. 

Spilepsy. — Hysteria. — Hystero-Epilepsy. — Catalepsy. — Neurasthenia. — 
Chorea. — Sunstroke. — Spinal Irritation. — Vertigo. — Sea-Sickness. . .1096-1124 



DESCRIPTION OF PLATE. 



No. 1. Bacillus Anthracis. — Section of liver of a white mouse inocu- 
lated with a pure culture of anthrax bacilli. Gram's method. Bismarck 
brown, x 500. 

No. 2. Bacillus Typhosus. — From a cover-glass preparation of spleen 
pulp. Loffler's solution and acetic acid, x 700. 

No. 3. Gonococcus Neisserii. — From a cover-glass preparation of gonor- 
rhceal discharge. Aqueous solution of methyl blue. x 1000. 

No. 4. Bacillus Tuberculosis (tissue). — Giant cell of a miliary tubercle 
of liver, containing bacilli. Erlich-Koch method. Methyl blue and Bis- 
marck brown staining, x 900. 

No. 5. Bacillus Tuberculosis (sputum). — Cover-glass preparation. 
Erlich-Koch method. x 900. 

No. 6. Spirillum (Jholerm Asiaticce. — Cover-glass preparation of intes- 
tinal discharge. Aqueous solution of methyl blue, x 900. 

No. 7. Spirochete Obermaieri. — Cover-glass preparation of blood, from 
case of relapsing fever. Aqueous solution of Bismarck brown, x 900. 

No. 8. Actinomyces. — Prepared from tumor of jaw of calf. Gram's 
method and Bismarck brown, x 850. 



LIST OF ILLUSTRATIONS. 



Fig. Page 

1. Inflammation of omentum 2 

2. Granulation cells, in various stages 3 

3. Inflammation of a serous membrane ' 5 

4. Inflammation of a mucous membrane 6 

5. Diphtheritic inflammation of a mucous surface ■ 8 

6. Parenchymatous degeneration in cells 13 

7. Fatty infiltration of cells 14 

8. Fatty degeneration of muscle fibres 15 

9. Amyloid degeneration 18 

10. ^Miliary tubercle 22 

11. Tuberculosis of liver 24 

12. Croupous membrane from the trachea 54 

13. Diagram showing position of the vocal bands in abductor and adductor paraly- 

sis as seen with the laryngoscope 62 

14. Multiple papilloma of the right vocal chord as seen with the laryngoscope. ... 65 

15. The trachea laid open, showing the same tumor as seen in Fig. 14 65 

16. Transverse section of a portion of a medium-sized bronchial tube in acute 

catarrhal bronchitis 68 

IT. Diagram illustrating the physical signs of bronchitis 70 

18. Bronchial wall in chronic catarrhal bronchitis 76 

19. Various forms of bronchiectasis 82 

20. Mould of bronchi in sputum of plastic bronchitis 84 

21. Morbid anatomy of first stage of acute lobar pneumonia 96 

22. Morbid anatomy of second stage of acute lobar pneumonia 97 

23. Morbid anatomy of second stage of pleuro-pneumonia 97 

24. Morbid anatomy of third stage of acute lobar pneumonia 99 

25. Morbid anatomy of purulent infiltration 101 

26. Temperature record in acute lobar pneumonia in an adult : 108 

27. Temperature record in acute lobar pneumonia, observations every six hours. . 109 

28. Temperature record in acute lobar pneumonia ending in purulent infiltration. 110 

29. Physical signs of the three stages of acute lobar pneumonia. 117 

30. Morbid anatomy of lobular pneumonia 120 

31. Temperature record in lobular pneumonia in a child 130 

32. Morbid anatomy of interstitial pneumonia 135 

33. Morbid anatomy of brown induration of the lung 143 

34. Hemorrhagic infarctions 149 

35. Morbid anatomy of emphysema of the lung 160 

36. Cancer of lung * 168 

37. Hydatids of luns; 173 

38. Temperature record in acute pleurisy 175 

39. Physical signs in acute pleurisy with a small amount of effusion 176 

40. Physical signs in pleurisy with effusion 182 

41. Physical signs of hydropneumothorax 195 



Xiv LIST OF ILLTJSTKATIONS. 

| 

Fig. Page 

42. Lung in acute tuberculosis 202 

43. Acute tuberculosis : alveolus filled with fibrin and cells 203 

44. Tubercle bacilli from phthisical sputum 207 

45. Temperature record in a case of acute tuberculosis 208 

46. Morbid anatomy of pneumonic tuberculosis 210 

47. Lung cavity 211 

48. Miliary tubercle in disseminated tuberculosis 213 

49. Tubercular nodule 214 

50. Physical signs of first stage of chronic tuberculosis 222 

51. Physical signs of cavities in third stage of chronic tuberculosis 224 

52. Oidium albicans . 241 

53. Stricture of the oesophagus 253 

54. Stomach wall in sub-acute gastritis 258 

55. Mucous membrane and stomach-tubules in chronic gastritis 260 

56. Sarcinae ventriculi from vomit of chronic gastritis 262 

57. Cancer of pyloric end of stomach 270 

58. Perforating ulcer of stomach 276 

59. Dilatation of stomach 284 

60. Acute enteritis, small intestine near middle of ileum 287 

61. Acute follicular enteritis ; transverse colon showing ulceration 288 

62. First stage of acute dysentery 302 

63. Second stage of acute dysentery 303 

64. Temperature record in acute dysentery. 305 

65. Tubercular ulcers ; ileum 318 

66. Intussusception (intestinal obstruction) 322 

67. Head of taenia solium (tape-worm) 339 

68. Mature segment of taenia solium „ 339 

69. Head of taenia saginata 340 

70. Oxyuris vermicularis with ovum; and ascaris lumbricoides 341 

71. Passive hepatic hyperaemia . . . . 372 

72. Interstitial hepatitis 375 

73. Interstitial hepatitis, same as Fig. 72 : more highly magnified 376 

74. Circumscribed suppurative hepatitis (pyaemic abscesses) 383 

75. Cells from a lobule in acute yellow atrophy of the liver 390 

76. Amyloid degeneration of the liver 401 

77. Three intralobular zones ; waxy, fatty and pigment degenerations of the liver. . 402 

78. Chronic atrophy of the liver 405 

79. Fatty infiltration of the liver 406 

80. Fatty degeneration of the liver 407 

81. Pigmentary degeneration of the liver.'. 409 

82. Same as Fig. 81 : more highly magnified 410 

83. Cancer of the liver 413 

84. Diagrammatic enlargements of liver 415 

85. Hydatids of liver: budding vesicles 419 

86. Hydatids of liver: head of echinococcus 421 

87. Gall-bladder filled with calculi 435 

88. Section of a large gall-stone showing layers 436 

89. Crystals of cholesterin 436 

90. Areas of splenic enlargement as shown by percussion 450 

91. Morbid anatomy and physical signs of sero-plastic pericarditis 455 

92. Physical signs of pericarditis with effusion 459 

93. Changes in mitral valve in diphtheritic endocarditis 465 

94. Changes in aortic valves in diphtheritic endocarditis 466 

95. Section of aortic valve in acute endocarditis 466 

96. Diagram showing the mode of production of cardiac murmurs 476 



LIST 01 ILLUSTRATIONS. 



XT 



Fig. Pagt; 

97. Diagram showing area of cardiac murmurs 478 

98. Vegetations on aortic valves in aortic obstruction 479 

99. Sphygmographic tracing of pulse in aortic obstruction 480 

100. Morbid anatomy of aortic insufficiency 482 

101. Sphygmographic tracing of pulse in aortic regurgitation 484 

102. Morbid anatomy of mitral stenosis 487 

103. Mitral orifice showing button-hole slit in stenosis 488 

104. Sphygmographic tracing of pulse in mitral stenosis 489 

105. View of left heart in mitral regurgitation 492 

106. Sphygmographic tracing of pulse in mitral regurgitation 494 

107. Physical signs in left ventricular hypertrophy 512 

108. Physical signs in right ventricular hypertrophy 512 

109. Section of heart-wall in acute myocarditis 522 

110. Teased fibres of heart-muscle in fatty degeneration of the heart 526 

111. Muscle-fibres showing fatty infiltration of the heart 527 

112. Chronic endarteritis : "atheroma" 548 

113. Section of kidney in general arterial fibrosis 551 

114. Diagrammatic representation of formation of thrombi and emboli 556 

115. Ke-establishment of circulation by anastomosis after embolism 558 

116. Morbid anatomy of spontaneous arterial aneurism. 560 

117. Hippuric acid 570 

118. Fat globules from chylous urine 571 

119. Leucin and tyrosin 571 

120. Uric acid crystals 572 

121. Urate of soda 572 

122. Urate of ammonia crystals 572 

123. Oxalate of calcium crystals 573 

124. Ammonio-magnesian, or triple phosphate 573 

125. Phosphate of calcium 573 

126. Cystine 574 

127. Epithelium from urinary deposits 574 

128. Blood in the urine 575 

129. Pus in the urine 575 

130. Epithelial casts in the urine 576 

131. Hyaline casts in the urine 576 

132. Granular casts in the urine 576 

133. Fatty casts in the urine 576 

134. Blood casts in the urine 576 

135. Spermatozoa in the urine 577 

136. Torula eerevisiae : penicilium glaucum ; and sarcina? ventriculi 577 

137. Section from Malphigian pyramid in passive renal hyperemia 584 

138. Hemorrhage from the vascular tuft of a glomerulus in renal hemorrhage. . . . 588 

139. Henal hemorrhage and renal infarction -. 589 

140. Cortex of kidney showing cloudy swelling in acute nephritis , 593 

141. Glomerulonephritis, scarlet fever 593 

142. Cortex of kidney showing advanced degenerative changes in acute nephritis . 594 

143. Cortex of kidney in chronic parenchymatous nephritis 605 

144. Cortex of kidney in early cirrhotic nephritis 611 

145. Cortex of kidney in advanced cirrhotic nephritis 612 

146. Cortex of kidney showing commencing waxy changes 617 

147. Medullary portion of kidney showing advanced amyloid change 618 

148. Longitudinal section of cystic kidney 629 

149. A cyst of the kidney : epithelial lining shown 629 

150. Renal calculi : ah embedded mulberry calculus 630 

151. Mucous surface of ileum in first week of typhoid fever 659 



XYi LIST OF I LLUSTK ATIOKS. 

Fig. Page 

152. Mucous surface of ileum in second week of typhoid fever 660 

153. Mucous surface of ileum in third week of typhoid fever 660 

154. Enlarged mesenteric lymphatics in typhoid fever 661 

155. Temperature record in typical (mild) typhoid fever 670 

156. Temperature record in non-typical typhoid fever 671 

157. Temperature record in yellow fever 698 

158. Temperature record in septicaemia 723 

159. Metastatic pyaemic abscesses of the lung 725 

160. Temperature record in pyaemia 727 

161. Temperature record in a case of facial erysipelas 747 

162. Temperature record in a case of acute miliary tuberculosis 751 

163. Temperature record in severe typhus fever 763 

164. Temperature record in a case of relapsing fever 782 

165. Temperature record in a case of discrete small-pox 789 

166. Temperature record in a case of confluent small-pox „ 793 

167. Temperature record in a case of varioloid 802 

168. Temperature record in a case of scarlatina 811 

169. Temperature record in a case of measles. 826 

170. Temperature record in a case of German measles 833 

171. Temperature record in a case of influenza 838 

172. Fever curve in quotidian intermittent ... 851 

173. Fever curve in tertian intermittent 852 

174. Fever curve in quartan intermittent 852 

175. Section of liver from a case of remittent fever 858 

176. Temperature record in remittent fever 861 

177. Temperature record in a case of continued malarial fever 869 

178. Temperature record in continued malarial fever (septic variety) 871 

179. Temperature record in pernicious fever (comatose variety) 879 

180. Temperature record in pernicious fever (algid variety) 881 

181. Temperature record in a severe case of dengue fever 888 

182. Temperature record in a mild case of acute rheumatism 897 

183. Temperature record in a fatal case of acute rheumatism 897 

184. Deformity from articular rheumatism (hand) 904 

185. Section of a gouty cartilage 909 

186. Vertical section of a Malphigian pyramid in gouty nephritis. 910 

187. Deformity from gout (hand) 912 

188. Blood from a case of leucocythaemia 931 

189. Section of leucocythaemic spleen 932 

190. Encapsulated trichinae in voluntary muscle 957 

191. Trichinae with calcareous deposits and degeneration of the capsule 957 

192. Temperature record in the fourth week of trichinosis 958 

193. Acute meningitis, showing also intact meninges .. . 978 

194. Temperature record in a case of acute meningitis 979 

195. Tubercular meningitis : — tubercular deposits along blood-vessels 986 

196. Temperature record in a case of tubercular meningitis 987 

197. Pachymeningitis interna — Vertical section of skull and cerebral meninges. . . 995 

198. Cerebral softening 1002 

199. Small blood-vessel from a focus of yellow softening (cerebral thrombosis and 

embolism) 1003 

200. Cerebral apoplexy ; newly formed clot in the left optic tract 1006 

201. Vertical section of the cerebrum 1011 

202. Fibroma of the cerebellum 1020 

203. Diagram showing connective-tissues of medullated nerve structure 1027 

204. Sclerosis of the brain 1028 

205. Acute myelitis 1038 



LIST OF ILLUSTEATIONS. XVII 

Fig. Page 

206. Chronic bulbar paralysis 1044 

207. Muscle of the tongue in chronic bulbar paralysis contrasted with normal 

muscle 1045 

208. Section of spinal cord in early stage of infantile spinal paralysis 1048 

209. Same as 208 after establishment of sclerotic process 1048 

210. Teased fibres from abductor pollicis in progressive muscular atrophy 1054 

211. Sketch of a hand in progressive muscular atrophy 1055 

212. Cerebro-spinal sclerosis 1057 

213. Regions of degenerative changes in spinal cord.- — Diagrammatic 1060 

214. Locomotor ataxia. — Section of cord in cervical region 1061 

215. Spinal apoplexy : clot in the left anterior cornu 1071 



A TEXT-BOOK 



OF 



PRACTICAL MEDICINE. 



INFLAMMATION. 

AccoediisG to the older writers the cardinal symptoms of inflammation 
are pain, heat, redness and swelling, features which are more striking in 
those forms of inflammation which come under the care of the surgeon than 
in those which the physician is called upon to treat. As the knowledge of 
tissues and processes became more detailed and complete, and as the hidden 
changes underlying these grosser ones were brought to light, pathologists 
sought to discover the essence of the inflammatory process, to find its cause, 
and to determine in which tissues or organs the primary change occurred. 
The history of the theories and definitions of inflammation is a record of 
the varying importance that has been attached to one or another of the 
changes observed. Into these theories, and the arguments by which they 
have been in turn supported and assailed, it is not desirable here to enter. 
It will be sufficient to describe the changes observed in the tissues, and to 
define the associated terms of which use will hereafter be made. The 
pathological results of inflammation are the product of three factors, com- 
bined in varying proportions, the vascular, the exudative and the paren- 
chymatous changes. According as one or another is prominent it deter- 
mines the character of the inflammation. 

Vascular Changes. — Except in the non-vascular tissues, as the cornea and 
cartilage, the earliest change observed is in the circulation, and this change 
is manifested by a change in the color of the affected part, which becomes 



2 



INFLAMMATION, 



red and congested. This redness is due to an increase of the quantity of 
blood in the part ; at first the hyperemia is active, that is, blood is brought 
to the part and passed through the capillaries in larger quantities than 
before ; but it may become passive, a condition in which, while the quan- 
tity of blood present in the part is greater than usual, the current is much 
slower, the amount which actually passes through the capillaries in a given 
time being less than normal ; finally, this retardation of the flow may end 
in actual arrest : stasis. That hyperemia is only an accompaniment, and 




Fig. 1. 

Inflamed Omentum from Human Subject. 

o, Normal fibrous trabecula ; 5, normal endothelium ; c, small artery ; d, vein with while blood-corpuscles 
peripherally disposed ; e, white blood-cells migrated or migrating ; /, desquamated endothelium ; multi- 
nuclear cell ; g, migrated red blood.— Zeigler. 

not the essence, of inflammation, is shown by the fact that the hyperemia 
which is caused by section of the sympathetic nerves is not accompanied 
by the other symptoms and changes observed in inflammation. 

Exudative Changes. — The swelling which has been mentioned as one of 
the four cardinal symptoms is due mainly to the presence of a liquid 
infiltrated through the tissues. This liquid comes from the blood by 
exudation through the walls of the capillaries ; but it is not simply the 
plasma or serum of the blood ; it contains large numbers of emigrated 
white blood-cells, which, w r ith the fixed cells of the part, furnish those 
peculiar constituents of the exudation which distinguish this liquid from 
the normal juices of the part, or from that of oedema, and which make 
it an inflammatory exudation. The character of the exudation, whether 
it be serum, fibrin, or pus, is determined also by the cellular elements, 
and more especially by the emigrated white cells. 

Examination of fresh normal tissues shows, scattered through them, free 



INFLAMMATION. 



3 



cells which closely resemble the colorless corpuscles of the blood and lymph. 
Like them, they possess the power of amoeboid movement, of rapidly chang- 
ing their shape by throwing out processes, of moving from place to place by 
means of this change of form, and of multiplying by division. They are 
called " wandering cells,*' or leucocytes, because of their supposed identity 
with the colorless corpuscles of the blood. Under normal conditions the 
leucocytes contained within the blood-vessels may occasionally be seen to 
pass through the unbroken wall of a capillary by means of this power of 
amoeboid movement which they possess ; when the tissue adjoining the 
capillary is inflamed, the number of cells "migrating 3 ' through its wall 
is notably increased. The emigrated white cells form the larger portion of 
the cellular part of inflammatory exudations, and play a most prominent 
part in both necrotic and reparative processes. The number of free cells is 
increased by the fixed corpuscles of the omnipresent connective-tissue, 
w T hich swell, as has been described, and give rise by proliferation to other 
cells, which cannot be distinguished morpho- 
logically from the normal wandering cells or 
leucocytes. 

Parenchymatous Changes. — The cellular 
elements of the tissues undergo change in 
form and nutrition. The chemical inter- 
changes which constitute normal nutrition, 
and which are carried on between the cells 
of the tissues and the liquid furnished to the 
cells by the blood, are modified in character 
or extent, and the cells themselves are cor- 
respondingly modified in form, 
hand the cells may show a tendency to re- 
turn to their earlier embryonal form, to be- 
come swollen, globular, pale and succulent, 
perhaps to divide, to form new cells, by pro- 
liferation ; on the other hand, the exaggerated activity of the cell may 
prove too great a strain upon it, and it dies or becomes disabled by pas- 
sage into the condition known as fatty degeneration. The former of these 
two results is the one seen most commonly in the connective-tissue frame- 
Avork and envelopes of the various parts and organs, and the latter in the 
specific cells that constitute their parenchyma. These modifications of 
nutrition vary with the nature of the irritant, and the extent of the tissue 
compression from the exudation. 

Terminations of Inflammation. — The inflammatory process, as thus de- 
scribed, may be arrested at any point. If the irritation is slight or of 
short duration, if the change has not progressed to the point of tissue 
destruction and formation of pus, the withdrawal of the primary cause is 
followed by a diminution of the swelling and congestion, and by return to 
the normal state ; — this is called resolution. When, however, the vitality 
of the tissues is impaired, by prolonged irritation, by compression or by 
the action of specific poisons, parenchymatous degeneration or necrosis of 




Fig. 2. 

Granulatiori-cells in Various Stages. 

On the One a, uninuclear ; a x , multinuclear migrated 
white blood-corpuscles ; b, vanous farms 
of uninuclear formative cells ; c, binu- 
clear ; c u multinuclear formative cells; 
d, formative cells developing into con- 
nective-tissue ; e, developed connective- 
tissue, x 250.— Zeigler. 



4 



INFLAMMATION* 



the tissues may occur. This necrosis may be preceded or followed by a 
localized or diffuse infiltration of the tissues by leucocytes. When these 
cells accumulate in great numbers (whether by transformation of connect- 
ive-tissue cells or by migration from the vessels), those which are in the 
necrotic area lose their vitality and constitute the cellular portion of pus, 
while those which fill the immediately adjacent parts pass on to the forma- 
tion of connective-tissue, producing the limiting wall of fibrin about the 
necrotic area. When this necrosis is gradual and attended by molecular 
disintegration of the tissues, it is called ulceration if upon a free surface, 
and abscess when the pus and necrotic tissue are retained in the substance 
of an organ. When necrosis affects palpable masses of tissue it is called 
sloughing. When necrotic changes have taken place, the simple arrest 
of the inflammation is not sufficient ; the losses must be made good, the 
destruction repaired. This is cicatrization, and it is accomplished largely 
by cells of the connective-tissue. As the conditions become more favor- 
able, the cells newly formed by proliferation no longer remain stationary, 
lose their vitality, and become pus, but they progress in the direction of 
a normal development and form new tissue. The irregular pink granula- 
tions seen within a wound or upon an ulcerated surface are formed of 
masses of young cells crowded with capillary loops of new formation. 
The cells, at first large, soft, finely granular and juicy, become smaller 
and firmer, and the intercellular substance increases and becomes fibrous. 
If the inflammatory process has taken place in the interior of an organ, 
involving only a small portion of tissue, and has stopped short of the 
formation of a distinct collection of pus, the result of the reparative pro- 
cess is a mass of fibrous connective-tissue, a cicatrix ; and if a collection 
of pus has actually formed, but is only of small size, the pus may disap- 
pear by liquefaction of its cellular elements and absorption. If, on the 
other hand, a larger abscess has formed and has been opened, its cavity 
becoming filled by the granulations, the same change into fibrous tissue 
follows, and a cicatrix is again the result. The same is true of ulceration 
of a free surface, with the addition that the surface of the cicatrix is 
covered by a layer of epithelium resembling more or less closely the origi- 
nal layer which has been destroyed by the ulceration. When the irrita- 
tion has been less active but more prolonged, and has perhaps involved an 
entire organ, although the cellular development is abundant, the elements 
retain their vitality, and neither suppurative nor necrotic changes occur, but 
the effect again appears in an increase of the connective-tissue of the part 
involved ; the consequences of this increase are most serious. The origi- 
nal " fixed cells" of the connective-tissue multiply as in the other case 
mentioned, and develop into fully formed tissue, and the amount of this 
tissue becomes in consequence much greater than normal. In its natural 
evolution it retracts, and by its quantity and its retraction it presses upon,' 
and , interferes with the nutrition of the specific cellular elements of the 
organ, so that they become less fit to perform their functions. This 
change is called induration or cirrhosis ; common examples are cirrhosis 
of the liver, and " contracted kidney " or interstitial nephritis. 



INFLAMMATION OF FREE SURFACES. 



5 



INFLAMMATION OF FREE SURFACES. 




First : Serous Surfaces. — The most common form of inflammation of serous 
membranes is that which results in the production of serum, fibrin, or pus, 
in variable proportions ; these products may infiltrate the substance of the 
inflamed membrane, be poured out upon its free or attached surface, or 
collect in cavities lined by it. The first change in this inflammatory pro- 
cess is in the blood-vessels, which contain more than their normal quantity 
of blood, and it is from 
the blood circulating in 
the vessels that most of 
the characteristic inflam- 
matory products are de- 
rived. After the initial 
hyperemia, the fibrino- 
gen of the exudation 
comes in contact with 
the fibrino-plastic mate-^^^ 
rial of the cellular ele- 
ments (there being a 
ferment present), coagu- 
lation takes place, and fig 

layers of fibrin Contain- Inflammation of Serous Membrane 

ing few or many cells are 
formed on the free sur- 
face. These layers are 
called pseudo-mem- 
branes, or coagulable lymph. If the inflammation occurs in a membrane 
whose normal conformation makes a free effusion possible (as the pleura 
and peritoneum) some serum is always present. It may be only infiltrated 
through the meshes of the tissues, or it may accumulate at some point 
as a serofibrinous collection. When leucocytes are present in great num- 
bers, the exudation is fibrino-purulent. The greater the intensity of the 
inflammation, and the more enfeebled the patient, the greater is the liabil- 
ity to pus formation. In certain serous inflammations the exudation may 
be hemorrhagic ; the blood may come from a ruptured capillary vessel, or 
the coloring matter of the blood-corpuscle may be set free and color the 
exudation without vascular lesion. Such inflammation of serous mem- 
branes may end in necrosis or in resolution. If the inflammation is intense, 
and stasis occurs throughout a wide area of tissue, it will result in necro- 
sis. Stasis is the expression of a higher degree of injury than that which 
exists in simple inflammation. 1 The intensity of the inflammation deter - 

1 If inflammation is an arrest of function, and not diversion of agents of nutrition into new channels 
of activity, restoration of a part to the natural state must be as simple as its departure from it, and reso- 
lution of inflammation means, either that the temporarily arrested process goes on again, or, if the process 
has proceeded to its ultimate issue (death of the affected part), that the destroyed part has to be repaired, 
not by a continuation of the morbid process, but simply by the restitution of the normal condition. 



Section through the Pericardium 
False Membrane, x 150. 

a, Visceral pericardium ; b, fibrinous false membrane ; c, distended 
blood-vessel; d, leucocytes infiltrating (issues; e, lymphatics filled 
with cells ; f, formative cells within the false membrane.— After 
Zeigler. 



6 



INFLAMMATION. 



mines whether the result shall be a return to the normal condition or a 
destruction of tissue. An uncomplicated serous inflammation is neither 
reproductive nor infective. It has no tendency except to stop as soon 
as its primary cause ceases to act. When resolution occurs, the emi- 
gration of leucocytes ceases, the serous fluid disappears, and the fibrin 
and the cell elements, after they have undergone molecular change, are 
absorbed. 

A second variety of inflammation of serous membranes is characterized by 

the production of new connec- 
tive-tissue cells either with or 
without a sero-purulent exuda- 
tion. It may be an acute or 
chronic process. The inflamed 
membrane becomes thickened, 
and there is abundant cell de- 
velopment in its substance and 
on its surface. If the inflamma- 
tory process is prolonged, or if the 
membrane becomes very much 
thickened, elevations are formed 
on the surface of the membrane, 
and thus adhesion takes place 
between opposing serous sur- 
faces, or the membrane be- 
comes thickened and indurated. 
If bands of adhesion form, they 
have the appearance of delicate 
membranes. This new tissue at 
first is exceedingly rich in capil- 
lary vessels, which are distin- 
guished from the normal capilla- 
ries of the membrane by their 
large calibre and # thin walls. As 
the new tissue contracts, it may 
shut off its own blood supply, 
and then undergo fatty change 
and be absorbed, leaving no 
trace of its existence. 
Second: Mucous Surfaces— Inflammation affecting mucous membranes 
may be either catarrhal, croupous, or diphtheritic. Catarrhal mucous 
inflammations are either acute, sub-acute, or chronic. In the acute variety 
the affected mucous membrane, at the very beginning of the process, is 
congested and dryer than normal, the functional activity of the mucous 
glands being diminished. After a time an abnormal quantity of mucus is 
poured out on its surface, the result of an increase in the functional 
activity of the glands. This mucus may be thicker or thinner than 
normal, and may have an acrid or irritating quality. Mucous exudations 




Fig. 4. 

Inflammation of Mucous Membrane. 

Vertical section of nasal septum. 

a. Pus corpuscles and degenerating epithelium on the 
free surface. 

b. Superficial layers of epithelium, 
c Sub-epithelial tissue. 

In the submucous tissue beneath the last will be seen— 
ff 0 <7> Longitudinal and transversely divided arteries, 

increased in number and size, 
h h. Veins. 

i i. Portions of enlarged mucous glands, 
jj. Gland ducts. 

A portion of the cartilage of nasal septum is seen at (d), 
with its pterichrondrium (<?). x 200. After Thierf elder. 



INFLAMMATION OF FREE SURFACES. 



7 



do not coagulate, but adhere somewhat closely to the surface of the 
inflamed membrane ; these changes are accompanied by desquamation 
of the superficial epithelial cells. If the catarrh assumes a purulent 
character in addition to the above changes, the mucous surface assumes 
a darker and livid hue, and pus cells are developed both in the mucous 
membrane and in the deeper substance. The amount of pus will indicate 
the intensity and character of the inflammation. In some cases there 
are very few pus cells, in others the quantity of pus is very large, and the 
tissues are extensively infiltrated. In chronic catarrh the blood-vessels 
of the inflamed membrane are either increased in size and number, or 
they are less numerous and more swollen than normal, giving to the mem- 
brane a grayish appearance. The production of mucus will be increased 
or diminished, according as the functional activity of the mucous glands 
is increased or diminished. When it is diminished, the membrane assumes 
a dry and shining appearance. The stroma of the affected membrane 
may be hypertrophied or atrophied. The mucous glands may also undergo 
hypertrophy or atrophy. If their ducts become obstructed they may 
suffer cystic change ; superficial erosions sometimes occur from a rapid 
epithelial desquamation. 

Croupous Inflammation of Mucous Membranes. — In croupous inflammation, 
the hyperemia is more intense than in catarrhal, so that the mucous sur- 
face usually assumes a dark livid color and becomes swollen ; soon its free 
surface is covered with a fibrinous exudation, which takes the place of 
the epithelium, and lies upon the sub-epithelial structures in the form of 
a network or in irregular masses. Enclosed in its meshes are epithelial 
and pus cells ; it varies in thickness from an exceedingly thin semi-trans- 
parent membrane to one that may be an eighth of an inch in thickness. 
This membranous exudation may be limited to small patches, or extend 
over a large surface. At first it is firm in consistency, and adheres closely 
to the tissues which it covers ; afterward it becomes soft, and is easily 
separated from the subjacent membrane ; when fully formed it may be 
cast off m patches or shreds. Its separation is accomplished by the return- 
ing secretion of the follicles which have been obstructed, as well as by 
the serous effusion from the inflamed surface. It may sometimes undergo 
fatty, and more rarely a mucous degeneration, and so become a fluid re- 
sembling mucus- Generally in simple croupous inflammation the sub- 
mucous tissue is but slightly involved, and its meshes are rarely infiltrated. 

Diphtheritic Inflammation of Mucous Surfaces. — By some this is regarded as 
identical in character with croupous. It differs from it in a more intense 
hyperemia, and a more extensive infiltration of the affected tissue. The 
fibrinous exudation is more abundant and granular, and there is a greater 
metamorphosis of the epithelial and tissue cells. The membranous exuda- 
tion seems to be a part of the mucous and sub-mucous tissues, and cannot 
be removed without the loss of their substance. In the surface exudation, 
and in the infiltrated tissues underlying it, are found multitudes of bacteria, 
especially the micrococci. When the mucous and sub-mucous tissues are 
so infiltrated as to cause undue pressure, and to cut off their nutritive sup- 



8 



INFLAMMATION". 




ply, the affected tissue dies and sloughs away. Between simple croupous 
and diphtheritic exudation there is every possible gradation. Some claim 

that the fibrinous de- 
£f $ generation of the epi- 

thelial cells is the 
cource of the diphthe- 
ritic exudation ; 
nearly all agree that 
the primary changes 
are epithelial. This 
form of inflammation 
must be regarded as 
the local expression of 
a constitutional affec- 
tion. 

Ulceration of Mucous 
Surfaces. — N e c r o t i c 

processes may be the 
result of intense puru- 
lent catarrhs or diph- 
theritic inflamma- 
tions of mucous sur- 
faces. Superficial 
loss of substance from 
rapid epithelial degen- 
eration, and ulcers formed by the bursting of small abscesses, are the chief 
varieties of necrosis, except in those catarrhal inflammations where the 
blood supply is so suddenly and completely shut off that the mucous mem- 
brane dies in bulk and sloughs away (as in acute dysentery). Most of 
the little abscesses that produce ulceration of mucous surfaces are due 
to obstruction of the follicles and lymph structures that lie in the sub- 
stance of the membrane ; in consequence of their obstruction their con- 
tents degenerate, an abscess is formed, and an ulcer is the result. 

Parenchymatous Inflammation. — In parenchymatous inflammation, the 
cells which perform the functions of the organ, the blood-vessels, and the 
stroma are in a greater or less degree involved in the inflammatory process ; 
and this may pursue an acute or chronic course. In a mild type of paren- 
chymatous inflammation the cells are enlarged, granular, and opaque, and 
their functional activity is increased, the blood-vessels contain more than 
their normal quantity of blood, and the stroma is infiltrated with serum. 
The affected organ is slightly increased in bulk, but returns to its normal 
size if the inflammation terminates by resolution. If the inflammatory 
process is very intense and prolonged, the cells are destroyed, the circula- 
tion is checked or arrested, and the stroma is extensively infiltrated with 
serum and pus. The inflamed organ is greatly increased in size, assumes 
a livid or purple hue, and its functional activity is arrested. In chronic 
parenchymatous inflammation the cells undergo fatty degeneration and 



Diphtheritic Inflammation of Mucous Membrane. 

Section through the uvula. 

a, Normal epithelium ; b, normal areolar tissue ; c, necrosed epithelium 
transformed into a coarse mesh-work ; d, areolar tissue infiltrated with 
fibrin and leucocytes ; <?, blood-vessels ; /, hemorrhage ; g, heaps of mi- 
crococci, x 75.— After Zeigler. 



HYPERTROPHY. 



9 



disintegration. The walls of the vessels Undergo extensive thickening, 
their calibre is diminished, and they may be obliterated. The stroma is 
increased by the development of new tissue. The function of the affected 
organ is impaired, and never returns to its normal condition, as the result- 
ing changes are permanent. 

In interstitial inflammation the connective-tissue or stroma of the organ 
in the part involved is affected. If the inflammation is acute, it is usually 
suppurative. The pus formation may be limited to small areas, or it may 
be diffused. When the pus cells are few, resolution is possible, but if they 
are numerous and infiltrate a large area of the organ, abscesses are formed 
with dense, firm walls. If the inflammation is chronic, it ends in indura- 
tion and cirrhosis, by the formation of new connective-tissue, but does not 
form pus. The new tissue corresponds in kind to the original stroma of 
the organ, and is permanent. The affected organ never returns to its nor- 
mal condition. 

Fate of Pus. — Pus may undergo absorption, be evacuated, become inspis- 
sated, or undergo caseous transformation. To be absorbed it must undergo 
fatty degeneration and become converted into granular matter ; its absorp- 
tion is accomplished by the lymphatics. Its evacuation is accomplished by 
an ulcerative process, established in the tissues which contain it. When 
it has been converted partly into fatty and partly into granular matter, it 
may become inspissated by the absorption of its liquid portion and remain 
unchanged for a long period. If it becomes incapsulated, it changes into 
caseous matter and remains as a cheesy mass. 



HYPERTROPHY. 

Hypertrophy is an enlargement of an organ or tissue, due either to an 
increase in the size of its elements or to an increase in their number. The 
former is called simple hypertrophy, and the latter numerical hypertrophy 
or hyperplasia. 

In most cases of hypertrophy these two forms are found associated. 

Examples of physiological hypertrophy are the enlargement of the uterus 
during pregnancy ; the increase in the size of the mammary gland in cer- 
tain uterine changes ; the hypertrophy of the prostate in old men, and the 
increase in size of muscles following persistent exercise. 

Causes of Hypertrophy. — 1. Increased functional activity is a prominent 
cause of hypertrophy, as is shown in the heart when called upon to per- 
form extra work in overcoming obstructions at its orifices, or an impeded 
circulation from obliterating changes in the arteries. 

Also in long-continued obstruction to the outflow of urine from the 
bladder, requiring an increase of force to overcome the obstruction, the 
muscular coat of the bladder becomes hypertrophied, and in the same way 
the coats of the stomach and intestines become hypertrophied above old 
obstructions. 

Hypertrophy of one kidney after removal or destruction of the other 



10 



ATROPHY. 



is the result of enforced functional activity thrown upon the remaining 
organ to enable it to carry on the normal elimination. All these are 
examples of what may be called conservative hypertrophy. 

2. Increased supply of nutrition caused by augmented blood supply is 
a less frequent cause of hypertrophy. The formation of the corpus 
luteum of pregnancy, in contradistinction to what is known as the " false 
corpus luteum," is possibly the best example of this. The hypertrophy of 
the cheeks and nose, as seen in acne rosacea, is another illustration. 

On account of the excessive amount of blood which surrounds areas of 
long-continued inflammation, there is often an excessive outgrowth of 
tissue. This is seen in the well-marked hypertrophy of bone which follows 
inflammation of the periosteum. Another example is the rapid outgrowth 
of hair in the neighborhood of ulcers and diseased joints. 

3. A partial arrest or delay of the normal retrograde changes in tissues 
may equally result in hypertrophy when the nutritive changes are not 
lessened. Many cases of obesity are thus induced. 



ATROPHY. 

Atrophy is either a diminution in the size of the histological elements 
of a part, or a decrease in their number. The former is called simple and 
the latter numerical atrophy. 

Simple atrop>hy occurs in ordinary emaciation, which affects first the sub- 
cutaneous adipose tissue, then the muscles, omentum, intestines, heart, and 
last of all the brain and skeleton. The fat is removed from the cells more 
or less completely, and they diminish in size, their walls and nuclei becom- 
ing more distinct. This process is a physiological one in certain tissues 
and organs, especially in those which have only a temporary function, as the 
supra-renal capsules, mammae, female genital organs, and thymus gland. 

In all pathological forms the simple atrophic tissue elements remain 
unchanged except in size. Degenerative changes are sometimes associated 
with this form of atrophy. 

Numerical Atrophy. — In numerical atrophy the elements of an organ or 
tissue are diminished, not only in size, but in number. Gradually, isolated 
elements or groups of elements of a part become involved. In many 
respects this change is quite as important as necrosis, and very much more 
so than simple atrophy, for it involves absolute loss of tissue, a loss which 
cannot be restored except by the production of new elements, which is 
very seldom, if ever, possible. 

Atrophied organs are firmer and more anaemic than normal. 

The causes of atrophy may be either general or local. 

General atrophy may be due — 

First. To deficient supply of nutritive material. 

Second. To excessive waste. 

Third. To impaired nutritive activity. 

Deficient supply of nutritive material is present in cases of gradual 



DEGENERATIONS. 11 

starvation, in obstruction in the alimentary canal (as occurs in cancer of 
the pylorus), in mal-assimilation due to diseases of the alimentary tissues, 
obstruction of the thoracic duct or lacteals, or disease of the mesenteric 
glands. 

Excessive waste is the exciting cause when it is due to prolonged hemor- 
rhages, suppurations, diarrhoeas, and the excessive loss of albumen or sugar. 

Impaired nutritive activity is an accompaniment of senile atrophy, where 
the vitality of the tissues gradually diminishes, and they become less able to 
assimilate the nutritive material brought to them by the blood. 

Sometimes general atrophy results from a combination of these causes, 
as occurs in chronic phthisis. 

The causes of partial atrophy are — 
First. Insufficient supply of blood. 
Second. Diminished functional activity. 
Third. Excessive functional activity. 
Fourth. Nervous influence. 

Insufficient supply of blood may be due to partial obstruction of an 
artery by pressure of a tumor, by the contraction of new connective- 
tissue on the smaller vessels, the result of an inflammatory process. 
Pressure upon the skull in hydrocephalus, upon bone by an aneurism, 
are also examples of local atrophy from pressure. 

Local or partial atrophy from diminished functional activity may be 
physiological or pathological. Examples of physiological atrophy are 
furnished by those parts which have a use only at certain periods of 
life, such as the ductus arteriosus, umbilical vessels, thymus gland, the 
mammae, the female sexual organs, and the jaw after the falling of the 
teeth. Pathological examines of atrophy depending upon diminished func- 
tional activity are seen in the wasting of muscles after paralysis, disloca- 
tions, anchylosis, or chronic disease of bone or joints, and in the rectum 
after establishment of an artificial anus. 

Examples of local atrophy from excessive functional activity are seen in 
the class of hyperkinetic diseases, of which writer's cramp, acute cardiac 
dilatation from violent exercise, and atrophy of the testicles from sexual 
excesses are examples. 

Nervous Influence. — Muscles which have been cut off from their trophic 
nerves, as in hemiplegia after injury of the anterior cornua, show atrophy 
depending upon this cause. The atrophy of the muscles which occurs 
after degeneration of the nerve-cells in the anterior horn of the spinal 
cord is also an example. It has also been proven that nerve fibres which 
are cut off from their ganglia all soon atrophy. 



DEGENERATIONS. 

The tissues of the body may undergo certain morbid processes charac- 
terized by alteration in their quality. They degenerate, and, as it were, 
take a step backward in their development. 



12 



DEGENERATIONS. 



These changes may lead to an impairment of their function, and often 
to a complete destruction of their elements. 

The term degeneration, in its strict sense, is synonymous with meta- 
morphosis, and implies a direct transformation of the albuminous elements 
of the tissues into a new material. 

It is often used, in a broad sense, to include infiltration ; but, strictly 
speaking, infiltratioDs are characterized by the introduction into the tissues 
of a new material brought from without. 

There are certain prominent type's of degenerative changes whose histo- 
logical characteristics are much the same wherever they occur. All struc- 
tures of the body are more or less liable to them ; so that when one is famil- 
iar with one of these types of degeneration in one tissue, he is practically 
familiar with it in every tissue of the body, and has only to recall the histo- 
logical elements of a part, to understand the changes in any particular 
degeneration. 



TABLE OF DEGENERATIVE PROCESSES AND INFILTRATIONS. 



Parenchymatous. . 
Fatty 



Natuke of Process. 



Degeneration. 
Infiltration . . 



Degeneration 

Degeneration 
Degeneration 

Deposit 

Deposit 

Infiltration . 



Parts Affected. 



Epithelium, muscle 

j Gland cells, connec- \ 
\ tive tissue. \ 

( Gland cells, coats of 
< small arteries, mus- 

( cle. 

Epithelial cells 

Connective-tissue 

Connective-tissue, epi 
thelium. 

(Normal situations, 
| seats of hemorrhage 

Blood-vessels 



Cause. 



Fever, poisons, etc. 
Imperfect oxidation. 

Impairment of quality 
or quantity of blood, 
etc. 

Unknown. 

Unknown. 

f 1. Excess of salts in the 
J blood. 

1 2. Anaemic and atrophic 
[_ tissues. 

Hemorrhage, stasis, ca- 
chexias, 
j Syphilis, prolonged sup- 
( puration. 



PARENCHYMATOUS DEGENERATION. 

{Cloudy Swelling.) 

Parenchymatous degeneration consists in an alteration of the anatomical 
elements of the body, especially the epithelial cells and muscle fibres, so 
that they appear swollen, cloudy, and filled with minute granules which 
look like fat granules, but differ from them in being soluble in acetic 
acid. 

This condition has also been called albuminous, serous, and granular 
degeneration. The name cloudy swelling is the one by which it is now 
generally designated. 



FATTY INFILTKATIOtf. 



13 



The parenchymatous cells of the glandular organs — as the liver and 
kidneys — are especially liable to be affected with this change. The 
organ becomes enlarged and of a pale color. If a microscopic exam- 
ination is made, the cells appear swollen and opaque ; the body of the 
cell is filled with albuminous granules, which give the appearance as if 
the cell was sprinkled with fine sand. 
The normal markings of the cell 
are lost, and the nucleus is obscured. 
Slight grades of this form of degen- 
eration are very difficult to appreci- 
ate, for many of the cells are normally 
granular, and we must not forget 
that all cells after death become 
somewhat granular. A cell which 
has undergone this form of degen- 
eration is not necessarily destroyed ; 
if the change is only transitory, the 
cell may return to its normal con- 
dition. As a result of this form of 
degeneration the cardiac muscle and 
the muscles of the skeleton undergo 
exactly the same change as the epi- 
thelial cells. 

Parenchymatous degeneration occurs in most febrile diseases, especially 
the specific fevers, as pyaemia, diphtheria, scarlet fever, typhus, and 
typhoid fevers. 

It is also seen after poisoning by arsenic, phosphorus, and the mineral 
acids. 

High temperature was at one time supposed to cause it, but this has 
lately been abundantly disproven. This form of degeneration was at first 
supposed to represent the first stage of inflammation, and hence was called 
parenchymatous degeneration. While in a certain number of cases it may 
be considered as the result of the action on epithelial cells of the same 
influence which, acting upon the blood-vessels and connective-tissue, pro- 
duces hyperemia, exudation, and cell proliferation, still, in the majority 
of cases it cannot be considered a true inflammatory process. 



FATTY IINTILTKATION". 

In fatty infiltration, fat is deposited within the cells of a tissue in the 
form of distinct drops. 

In the earlier stages the drops are small, but as they increase in number 
they run together, and larger drops are formed, which gradually displace 
the nucleus of the cell and obscure more or less of its protoplasm. The 
vitality and function of the cell is but little impaired by the accumulation 
of fat ; and the protoplasm, although compressed by the fat globule, is 




Fig. 6. 
Cloudy Swelling of Cells. 

a, Normal epithelium. 
6, Commencing cloudy swelling. 
o, d, Cells in extreme degeneration. 



14 



DEGENERATIONS. 



still unaltered, and quickly assumes its normal condition when the fat is 
removed. 

Fatty infiltration is a normal physiological process under certain condi- 
tions, as during the growth of adipose tissue, or in the liver cells during 

the process of digestion. More or less 
fatty infiltration takes place in the liver of 
many healthy persons after a hearty meal, 
but in a few hours the fat is "burnt up," 
or oxidized, and the liver cells return to 
their normal condition. 

When for any reason the fat is not com- 
pletely oxidized, then it collects in the tis- 
sues. This occurs under two opposite 
conditions : the one associated with gen- 
eral obesity, where an excess of fat, or 
substances capable of being converted into 
fat, are taken into the system, while the 
amount of oxygen received is insufficient 
to oxidize the excess, and it consequently 
accumulates in the cells ; the other, in 
which there is general emaciation and a 
consequent impairment of the oxygenating power of the blood. As a 
result of this imperfect oxidation the fat contained in the food is incom- 
pletely oxidized, and so accumulated. This is well illustrated by the fatty 
infiltration often present in chronic phthisis. Fatty infiltration usually 
begins and is most marked in those cellular elements which are adjacent 
to the radicles of the nutrient vessels. 




Fig. 7. 

Fatty Infiltration of Liver Cells. 

«, b, Early stages. 

c, Nucleus of cell displaced by fat glob 

ule. 

d, Cells completely filled by fat globule. 



FATTY DEGENERATION. 

This differs from fatty infiltration in that the fat is derived from the 
albuminous constituents of the tissues themselves. 

It is a far more serious process, as it ends in the destruction of the cells ; 
and, there being no provision for the production of new cells, the loss is a 
permanent one. 

The fat makes its appearance as minute globules or granules in the 
protoplasm of the cell, the cell itself furnishing the fat from its own sub- 
stance, and in time the cell is converted into a mass of granular fat, and 
is destroyed. In fatty infiltration the protoplasm is displaced by the 
fat which is deposited in the cell, but it does not suffer materially in 
its integrity ; remove the fat, and the cell returns to its normal condi- 
tion. 

As, in fatty infiltration, the well-known physiological deposit of fat in 
the cells of the liver during digestion furnished a type of what might 
become a pathological process, so in fatty degeneration the secretion of 
milk illustrates a fatty degeneration which is perfectly normal. The 



COLLOID DEGENERATION. 



15 



young cells in the acini of the mammary gland become converted into fat, 
they break up, and the fatty matter constitutes the milk corpuscles. 

Fatty degeneration depends upon all those conditions which interfere 
with the quality of the blood, so that the tissues are imperfectly nourished ; 
as a result there is an interference with the oxidizing process in the cell, 
which loses its vitality and undergoes this form of 
degeneration. The diseases in which this change is 
apt to occur are, acute yellow atrophy of the liver, 
chronic alcoholism, progressive pernicious anaemia, 
and pulmonary phthisis. 

It is also seen in poisoning by phosphorus, arsenic, 
and antimony. 

The tissues which are most commonly the seat of 
fatty degeneration when it depends upon a general 
condition are the liver, kidneys, glands, heart, walls 
of the arteries, and voluntary muscles. 

When the cause of this degeneration is local, it 
is due generally to an insufficient supply of blood 
to a part, as would result from narrowing of the nutrient blood-vessels. 
This is well seen in the heart, as the result of atheromatous changes in 
the coronary arteries. Nerves which have been separated from their nerve- 
centres undergo this degeneration. Organs and tissues which have been 
long disused, and in which, consequently, the quantity of circulating 
blood is diminished, also undergo fatty degeneration. 

This change is often seen in the tissues of old persons, especially in the 
cartilages, the walls of the arteries, the edge of the cornea (arcus senilis) 
and the lens (cataract). Cerebral softening is only fatty degeneration of 
brain tissue, caused by the cutting off of the normal blood-supply to the 
softened part. 




Fatty Degeneration of 
Cardiac Muscle. 



COLLOID DEGENERATION. 



Colloid degeneration is closely allied to mucoid, but differs from it in 
affecting principally the epithelial cells. The cells become filled with 
colloid material, which is derived from their substance. This material 
appears at first as minute spherules in the body of the cells, but eventually 
it escapes or is set free by the breaking down of the cells, and then the 
globules coalesce and form colloid masses. 

Colloid matter resembles mucine, but differs from it. It is more dense, 
contains sulphur, and is not precipitated by acetic acid. 

As a physiological process, colloid material is deposited in the thyroid 
gland, especially in the aged. When there is a large accumulation of this 
material in the follicles of the gland, then a goitre is formed. 

Colloid change is met with in lymphatic glands, in the tubules of altered 
kidneys, in the choroid plexus, and in certain new growths, as compound 
ovarian cysts and colloid cancers. 

The cause of this change is unknown. 



1G 



DEGENERATIONS. 



MUCOID DEGENERATION. 

Mucoid degeneration consists in a transformation of the albuminous 
elements of the tissues into a transparent, homogeneous, colorless, jelly- 
like material called mucine. 

Mucine is closely allied to albumen. Like albumen it is coagulated by 
acetic acid, but differs from it in not being redissolved by an excess of the 
acid, and in not containing sulphur. Mucoid change has its physiological 
prototype in the secretion of mucus by the goblet-cells of mucous mem- 
branes and the epithelium of certain mucous glands. The material is 
formed by metabolism from protoplasm of the cells. 

Mucoid degeneration affects both cells and intercellular substance. 

In epithelial structures mucoid degeneration can hardly be called a 
pathological process. In any catarrh of a mucous surface there will be 
found in the secretion cells which have undergone this degeneration. 

Fibrous tissue is especially liable to undergo mucoid degeneration, and 
the albuminous intercellular substance is replaced by mucoid material. 
This is a return of the tissues to their foetal elements, for mucine is found 
distributed in foetal structures. 

Mucoid degeneration is frequently met with in the intervertebral and 
costal cartilages of old people, in certain tumors, in bone, and in the 
disease known as myxcedema. 

The causes of this degeneration are unknown. 

CALCAREOUS DEGENERATION. 

(Calcification.) 

This form of degeneration is characterized by an infiltration in the 
tissues of calcareous particles composed mainly of lime and magnesia salts. 
It occurs physiologically in the formation of the bones of the skeleton, 
preceding actual ossification, and also in the formation of a deer's-horn. 
It is often confounded with ossification, but must be distinguished from it, 
for it never results in the formation of true bone. 

The degeneration is common in old age in the coats of the arteries. 

Tissues which have undergone calcareous degeneration are rendered hard 
and gritty. When tbe process has not advanced very far, the tissues feel 
as if they had been sprinkled with sand, as the deposit occurs in the form 
of irregular granules. 'At a later stage large masses are formed of a 
gray or whitish color, the result of an increase in the number and size of 
these granules. Under the microscope the affected tissue appears as an 
opaque mass in which no trace of structure can be distinguished, or at an 
early period the tissue and cells can be recognized, filled with small dark 
particles. If the tissue be treated with dilute hydrochloric acid, the salts 
dissolve, bubbles of carbonic acid gas appear, and the original structure of 
the part may be recognized. 



PIGMEXTATI0J5". 



17 



The deposit occurs first and most abundantly in the intercellular tissue ; 
afterwards the epithelial cells are involved. 

The effect of this degeneration is to destroy the life of the part, which 
remains as an inert mass ; but the histological structure of the part is not 
destroyed ; the calcified cells remain, but they are dead ; no further change 
occurs, and there is no softening. In these respects it differs from fatty 
degeneration, and is in fact a favorable termination of the latter. 

The results of this change are very serious when it occurs in the arteries, 
for it destroys their elasticity and leads to rupture and aneurism ; so also 
when it takes place in the valves of the heart. 

It occurs as a conservative process when it checks the growth of tumors 
and renders pathological products inert, as is often seen in the lungs in a 
case of arrested phthisis. 

Calcareous degeneration may occur under two conditions. 

1. When there is an excess of salts in the blood. 2. When there is 
no such excess, and the deposit takes place when certain alterations have 
occurred in the blood or tissues. 

The first is by far the least frequent ; it occurs in certain forms of soft- 
ening of bone, osteomalacia, and extensive caries. Apparently as the bone 
breaks down, its salts are taken up by the blood and deposited in other 
places. In such cases it is usually quite general, involving the kidneys, 
lungs, dura mater, liver, stomach, and intestines. 

In the second it is local and due apparently to a diminution of vitality in 
the tissues by which the normal relation between the tissues and the small 
amount of calcareous salts in the blood is destroyed. 

Atrophic and retrogressive processes are apt to be accompanied by it. 

The favorite seats of calcific deposits are tumors, in and about parasites, 
old blood clots in veins, cheesy deposits, false membranes, and other patho- 
logical products. 

PIGMEOTATTOI*. 

Pigmentation is characterized by the presence in the tissues of a colored 
substance, amorphous or crystalline, which is derived from the coloring 
matter of the blood. 

Normal pigmentation occurs in the choroid, rete mucosum, and in some 
motor cells of the cerebral peduncles. 

An absence of this normal pigment is seen in albinos ; an increase in 
Addison's disease, freckles, melanotic tumors, and brown atrophy of 
muscle. 

Pathological pigmentation follows the extravasation of red blood-corpus- 
cles, and the escape of their coloring matter, w r hich may also be liberated 
from the corpuscles while in the vessels. 

This coloring matter (haemoglobin) infiltrates the tissues and stains 
both the cells and intercellular substance. It becomes converted into 
haematoidin, and appears as minute yellow and reddish-brown granules, 
or as orange-colored needles and rhombic prisms. 
2 



18 



DEGENERATIONS. 



Pigmentation occurs in most cachectic conditions ; especially in chronic 
malarial poisoning by a destruction of the corpuscles in the blood. Local 
causes are rupture of small vessels, and those which cause obstruction to 
the flow of the blood and. favor diapedesis of the red blood-corpuscles, as 
in a nutmeg liver and brown induration of the lungs, dependent upon 
heart disease. 

The staining of the tissues yellow with the coloring matter of the bile, 
as occurs in "jaundice," is not true pigmentation. 

Pigmentation may follow the introduction of extraneous substances into 
the body, as occurs in the lungs by the inhalation of coal dust, soot, and 
particles of iron, and in the skin and lymphatic glands by tattooing. 

AMYLOID DEGENERATION. 

This form of degeneration is characterized by the presence in the tissues 
of a homogeneous, structureless, translucent substance, differing but little 
from albumen, and giving peculiar reactions with certain staining reagents. 

Iodine in solution gives it 
a mahogany brown color ; io- 
dine and sulphuric acid a blue 
color ; methyl blue, and gen- 
tian violet a bright red or pink 
color. 

The nature of this material 
is still in dispute. Virchow 
held it was starchlike, and gave 
it the name "amyloid ;" other 
writers, from its resemblance 
to wax or lard, have called 
this change " waxy " or " lar- 
daceous " degeneration. 

Amyloid material is an al- 
buminoid rich in nitrogen, and 
is in all probability derived 
from the fibrin of the blood 
by direct metamorphosis (amy- 
loid reaction having been ob- 
tained in the fibrin of a nasma- 
tocele). As this material is 
found in its earliest stage in 
close proximity to the blood-vessels, it in all probability soaks out from 
the blood into the tissues and is in reality an infiltration. 

The change is a pathological one. There is no physiological analogue 
unless we consider senile changes physiological, for amyloid degeneration 
is an almost constant accompaniment of senility, in the cartilages of joints, 
especially the sterno-clavicular and vertebral. 




Fig. 9. 



Amyloid Degeneration of Kidney. 

a, Normal capillary loop. 

b, Amyloid capillary loop. 

c, Normal epithelium in tube. 

d, Hyaline tube cast. 

e, Amyloid arteriole. 

f, Amyloid capillar;/. 

g, Loosened fatty epithelium, x 300. 



NECROSIS. 



19 



Under other more strictly pathological circumstances, amyloid degenera- 
tion may involve almost every kind of tissue ; but the change shows itself 
at first always in the walls of the capillaries and the small arteries. 

They become thickened, have a homogeneous look, and their lumen is 
diminished. Not every vessel is affected, nor is the change regularly dis- 
tributed over the same vessel. In time, as the process advances, the con- 
nective-tissne may become involved, and last of all, and this but seldom, 
the epithelial cells may show this change. 

Amyloid degeneration may be local, but usually a number of organs are 
affected at the same time. 

The affected organ is enlarged, and heavier (denser) than normal, its cap- 
snJe is tense, its borders rounded, its surface paler and dryer than normal, 
and of a grayish appearance. 

The organs which are most frequently affected with this change, in the 
order of their frequency, are the spleen (sago-spleen), kidneys, liver, lym- 
phatic glands, mucous membrane of the stomach and intestines, and occa- 
sionally the pancreas, thyroid, lungs, ovaries, and supra-renal capsules. 

Although this degeneration is a constant accompaniment of old age, it 
occurs pathologically principally between the ages of twenty and forty. It 
depends upon some nutritive disturbance, and in a large proportion of 
cases is associated with prolonged suppuration of bone (out of 96 cases 
examined by Wilks, bone suppuration existed in 68 and had been present 
in 17 others). 

It is common in persons suffering from certain cachexias. Pulmonary 
phthisis is one of its most common antecedents. Syphilis and chronic 
malaria are apt to lead to it. 

The prognosis of the disease is very unfavorable, and, considering the 
resistance of this substance to all reagents, it seems improbable that we 
shall ever be able to combat it successfully. 

Corpora amylacea are concretions which have been supposed to be identi- 
cal with amyloid material ; they give the same color-reaction with iodine, 
and with iodine and sulphuric acid. It is now known that they have no 
relation to amyloid degeneration, and are of no special significance. They 
are hard, stratified concretions found in the prostate, seminal vesicles, and 
in the central nervous system, and are very common in the aged. 



NECROSIS. 

Necrosis is a term applied to the death of a portion of the body. In the 
soft tissues the process is mortification, and the dead tissue a slough. 

As soon as a tissue dies, it becomes subject to the conditions of inorganic 
bodies. Its materials are held together only by cohesion, and that cohesion 
usually yields promptly to the forces of decomposition due to the action 
of a ferment generated by certain bacteria. When the entire body dies, 
its component parts are no longer capable of taking up new material and 
changing it into living tissue ; as a result the body is unable to resist 



20 



DEGENERATIONS. 



decomposition, and this inability is made manifest when the first symp- 
toms of dissolution appear. All the elements of the body do not lose 
their vitality at the same time ; as a rule the epithelial cells die sooner 
than the connective-tissue framework. When a part of a living body 
dies (necrosis), it undergoes similar changes to those occurring after 
death of the whole body, being modified only by the locality in which it 
occurs. 

The causes of necrosis are : 

1. Arrest of blood supply, caused by obstruction in the arteries, veins, or 
capillaries, — in the arteries by ligature, compression, embolism, thrombosis ; 
in the veins principally by pressure or thrombosis ; but the anastomoses 
are so free in the veins that death of the part seldom occurs from this 
cause alone. Obstruction in the capillaries is much more serious ; for 
when complete capillary stasis occurs, — as from pressure or diminished 
heart power, — the vitality of the capillary walls is destroyed, and necrosis 
results. 

2. Direct Injuries to the Cells.— Such injuries are : 

a. Mechanical, as chemical corrosives, crushing, and animal poisons. 

b. Bacteria, setting up septic processes, as from putrid pus, dead tissue, 
decomposing urine, etc. 

3. Abnormal Temperatures. — All changes which cause slight increase or 
decrease of temperature produce inflammation, but when the variations of 
temperature are excessive, necrosis is the result : this is seen after frost- 
bites or a burn. 

The above causes of necrosis do not always act singly, but are often 
combined ; for example, in a part which is imperfectly supplied with blood, 
only a slight injury to the cells may cause necrosis ; or, again, let the vitality 
of the tissues be weakened by an extreme cachexia, and a slight interference 
with the blood supply will cause necrosis. An illustration of the first is 
seen in senile gangrene, and of the second in gangrene in children (noma), 
Certain general pathological conditions may so lower the vitality of the 
whole body that slight causes will produce necrosis. This is illustrated 
by the sloughing bed-sores which form in adynamic fevers and exhausting 
diseases on parts of the body exposed to pressure, and in the liability 
to senile gangrene, which is increased by the diminished heart power and 
arterial changes that accompany old age. 

The rapidly forming bed-sores which result from injury to the spinal 
cord are regarded by some as due to special trophic changes, but it seems 
more probable that they are the result of a general vaso-motor disturbance, 
which produces paralytic hyperemia, and so necrosis. 

Varieties of Necrosis. — Restricting the term " necrosis " to a local death 
of tissue, the following varieties are met with : 

1. Dry Gangrene or Mummification. — If tissues that are the seat of this 
change contain little water, and are composed largely of earthy matters, 
they may preserve their outline and appearance for a long time. If the 
water contained in them evaporates rapidly, they shrivel and become 
hard. 



TUBERCLE. 21 

2. Moist Gangrene. — Tissues that are the seat of this variety of necrosis 
undergo putrefaction, and, as the evaporation of the water contained in 
them is prevented, they are moist, soft, and doughy, and in time gases are 
formed, and their color becomes dark. Such changes are similar to those 
that occur in the body after death. Moist gangrene always has its seat in 
parts which are exposed to the air. 

3. Hospital Gangrene. — This is a progressive necrosis which affects 
wounds, and is due to a special micro-organism (septic). 

4. Senile Gangrene. — It affects the aged, and is due to an impeded cir- 
culation from atheromatous, or calcareous changes in the arteries. 

5. Coagulation Necrosis. — In this variety of necrosis the cells of a tissue 
undergo a change analogous to the coagulation of the fibrin of the blood. 
Their protoplasm becomes rigid and converted into a homogeneous hyaline 
substance ; their nuclei disappear, and finally the cell breaks up into a 
granular-looking debris. Coagulation necrosis may affect entire organs, 
or portions of organs or cells. It occurs in infarctions, tubercular nodules, 
tumors, waxy degeneration of muscles, and in diphtheria, typhoid and 
relapsing fevers. 

The terminations of necrosis, when putrefaction is absent, are : 

1. Liquefaction. — In tissues where there is an abundance of liquid, 
and its removal is prevented by non-evaporation, or the action of the 
lymphatics is imperfect, the softened tissue becomes converted into a thick 
creamy fluid. This occurs especially in brain necrosis, and in the soften- 
ing of infarctions and thrombi. 

2. Caseation. — This is a change which results in the formation of a 
more or less dry, whitish-yellow mass resembling cheese. It is met with 
most frequently in encapsulated collections of pus, in tubercular masses, 
and in inflammatory products of low vitality. As the cell elements of such 
masses die, their watery portions are absorbed, they become granular and 
dry up. The fat contained in them becomes partly saponified, and crys- 
tals of cholestrine are deposited. If there are any cells which have not 
been entirely destroyed, they shrivel and atrophy. This cheesy change is 
not always a final one, for the cheesy mass may become calcified, calca- 
reous matter (lime salts) being deposited in and about it. The physical 
organism behaves towards all necrotic tissues the same as it does towards 
foreign bodies. If possible, it removes them ; when unable to do this, it 
surrounds them with a fibrous capsule and so renders them inert. 



TUBERCLE. 

To-day experimental research teaches that tubercle is the result of an 
infectious inflammatory process, and that the infection which excites the 
inflammation is a specific vegetable parasite, the "tubercle bacillus," 
which gains entrance into the body through the respiratory and digestive 
tract, rarely through the geni to-urinary passages or wounds of the skin. 

Wherever the bacillus lodges and finds conditions suitable for its develop- 



,22 



TUBERCLE. 



ment and multiplication, there are found in a short time small, gray, 
translucent nodules, looking like particles of coarse sand, which are called 
miliary tubercles. If a tubercle is examined microscopically before any 
degenerative changes have taken place, it will be found to be composed of 
a reticulated basement substance, lymphoid, epithelioid and giant cells 
arranged in the following manner : near its centre are one or more large 
branching cells, the processes of which blend with the surrounding growth. 
These are the giant cells, which have a homogeneous cell body and a 
number of nuclei arranged around the periphery like a belt or ring ; sur- 
rounding these giant cells are a large number of epithelioid cells with 
single nuclei, packed so closely together that it is almost impossible to 
distinguish individual cells. Beyond these cells, as one looks towards the 

periphery of the nodule, is seen 
a large number of lymphoid 
cells. These three varieties of 
cells are enclosed and supported 
by a fine reticular stroma, sim- 
ilar to that of a lymphatic 
gland. The explanation of the 
formation of a tubercle is as 
follows : The tubercle bacillus, 
acting as a specific poison, sets 
up an inflammatory process, 
which leads first to an accu- 
mulation of lymphoid cells 
with some proliferated fixed 
cells of the part ; some of the 
lymphoid cells change into epi- 
thelioid cells, and a few of the 
latter become giant cells by 
the enlargement of the cell 
body and a repeated division 
of their nucleus. Tubercles are non-vascular structures, no vessels have 
ever been found in them ; sometimes they start from the wall of a ves- 
sel, and often, in early growth, the remains of a partially obliterated 
vessel are seen in them, which has given rise to a dispute whether they 
were vascular or non-vascular growths. The changes which take place in 
tubercles are as follows : 

1st. They undergo caseous or cheesy degeneration. As they are non- 
vascular, their centres are shut off from nutrition, and as they are sub- 
jected to the necrotic action of the tubercle bacilli, in a short time they 
die and undergo what is called " coagulation necrosis," so that in old 
tubercles no cells can be found in the centre of the tubercular nodule. 
Just outside of the caseous centre will be found giant cells blended with a 
few epithelioid cells, while still further from the centre, constituting the 
peripheral zone of the nodule, are a large number of lymphoid cells. By 
special methods of staining the tubercle, bacilli may be found in the 




Fig. 10. 
Miliary Tubercle. 

a, Giant cell. 

b, Nuclei of giant cell. 

c, Ejrithelioid cells. 

d, Lymphoid cells. ; 



TUBERCULOSIS. 



23 



caseous centre and often in the giant cells. The ultimate change in a 
tubercle which has undergone caseous degeneration is disintegration with 
the formation of an irregular abscess cavity. If a number of miliary 
tubercles are united to form a tubercular mass, as is often seen in the 
lungs, the union of several of these small abscesses forms cavities of con- 
siderable size, in the walls of which are generally found a large number of 
tubercle bacilli. 

These cheesy masses may become encapsulated, calcified, and remain as 
inert masses for an indefinite period. 

2d. Tubercle may undergo fibroid change. The tissues which surround 
the tubercle taking on a chronic fibroid inflammation, the newly formed 
connective-tissue contracts, and, compressing the tubercle, converts it into 
a fibrous nodule. This change is most likely to occur in the aged, and in 
those of a strong fibrous diathesis. 

The characteristics of a typical tubercle may be briefly summarized as 
follows : First, a non-yascular nodular growth ; second, a growth com- 
posed of reticular basement substance and giant epithelioid and lymphoid 
cells ; third, this growth has a tendency to undergo coagulation necrosis 
due to its non-vascularity and the direct action of the tubercle bacillus ; 
fourth, the special and distinguishing characteristic of this growth is the 
tubercle bacillus. 

TUBEECULOSIS. 

We now understand, by the term tuberculosis, a diseased condition 
caused by the introduction into the body of tubercle bacilli. Its anatom- 
ical characteristic is the development of specific nodules. Its clinical 
characteristic is the consecutive invasion of one organ or of the entire 
system. 

Tuberculosis may be local or general : local, when it is limited, and 
gradually destroys the organ or tissue primarily involved, as occurs in 
tuberculosis of the lungs, kidney, liver, or peritoneum ; general, when large 
numbers of tubercle bacilli gain entrance into the general blood current, 
and in a few weeks develop in the various organs of the body a multitude 
of miliary tubercles, called acute miliary tuberculosis. 

It has been shown by experiments on animals that the tubercle bacilli 
and their spores are alone the infectious agent, and that they travel in the 
blood current ; and wherever they lodge, there the characteristic cellular 
changes take place, and a tubercle is developed. We consequently reach 
the conclusion that tuberculosis is an infectious disease, and that its cause 
is the tubercle bacillus. 

The danger of local tuberculosis is that it may become general ; for the 
first irruption of tubercles in the neighborhood of an existing tubercular 
focus is usually followed, sooner or later, by the appearance of nodules in 
the lymphatic system. It is in the glands that these tubercular irruptions 
are most intense ; generally the process makes a kind of halt in these 
gland stations, but in time spreads onwards, and at length reaches the 
thoracic duct, and through it the general blood current. 

We therefore conclude that tubercular infection may take place in the 



24 



BACTERIOLOGY. 



following way : First, by the blood, as when tubercular masses grow into 
the pulmonary veins. Second, by the lymphatic system. Third, by con- 
tinuity, as on the surface of mucous or serous membranes. Fourth, by 

the direct application of the 
- *W*^-'~ - bacilli to a part, as when a 

.^^^^^^H&j^fe^ * ^-—-^ tubercular mass is coughed 
£" 4 '---?V-~^ v *<l^ l ^^ 7 Z^r<^ up, and, before it can be ex- 

pectorated, falls back into an- 
i other bronchus, 
j At the present time the fol- 
j lowing questions in the pathol- 
j ogy of tuberculosis are being 
| discussed by scientists : 
j 1. Can man become infected 
j with tubercle by eating tuber- 
j cular meat, or by drinking the 
\ milk of tubercular cows ? 
j 2. May not the tubercle ba- 
- cilli contained in the sputum 
and other discharges from 
tubercular subjects be infect- 
ing agents, and thus render 
tuberculosis a contagious dis- 
ease ? 

3. As the tubercle bacilli 
preserve their vitality for a 
long time outside the body, 
may not those contained in the sputum of tubercular subjects, after the 
sputum is dried and becomes pulverized, be inhaled with the air as dust 
particles, and set up tubercular processes in the respiratory organs of non- 
tubercular subjects ? 

4. As a preventive measure for the spread of phthisis, should not the 
sputum and other discharges be burned or disinfected in their fresh state ? 

Accepting the doctrine that the tubercle bacillus is the only cause of 
tuberculosis, we are compelled to answer these questions affirmatively, and 
to say that the doctrine of heredity of tuberculosis must be abandoned, 
the tubercular taint being nothing more than a hereditary enfeeblement, 
which furnishes a better soil for the lodgment and development of the 
tubercle bacilli, or a physical condition which is less able to resist their 
invasion. 

BACTERIOLOGY. 

Bacteria are microscopic organisms belonging to the vegetable kingdom, 
whose characteristics are the absence of chlorophyl and their peculiar 
method of reproduction by transverse scission, or by means of small sphe- 
rules called spores. The science of bacteria is termed Bacteriology. 

To facilitate bacterial studies I shall divide the subject into four 
sections : 



|C : ; 



Fig. 11. 
Miliary Tubercles in the Liver. 

x 250 drawn by camera Ivcida. 

a, Miliary tubercle. 

b, Giant cells. 

c, Tubercle with cheesy centre. 

d, Normal liver cells. 




PATHOGENIC BACTERIA. 
PREPARED IN THE LOOMIS LABORATORY BY J.M.BYRON. M.D. 
PLATE DESCRIPTION SEE PACE XI i. 



TECHNOLOGY. 



26 



First. Their technology, or the consideration of the principal facts 
relating to cultures, staining, etc. 

Second. A consideration of their forms, dimensions, classification, etc. 

Third, Their biology, including their origin, nutrition, constitution, 
reproduction, and special action. 

Fourth. A description of those whose pathogenic action on man has 
been established. 

TECHNOLOGY. 

In order to study the life history of the different known organisms, pure 
cultures must be obtained. A pure culture is an artificial growth on 
nutrient media, of a single species of micro-organisms. 

Media. — Xutrient media are either artificial or natural. Natural media 
are obtained directly from man or animals, as blood serum, pleuritic fluid, 
hydrocele fluid, etc. 

Artificial media are prepared from different substances and in different 
ways. Media may be liquid or solid. 

All media must be sterilized before using for cultures; that is, they 
must be made free of all germs that by contamination may be contained in 
them. This is accomplished by subjecting the media several times to a 
temperature ranging from 50° C. to 120° C. 

All vessels and instruments used must be sterilized by heating in dry air 
to a temperature of 150° 0. for an hour. 

Natural Media. — Blood serum is obtained by leaving in a cool place, for 
twenty-four to forty-eight hours, the blood of an animal in a sterilized jar. 
The blood-corpuscles precipitate with the clot, and the clear serum is 
then transferred to tes.t tubes plugged with cotton- wool, which have been 
previously submitted to a dry temperature of 150° C. for an hour. The tubes 
and serum are then submitted during eight days — one hour every day — to a 
temperature of 50° C. If solid blood serum is desired, after the eighth day 
the tubes are transferred to the serum inspirator, and the temperature 
slowly raised to 70 cr 80° C, when the blood serum coagulates. Pleuritic 
and hydrocele fluids are treated in the same way. 

Potatoes and other vegetables, as well as eggs, can be used for cultures with 
advantage in some cases. They are sterilized by boiling them, or keeping 
them fifteen minutes a day, during three days, at a temperature of 100° C. 

Artificial Media. — Pasteur's, Cohn's, and other fluids classed as mineral 
media, are made by mixing certain salts and water. 

Bouillon is the principal ingredient used, either as a medium itself or in 
the preparation of the artificial media used in bacteriological culture. It 
is prepared by boiling one part of lean chopped beef and two parts water. 
Filter, and add peptone, Vf, ; salt, \$> : filter again, and sterilize. To 
make gelatine : To 100 parts of bouillon add 7 to 10 parts good gelatine 
which has been previously soaked in water, heat in water bath, and pour 
in sterilized test tubes. If agar is needed, take 1 part agar and soak for 
a night in salt water; rinse and add it to 100 parts bouillon, heat till 
completely dissolved, filter, and pour in tubes and sterilize. All media 
should be made slightly alkaline in re-action ; sodium carbonate is best 
suited for this purpose. 



26 



BACTERIOLOGY. 



Cultures. — To obtain pure cultures, inoculate, by means of a recently 
sterilized platinum needle, with the substance suspected to contain micro- 
organisms, gelatine and agar tubes ; the former are kept at a constant tem- 
perature of about 22° ; the latter at a temperature of 37° to 40° C. 

If a pure culture is obtained from the beginning, which is seldom the 
case, the micro-organism can be directly studied ; but if an impure culture 
is obtained, which is the most frequent case, the cultures are plated ; that 
is, very dilute cultures are spread out on sterilized glass plates, in order to 
allow every microbe to grow separately. This operation is done as follows : 
Three tubes of gelatine or agar are heated to the melting-point, then w T ith 
a platinum needle inoculate from the impure culture one of the tubes ; 
sterilize needle, and from this first tube inoculate a second tube ; and from 
this in the same manner a third tube ; thus very few micro-organisms are 
contained in the last tube, perhaps six or eight only. Now spread the con- 
tents of those tubes on pieces of sterilized glass 5x6 inches. After the 
gelatine or agar has hardened, the glass plates are allowed to remain at 
an even temperature ; then the colonies of bacteria begin to grow. Each 
colony is inoculated with the platinum needle in a separate tube, and cul- 
tivated. 

Most bacteria grow freely in nutrient gelatine or agar, as above described, 
but some require particular media, as tubercle bacilli, gono-cocci, etc. ; 
others do not grow in any of the known media, as the spirillum of relapsing 
fever, bacillus of syphilis, etc. 

EXAMINATION" AND STAINING OF BACTERIA. 

Micro-organisms are very resistant to the action of acids and alkalies. 
This property was utilized to recognize them before the staining methods 
were used. If a section or specimen be treated by acetic acid, or with a 2$ 
solution of caustic potash, all the components disappear, and the bacte- 
ria only remain visible. Some protoplasmic granules and crystals may 
resist the action of such treatment, but the special form of the micro- 
organisms, their uniform dimensions, and their peculiar grouping, make 
their recognition easy. This method is known under the name of its 
author, — Baumgarten's method. Giinther has modified this method, prin- 
cipally when treating specimens kept for a long time in alcohol. In such 
cases it frequently happens that the granular protoplasm is affected neither 
by acids nor alkalies ; Giinther treats them with a 3</o solution of pepsine, 
which, peptonizing all the albuminoids, clears the field, leaving the micro- 
organisms unaffected. 

Staining.— -The best method of staining micro-organisms is important ; 
for by it the bacteria are made more distinct, and a chemical action takes 
place which in many cases is characteristic of a determined species. 

Aniline colors are chiefly used for staining. Acid dyes have the prop- 
erty of diffusely coloring tissues ; the principal ones are eosine, aurine, and 
acid fuchsine. Basic dyes have an elective tendency to color the nuclei of 
cells and bacteria : these are methyl blue, methyl violet, gentian violet, 
dahlia, basic fuchsine, Bismarck brown, etc. 



EXA^II^ATIOX AXD STAINING OF BACTERIA. 



■27 



Any water solution of a basic color will clo for coloring bacteria. It is 
well to beat the specimens after staining with acetic acid, as in Baumgar- 
ten's method ; by thus dissolving the nuclei, the colored bacteria are much, 
more distinct. This method gives excellent results in the study of the 
spirillum of relapsing fever. 

Not all micro-organisms can be colored by this method. Those that 
resist it may be treated with Loffier's solution (concentrated alcoholic solu- 
tion of methyl blue 30 parts, iq^-qq water solution of caustic potash 100 
parts). After leaving the sections for a few minutes in this solution, treat 
them with lf 0 acetic acid, then pass to absolute alcohol and clear with cedar 
oil. This method shows very distinctly the bacillus of typhoid fever in 
tissues. 0 

Gram's method is a general method for staining. The sections are first 
treated with water solution of aniline oil 100 parts; saturated alcoholic 
solution gentian violet 5 parts (the sections must have been kept, previous 
to staining, in concentrated alcohol). After a few minutes they are trans- 
ferred to a solution of iodine (iodine 1 part, potassium 2 parts, water 
300 parts), where they are left for two or three minutes ; from this solu- 
tion the sections are put in absolute alcohol, where they decolorize almost 
entirely ; clear in oil of cloves and mount in balsam. By this method the 
micro-organisms are deeply stained, while the tissues remain colorless ; 
such preparations can be stained with a contrast stain, as a water solution of 
Bismarck brown — and the relations of tissues and micro-organisms studied. 

Giinther has modified Gram's method, and his modification is to be 
recommended where oid sections, kept in impure alcohol, are dealt with. 
The sections are kept for a minute at ordinary temperature in the violet 
solution, dried with blotting-paper, and transferred to the iodine solution 
for two minutes, then placed in alcohol for one minute, treated for exactly 
ten seconds by a ofo hydrochloric acid, alcoholic solution, and washed in 
alcohol again. Clear with oil of cloves, keep in balsam. 

Weigert has also modified Gram's method : when the sections are taken 
from the iodine solution they are decolorized by aniline oil instead of alco- 
hol ; thus not only micro-organisms remain colored, but also fibrin, which 
is important in certain cases. 

The micro-organisms that stain by Gram's method and its modifications 
are : 

Pneumococcus of Friedlander. 
Diplococcus pneumonias of Frankel. 
Bacillus anthracis (Davaine). 
Bacillus leprae (Hansen). 
Bacillus tuberculosis (Koch). 

Streptococcus erysipelatis (Fehleisen), all pyogenic bacteria and actin- 
omyces. ( 
Those that do not stain are : 
Gonococcus (jSTeisser). 
Bacillus typhosus (Eberth). 

Diplococcus intercellularis meningitis (Weichselbaum). 
Bacillus mallei (glanders). 



28 



BACTERIOLOGY. 



Spirillum cholera asiaticae (Koch). 
fSpirochaete Obermaieri (relapsing fever). 

Gonococci, diplococcus intercellularis, and bacillus typhosus stain well 
with Loffler's solution as already indicated ; bacillus mallei, spirillum 
cholera asiaticse, and spirochete Obermaieri, stain with ordinary water 
solutions of dyes, and afterwards are treated with 1$ acetic acid. 

All these preparations can be double-stained with a contrast color in water 
solution, or with picro-lithio-carmine, excepting* the streptococcus erysipela- 
tis. For this micro-organism the sections are first treated with any of the 
carmine solutions, washed in water, transferred to alcohol, and treated by 
Gram's method. Thus the nuclei and tissues remain colored by the car- 
mine or picro-carmine solutions, while the bacteria are of a deep-blue color. 
These preparations are exceedingly beautiful, and the staining, first of the 
tissue and then of the bacteria, gives such distinctness that it ought to be 
recommended for general use. 

The importance of tubercle bacillus in diagnosis is such that a special 
mention should be made of the particular method of its staining, which 
makes it easily distinguished from all known bacteria excepting lepra 
bacillus. The property of retaining the color when treated by strong 
mineral acids is peculiar to this bacterium. The sections, or cover-glass 
preparations (sputum, pus, blood, etc.), are first treated by a solution 
composed of — 

Aniline water 100 parts. 

Alcoholic solution of fuchsine, methyl blue, or 

methyl violet 11 parts. 

Absolute alcohol 10 parts (Erlich). 

If sections, they should be heated for a few minutes in this solution 
(rapid process), or kept for twenty-four hours at ordinary temperature ; if 
cover-glass preparations, pass them over a burner three or four times until 
steam begins to arise. Then wash with — 

Nitric acid 1 part 

Water 2 or 3 parts, 

until nearly decolorized, then wash in abundant water or alcohol, and 
stain with contrast color in water solution. If section, treat with alcohol, 
clear with oil of cloves, and keep in balsam. 

By this method the tubercle bacillus alone remains colored after the 
action of the nitric acid ; the contrast stain colors the tissues. 

This is the classic method of staining tubercle bacilli, and is called — after 
the authors — Erlich-Koch's method. Many others have been proposed, but 
all are more or less a modification of the one given. Lepra bacilli also 
react in the same manner as tubercle bacilli. To distinguish them, pour 
four to six drops of a saturated alcoholic solution of fuchsine in a watch- 
glass filled with water, dip the cover-glass preparation for six to eight 
minutes in it, and afterwards treat with of nitric acid in alcohol for 
twenty seconds, wash in distilled water, and treat with aqueous solution 
of methyl blue, clear, and examine. If sections, treat with Erlich's fluid 
for two or three minutes ; pass through the nitric alcoholic solution for 



BIOLOGY OF BACTERIA. 



2ij 



one-half a minute ; then stain with water solution of methyl blue ; treat 
with absolute alcohol, then with oil of cloves ; keep in balsam. 

Thus only the lepra bacilli are colored, even if the tubercle bacilli are 
present (Baumgarten's method). 

To keep ordinary preparations, balsam dissolved in xylol is good if they 
are cleared with xylol instead of other oils. Tubercle bacilli after a time 
lose their color. This is due to the acid retained in the preparation. To 
avoid such an inconvenience, after treating as usual, dry the preparations 
first with blotting-paper, then clear with xylol and keep in balsam. 



BIOLOGY OF BACTERIA. 

During the various stages of their life, bacteria present different forms 
according to the time at which they are examined ; but it is established 
that one species of bacteria in the adult state and under the same circum- 
stances presents constantly the same forms. Experimentation has also 
proved that each species has an individuality of its own, capable of repro- 
ducing itself under the same circumstances, with its characteristic form 
and biological properties. The principal forms are micrococci and ba- 
cilli. The micrococci, or spherical micro-organisms, are sometimes ellip- 
tical, but they never exceed in length twice their diameter. They can be 
grouped as follows : When alone, they are called micrococci ; if in twos, 
diplococci ; if in chains, streptococci; if in irregular bunches, staphil- 
ococci ; if those bunches are surrounded by a gelatinous envelope, asco- 
cocci ; when the cocci divide in two directions, forming squares, they are 
called merismopedia ; if in three directions, forming packs or cubes, sarcina. 

The elongated or bacillary forms are those whose length is more than 
twice their diameter. They are of various shapes ; some are perfectly 
cylindrical, others elliptical, lanceolate, fusiform, spiliform. A distinction 
has been established by some authors between bacillary forms containing 
spores, and those where spores are absent ; calling the first bacilli and 
the second bacteria. Such a distinction is not generally accepted. If the 
bacillary forms are curved, they are called spirilla ; if corkscrew in shape, 
spirochete ; some of them have prolongations called flagella. Long and 
slender bacilli, without any difference between base and apex, are lepto- 
thrix ; if they have false branchings, cladothrix ; large bacilli, containing 
sulphur granules, are called beggiatoa. All these forms can readily be 
reduced to two general classes : the spherical, or coccacea? ; and the elon- 
gated, or bacillary. 

The dimensions of bacteria vary ; the unit of measure adopted by bac- 
teriologists is the micro, which is the thousandth part of a millimeter, or 
the 25,000th part of an inch. 

Structure. — Bacteria are cellular, formed of an involving membrane, the 
constituents of which are principally an albuminoid substance called micro- 
proteine. Their protoplasm is homogene. In addition to these constitu- 
ents they may contain sulphur granules (beggiatoa) or amyloid substance. 

Nutrition. — Nitrogen, oxygen, carbon, water and some mineral salts are 



30 



BACTERIOLOGY. 



elements indispensable to the life of bacteria. No bacteria grow without 
water, and most of them are seriously affected, if not destroyed, by a pro- 
longed desiccation. Oxygen is essential to their life. Some need free 
oxygen, which they take from the air ; others take their oxygen from the 
media in which, they live, and will not grow in the free air ; a third class 
obtains oxygen either from the air or the media, or from both. The first 
are called gerobii, the second anaerobii, and the third indifferent, or ana?- 
robii by election. They also receive their carbon from the media in which 
they grow. They differentiate themselves from the plants with chlorophyl 
by not taking carbon from carbonic acid. They obtain nitrogen princi- 
pally from the albuminoids. The salts required principally by bacteria are 
the sulphate and phosphate of magnesia and soda, of which they contain 
from three to six per cent. Bacteria produce such changes in the media in 
which they grow that they have been divided into three general groups, 
viz. : chromogenic or color-forming bacteria, zymogenic or putrefactive bac- 
teria, and pathogenic or disease-producing bacteria. This is an empirical 
division that has no scientific base, but the division, from a practical 
standpoint, facilitates their study. Bacteria decompose the media in 
which they live, and give rise to new compounds, w T hich may be a color, a 
putrid substance, or a virus. The temperature best suited to the life of 
microbes is between 20° and 40° Centigrade ; those that have been accli- 
mated to the animal body need the temperature of 37° and 40° C. Extreme 
temperatures are antagonistic to microbes, although they can stand extreme 
low temperatures. Some lose their vitality at — 37° C. and others only at 
— 110° C. High atmospheric pressures destroy them. Light does. not affect 
them ; electricity affects them only when the current is sufficiently intense 
to cause electrolysis. 

Movement. — Most bacteria have movements of their own, whenever the 
conditions of their nutrition excite them. These movements are either 
rotatory, oscillatory, or dancing, and are produced either by the contrac- 
tion of their protoplasm, or by the cilia in those bacteria that have cilia, or 
by both. 

Reproduction. — Bacteria, under favorable conditions of existence, repro- 
duce themselves by transverse scission in one, two, or three directions ; 
thus their name of schizomycetes (from cjzc^zV). When they reach 
their maturity, their protoplasm contracts, they become trabeculated, 
and two or more cells are developed. If the media is exhausted, or other 
conditions interfere, another change takes place, viz., the formation 
of spores. When the spores are about to be produced, the protoplasm first 
swells in one or more points of the bacilli, and little by little gets brilliant 
until the spore appears as a very refulgent point. The remainder of the 
protoplasm undergoes a process of atrophy, and the spore remains free. 
Spores are much more resistant than the mother cell, and keep their vital- 
ity for a very long time, until they find the necessary conditions for their 
growth. When this happens, their contents get opaque, the spore swells, 
its membrane atrophies in one of its poles, and a new bacillus escapes, which 
begins again the process of reproduction. 

Biological Action. — As has been stated, bacteria have been divided into 



BIOLOGY OF BACTERIA. 



31 



three general classes, according to their influence on the media upon which 
they grow. The chromogenic and zymogenic are of little importance to the 
physician. 

The third group, or pathogenic bacteria, are of the greatest interest to 
the physician, and their discovery has led to many practical and useful 
conclusions. 

A micro-organism is pathogenic, according to Koch, when it answers to 
the following conditions : 

1. It must be found in the humors or tissues of the animal suffering 
or dead from the disease. 

2. The micro-organism must be cultivated out of the organism (if pos- 
sible). 

3. A pure culture inoculated in an animal must reproduce the disease. 

4. The organism ought to be found in the humors or tissues of the 
artificially diseased animal. 

Bacteria that fulfil such conditions are pathogenic. They produce dis- 
ease whenever introduced into an organism which presents conditions favor- 
able for their development. The second condition must be taken into 
consideration as much as the existence of the micro-organism itself. 
Myriads of germs float in the atmosphere and are taken into the blood ; 
nevertheless the amount of disease produced by them is small. This can 
only be explained on the basis that the exposed organism has the power 
to resist the invasion of the germs. The tissue cells — principally the sur- 
face cells — are constantly at war with bacteria. If the vitality of the surface 
cells is normal, and the bacterial invasion is not overwhelming, the sys- 
temic infection is prevented ; but if the vital resistance of the cells is not 
sufficient to arrest the action of bacteria, disease results. Hence there are 
two conditions which are necessary for infection, viz. : the specific germ 
and a low vitality of the organism. 

Whether the micro-organism itself, or its products, is the cause of the 
disturbances observed in disease is still an unsettled question. Since the 
discovery of ptomaines by Gautier, and the experiments made by inocu- 
lating them in animals and producing the symptoms of the disease incited 
by the specific bacteria, scientists are inclined to attribute to the pto- 
maines, and not to the bacteria, the direct action in the development of the 
disease symptoms. Such facts, however, do not affect the doctrine of para- 
sitism, as many of those opposed to it thought. The microbes generate 
the poison and are thus the cause of the disease. 

Most of the infectious diseases have been studied bacteriologically, and 
many bacteria have been claimed as pathogenic of certain diseases which 
further experiments have shown to be innoxious. 

Attenuation of Virus. — Bacteria are differently affected in their vital 
characteristics by the soil in which they grow, or by the atmosphere, tem- 
perature, light, electricity, etc. Some lose their primitive properties ; 
their infective power is either changed to a higher degree or rendered 
almost inert. 

Anthrax bacilli ordinarily, at a certain period of their growth, begin the 
formation of spores ; but if kept at a certain temperature, — about 42° 



32 



BACTEKIOLOGY. 



C, — for some time, spores cease to form, and their virulence is greatly 
diminished. 

The virus of rabies, if passed through a series of rabbits, increases in 
virulence, while if subjected to a dry atmosphere it gradually loses its 
virulence. 

Cholera bacillus, inoculated from man to pigeons, produces no results, 
but if inoculated first to guinea-pigs and from them to pigeons the phe- 
nomena of cholera are developed. 

These facts, and many others stated, have given rise to the theory of 
attenuation of virus. Upon the basis of this theory, inoculation of the 
attenuated germs has been practiced with the purpose of producing a mild 
form of disease, which would render the individual unsusceptible to the 
more severe form. Practically this theory has been proved to be true, and 
inoculations of an attenuated virus are now employed as prophylactic or 
therapeutical measures. Among those can be mentioned vaccine, anthrax, 
rabies, etc. As to how they act upon the organism to render it refractory 
to the action of a new invasion of micro-organisms is a question not yet 
answered. 

The discovery of ptomaines and their action tends to establish a chem- 
ical action of the virus. In such a case the micro-organisms would not be 
the agents of disease, but their exchange products act as so many poisons. 
By modifying bacillary vitality, such poisons may somewhat affect the 
composition or biological action of the bacilli themselves. 

This assertion has to a certain extent been proved by inoculating the 
ptomaines of certain micro-organisms (tetanus, cholera, etc.), and pro- 
ducing symptoms similar to those observed in the diseases of which they 
are supposed to be the cause. 

If the conditions of attenuation be carried to a further extent, the 
micro-organisms not only lose the power of producing disease, but also 
of existence, and die. Extreme temperatures, the lack of humidity, 
or the action of certain chemicals, are apt to produce it. In such cases 
we disinfect or sterilize the cultures. By properly applying those prin- 
ciples, the hygienist can avoid the spreading of infectious diseases. 

Pathogenic Bacteria. — The specific character of some bacilli is well 
determined. The pathological processes which they incite, although 
essentially the same in character, are modified according to their localiza- 
tion. Some have a predilection for certain organs, but can localize them- 
selves and excite pathological processes in any part of the body where they 
find proper conditions for their existence. 

Acting thus as the cause of disease, they incite similar morbid processes, 
which receive different names according to the organ in which they are 
developed. 

Let us take, as an example, inflammation of the lungs. 

In addition to the micro-organisms usually regarded as the cause of 
pneumonia, many others can produce inflammation of the lung. 

The intensity of the inflammations, or even the ultimate characters of 
the processes, may differ; but clinically it is impossible to distinguish the 
diseases produced by FrankeFs diplococcus, Friedlander's bacillus, typhoid 



PATHOGENIC BACILLI. 



33 



bacillus, etc., from each other. Some bacilli destroy the tissues which 
they penetrate ; others provoke hyperplasia of the anatomical elements, 
and either organize, or perish after a short existence. 

Thus, lesions dependent upon a single cause vary. In one case a rapid 
pyogenic gangrene is established, while in another a neoplasm is developed, 
which may, as in tuberculosis, undergo coagulation necrosis, and become 
cheesy. Although many diseases are known to be of an infectious nature, 
their micro-organisms have not yet been determined. Many germs have 
been assigned as the causes of certain diseases, and afterwards proved to be 
harmless saprophytes. 

In this sketch only those germs the pathogenic nature of which in 
man we know has been thoroughly proved will be mentioned. 

PATHOGENIC MICROCOCCI. 

Staphilococcus Pyogenes Aureus. — Found in pus. Cells grouped in 
bunches. Yellow gold color of cultures. Melts gelatine. 

Staphilococcus Pyogenes Alius. — In pus ; similar to above, excepting 
color of culture, white. 

Staphilococcus Pyogenes Citreus. — Same as above, excepting lemon yel- 
low color of culture. 

Diplococcus Inter cellular is Meningitis. — In exudation of cerebro-spinal 
meningitis. Cocci united in twos. Does not melt gelatine. 

Diplococcus Pneumoniae, Lanceolatus. — In croupous pneumonia exuda- 
tion. Cocci united in twos. Capsulated when in the lung ; in cultures it 
loses the capsule. Does not melt gelatine. 

Gonococcus. — In gonorrhoeal pus. Cocci in twos, similar to grains of 
coffee. Cultures grow on agar and sugar or blood serum. 

Streptococcus Pyogenes. — Chains of cocci found in phlegmons. Culture 
does not melt gelatine. 

Streptococcus Erysipelatis. — In the lymph spaces of erysipelatous 
patches. Very fine cocci in chains. Does not melt gelatine. Considered 
by some authors identical with previous one. 

PATHOGENIC BACILLI. 

Bacillus Anthracis. — Rods single or in long chains when cultivated ; 
found in the lymph and blood of animals suffering from splenic fever. 
Cultures melt gelatine. 

Bacillus Tuberculosis. — Eods- about one third the diameter of a red 
corpuscle in length ; it appears as if formed of several minute buds. 
From tubercular tissue or sputum ; it grows in blood serum, agar, pota- 
toes, carrots, turnips, etc., very slowly ; temperature of 37° C. the best. 
Its coloring reaction differentiates it from all other bacteria. 

Bacillus Leprm. — Found in the tubercles of leprosy. It resembles tuber- 
cle bacillus, as shown in colored plate. Grows very slowly in blood serum. 

Bacillus Mallei. — Short, slender bacilli, resembling tubercle. Found 
3 



34 



BACTEKIOLOGY. 



in the tissues and secretions of animals affected with glanders. Grows as 
small shining drops on blood serum and potatoes. 

Bacillus (Edematis Maligna. — Rods straight, generally forming chains. 
Found in cases of malignant oedema in man and animals. It is anaerobic, 
and grows under the gelatine, giving rise to the formation of gas bubbles. 

Bacillus Typhosus. — Found in the dejections, mesenteric glands, and 
spleen of typhoid patients. Short rods with rounded ends ; it grows 
slowly without melting the gelatine. On potatoes it gives a colorless 
growth. 

Bacillus Pneumonia?. — Short bacilli, single or in chains ; capsulated 
when in the animal organism ; without capsule in cultures. Does not melt 
gelatine, and forms a characteristic nail form ; growth white in gelatine 
tubes. 

Bacillus of Rhinoscleroma. — Found in rhinoscleroma tubercles. It 
resembles the diplococcus pneumoniae of Frankel in form and in cultures. 

Spirillum Cholerm Asialicm. — Short, slender rods curved to resemble a 
comma, sometimes in S or corkscreAV forms ; it liquefies gelatine in a 
characteristic manner. Found in cholera discharges. 

Bacillus of Syphilis. — Short rods found in the syphilitic lesions. It 
has not been cultivated. 

Spirochete Obermaieri. — Long spirilliform rigid threads, found during 
the exacerbation of relapsing fever. It has not been cultivated, although 
it has been inoculated in animals from man, producing the disease. 

Pathogenic Fungi; Actinomyces. — Found principally in tumors in the 
jaws of cattle. It is a club-shaped fungus, growing as radii. It produces 
suppuration in man. Cultures on agar present themselves as small grayish 
dots. 

A chorion Schbnleinii. — Fungi of favus, found in patches of favus. Its 
growth on agar resembles the patches of favus in color. 

The micro-organisms just mentioned are those which have been proven 
to be pathogenic in man as well as in animals. Many others have been 
described as related to disease. Some of them are peculiar to animals 
only, and are out of our limits ; others, although considered as pathogenic 
in man, need to be more widely experimented with, in order to include 
them in the list of causes of disease. 

CLASSIFICATION OF BACTEEIA. 

A scientific classification of bacteria has not yet been given. All of those 
proposed are defective, as they rest only on empirical basis. It is known 
that bacteria are plants, that they belong to the Thallophytes without 
chlorophyl. To this point our knowledge of the place bacteria occupy in 
the living world is scientific. The subsequent divisions are based only on 
the form of each germ. As some classification has to be adopted until a 
truly scientific one is established, bacteriologists generally accept that 
proposed by Cohn as the one which is more advantageous and nearer to 
the actual exigency of this new science. 



SECTION I. 



DISEASES OF THE RESPIRATORY ORGANS. 

In considering diseases of the respiratory tract, I shall commence with 

DISEASES OF THE NASAL PASSAGES. 

The Medical diseases affecting these passages may be included under the 
general head of Nasal Catarrhs, for nasal catarrh appears, either as cause 
or effect, in all intra-nasal diseases. These diseases may be conveniently 
considered in the following order : 

I. Acute Coryza. III. Hypertrophic Nasal Catarrh. 

II. Chronic Coryza. IV. Atrophic Nasal Catarrh, 

V. Ozama. 

ACUTE CORYZA. 

Acute Coetza is an acute catarrhal inflammation of the nasal mu- 
cous membrane characterized by engorgement and tumefaction of the tis- 
sues over the turbinated hones. It is commonly called " cold in the head." 

Morbid Anatomy. — At the onset of the affection, the anterior portion of 
the nasal mucous membrane is markedly congested, its normal pink and 
red hue being replaced by a bright arterial red, while the inner margins of 
the turbinated tissues assume the blue color of intense venous engorgement. 
The turbinated tissues are tumefied because of the distension of the venous 
spaces with blood. Having lost their normal tonicity, they are unable to 
retract and reduce the turgescence. The distension is, after a time, relieved 
by an exudation, and the blood gradually resumes its natural flow. 

Etiology. — Acute coryza may result from momentary reduction of the 
surface temperature by chilling, which causes an unequal distribution of 
blood. As the nasal mucous membrane has less resistance than other mu- 
cous surfaces, its inflammation is the result. It may also be occasioned by 
external irritants, such as tobacco, dust, acrid fumes from chemicals, or by 
direct injury ; extensive desiccation of the nasal mucous membrane, inspis- 
sated mucus, and foreign bodies may also cause it. 

Symptoms.— An acute coryza may be ushered in by a slight chill. It is 
often preceded by a pricking sensation in the turbinated tissues. These 
structures are rendered extremely sensitive by the intense hyperemia, so 
that sneezing is provoked by touching them. The sudden tumefaction 
accompanying venous engorgement arrests secretion and causes an uncom- 
fortable sensation of dryness ; this is somewhat relieved by a free mucous 



36 



DISEASES OF THE RESPIRATORY ORGANS. 



discharge, which in a short time becomes muco-purulent. The accessory 
cavities of the nose may become involved, producing headache. 

Differential Diagnosis. — A persistent discharge, caused by foreign bodies 
in the nostrils, may be mistaken for an acute catarrh. Concealed scrofu- 
lous and syphilitic ulcers, with co-existing coryza, cause similar symptoms, 
but will hardly be mistaken for it. 

Prognosis.— The nostril generally returns to its normal condition in a 
few days. Repeated attacks of acute coryza may result in permanent struct- 
ural changes, and lead to a chronic nasal catarrh. The ear, lachrymal 
duct, accessory nasal sinuses and cavities may secondarily become involved. 

Treatment. — An effort to abort the disease in its incipiency may be made 
by the administration of ten or fifteen grains of quinine, given alone, or 
with an equal quantity of bromide of sodium. A full dose of opium at its 
very onset may restore the vascular equilibrium and abort the affection. 
Inhalations of ammonia, carbolic acid and alcohol, the vapor of solutions 
of carbolic acid inhaled through a cone, and fumes of iodine and cologne, 
inhaled through a sponge, often relieve the engorgement and tension of the 
mucous membrane by exciting exudation. Depletion of the turbinated tis- 
sues by puncturing them with sharp needles, relieves the turgescence and 
iavors their retraction. Spraying of the parts reduces the congestion by 
chilling the turgid tissues, and gives comfort and hastens recovery by re- 
moving acrid discharges. 1 Chloride of sodium, bicarbonate of soda and 
borax (two grains to the oz. of water) make efficient cleansing solutions. 

CHRONIC CORYZA. 

{Chronic Nasal Catarrh.} 

Chronic Coryza is a chronic catarrhal inflammation of the nasal 
mucous membrane characterized by an excessive and persistent discharge 
of mucus. 

Morbid Anatomy. — There is intense and persistent congestion of the nasal 
mucous membrane without pronounced tumefaction of the deeper tissues 
covering the turbinated bones. The abnormal cell production is not 
accompanied by a marked increase of the sub-mucous cellular tissues. 
A continuous discharge of watery mucus generally escapes anteriorly. 
Inspissation of the mucus seldom occurs, as the nares are constantly moist. 
Excoriation of the lips and integument about the nostril is often caused by 
the action of the acrid discharges. 

Etiology. — Constant watery mucous discharges are sometimes caused by 
the lodgment of foreign bodies in the nostril. It is frequently observed in 
young women having a constitutional tendency to catarrh. Cachectic 
children readily acquire the disease. An irritating atmosphere or abnor- 
mally moist or impure air may develop it. 

Symptoms. — Annoying paroxyms of sneezing are of frequent though not 
invariable occurrence. A burning sensation of the anterior nasal orifices is 



1 Delano's, Goodyear's, or Richardson's hand atomizers are best for this purpose. 



HYPERTROPHIC NASAL CATARRH. 



37 



often complained of. Discomfort is sometimes caused by the excoriation 
resulting from the acrid discharges. 

Differential Diagnosis. — Failure to find a foreign body in the nasal pas- 
sages will prove that the discharge is not caused by mechanical irritation. 
Absence of ulceration demonstrates the catarrhal nature of the affection. 
The chronicity of the complaint and freedom from nasal obstruction dis- 
tinguish it from acute coryza. The distinctive feature of hypertrophic 
nasal catarrh, thickening of the intra-nasal tissue, does not occur in chronic 
coryza. In hypertrophic nasal catarrh the secretions usually flow pos- 
teriorly. Concentration and inspissation of the nasal mucus rarely occur 
in chronic coryza. 

Treatment. — The nares should be first thoroughly cleansed, the acrid 
discharge being best removed by means of syringes and sprays. 1 Weber's 
nasal douche is convenient for cleansing. Solutions of bicarbonate of 
soda, boracic acid, and chloride of sodium, five to ten grains to the ounce 
of water may be employed, the fluid always being warmed before using. 

Alkaline solutions may be thrown into the nasal cavities by means of 
atomizers. After the nares have been thoroughly cleansed, it is well to use 
astringents. They should be applied in the form of sprays. Of these, 
ferric alum, five grains to the ounce of water, sulphate of zinc, and tartaric 
acid, three grains to the ounce of water, are the most efficient. Iodoform, 
applied by means of Ely's powder-blower, acts as a local anaesthetic, and 
sometimes affords great relief. Vaseline and benzoated oxide of zinc oint- 
ment may be employed to protect the margins of the nostril and heal 
excoriations. Constitutional vices and tendencies should be corrected by 
appropriate treatment. The general health should be improved by tonics 
and an out-of-door life. 



Hypertrophic ISTasal Catarrh is a chronic catarrhal inflammation, 
characterized by hypertrophy of the turbinated tissues and intra-nasal 
mucous membrane. 

Morbid Anatomy. — The nasal mucous membrane is in a constant state of 
engorgement, especially the soft turbinated structures, whose cavernous 
sinuses are so distended as to interfere with free nasal respiration. Hyper- 
trophic changes are most extensive in the loose turbinated tissues ; the 
hypertrophy is due to the general increase of the soft turbinated structures. 
Permanent dilatation of the turbinated blood cavities takes place, with con- 
sequent loss of " turbinated erection." Localized thickening of the tissues 

1 DobelPs is an efficacious cleansing solution, viz. : 



HYPERTROPHIC NASAL CATARRH. 



(Chronic Naso-Pharyngeal Catarrh.) 



R; Carbolic acid 

Bicarbonate of soda 

Borax 

Glycerine 

Water 



gr. j. 



.aa gr. v. 



38 



DISEASES OF THE KESPIBATOEY ORGANS. 



over the septum, with deviation of this structure, is of common occurrence. 
The nasal mucus, with epithelial debris, being retarded in its escape by the 
thickened mucous membrane, inspissates and accumulates in the nostril. 
The turbinated hypertrophies have a light pink hue ; wheu complicated by 
acute coryza they vary in color from arterial red to a venous blue. 

Etiology. — This disease sometimes results from repeated attacks of acute 
coryza. The constant irritation caused by a deviated septum, pressing 
upon the turbinated tissues or nasal mucous membrane, frequently gives 
rise to it. Distortion of the nasal gutter from deflection of the septum, 
with consequent accumulation of mucus, always develops it. The growth 
of gelatinous polypi is encouraged by the abnormal vascularity, and the 
irritation they produce intensifies the affection. The dusts of cities, facto- 
ries, and certain occupations act as excitants. Damp localities, irregu- 
lar living, insufficient clothing, and prolonged exposure to cold and wet, 
also predispose to it. 

Symptoms. — The symptoms of this affection are usually due to turbinated 
enlargement and accumulated secretions. Thick, tenacious mucus collects 
in the nostrils, and small masses drop into the pharynx, and thence 
pass into the larynx, producing irritation, coughing and retching. The 
nostrils may be permanently or temporarily occluded. Hearing is impaired, 
either by extension of the catarrhal processes, or collapse of the Eustachian 
tube from suction induced by nasal stenosis. Obstinate sneezing, head- 
ache, suffusion of the eyes, or the ordinary symptoms of cold in the head, 
may occur as the result of acute exacerbations. The pressure exercised by 
the thickened tissues sometimes produces persistent neuralgia. Nasal ste- 
nosis, combined with laryngeal irritation, may develop symptoms resem- 
bling spasmodic asthma. 

Differential Diagnosis. — The chronicity of the affection will prevent it from 
being mistaken for an acute coryza. A careful examination will show 
whether the disease is simple, or dependent upon the presence of foreign 
bodies or growths. The mistake of confounding turbinated hypertrophies 
with gelatinous polypi may be avoided by comparing the gelatinous appear- 
ance, mobility, and clear contour of the polypus, with the fleshy hue, firm 
attachment, and irregular shape of the hypertrophied turbinated tissues. 

Prognosis. — The cure of hypertrophic nasal catarrh depends upon the 
general health, the nature of the structural changes, and the complications. 
Patients, otherwise in good health, who have acquired the disease from 
prolonged exposure, may be permanently relieved by a change of climate, 
after the removal of the nasal obstruction. The part played by a deviated 
nasal septum, in chronic nasal catarrh, is pronounced, and its excision is 
as much called for as the removal of a foreign body. Turbinated hyper- 
trophies obstruct nasal drainage and respiration, and provoke and continue 
the disease which produced them. There are cases in which the simple 
excision of the offending structures, by removing the cause of the disease 
and restoring normal respiration, circulation and drainage, effects a cure. 
AYhen the health is much impaired, with a tendency to profuse catarrhal 
discharges, and with great distortion of the interior of the nostril, the 



ATROPHIC NASAL CATARRH. 



39 



prognosis is unfavorable. More or less relief, however, can be afforded in 
all cases. 

Treatment. — The treatment of hypertrophic nasal catarrh consists in the 
restoration of the symmetry of the nasal chambers, and the local cleansing 
of the part, with the prolonged local use of certain medicinal agents. 
Caustics and cutting instruments are now employed to remove obstructions 
and restore drainage and nasal respiration. The exfoliation produced by 
cauterization with chromic acid and nitrate of silver slowly reduces intra- 
nasal hypertrophies. They may be used when the tissues are easily acces- 
sible. The platinum knife, made incandescent by the galvanic current, is 
extensively used to diminish hypertrophied tissues. It acts either by 
eschar and cicatricial contraction, or by excision. Glacial acetic acid, ap- 
plied by means of Bosworth's nasal applicator, forms an eschar which can 
be easily limited, and immediately neutralized by an alkaline spray. Tur- 
binated hypertrophies and gelatinous polypi can be safely removed by the 
cold wire, with Jarvis' Ecraseur. After the removal of the hypertrophied 
tissues, Dobell's solution, or the bicarbonate or chloride of sodium, may be 
employed to cleanse the parts ; the addition of an antiseptic like carbolic 
or salicylic acid, or the permanganate of potash, is often of service. 
Nasal washes are most elfective when employed with the post-nasal syringe. 
Cleansing can be practised by the patient, by means of Warner's nasal 
douche. Astringents should only be used after thorough cleansing. They 
are usually applied by means of sprays. Insufflations of boracic acid and 
iodoform are sometimes advantageously employed. Insufflation should 
only be practised with powder-blowers working on the Ely principle. 

ATROPHIC NASAL CATARRH. 
{Dry Nasal Catarrh.) 

Atrophic Nasal Catarrh is a chronic catarrhal inflammation re- 
sulting in atrophy and desiccation of the nasal mucous membrane. 

Morbid Anatomy. — The nasal cavities are very much enlarged from atro- 
phy of the soft and osseous turbinated structures. The mucous membrane 
becomes thin, and loses part of its epithelium and some of its mucous 
glands ; and there is an unnatural dryness of the nasal and naso-pharyngeal 
mucous membrane from deficient glandular secretion. Crusts of decom- 
posing mucus adhere to the turbinated ridges, and occupy the sinuosities 
of the nostrils. 

Etiology. — This disease is local in character. It may be brought on by 
rapid absorption of moisture from the nasal mucous membrane, hence the 
frequency of its occurrence in persons continually subjected to the desiccat- 
ing influence of a dry or dusty atmosphere. Occupations which favor this 
desiccation, as wood-turning, soldering, milling, cigar-making, develop the 
affection. It is sometimes associated with a hypertrophic nasal catarrh, 
and in such cases probably owes its existence to a local modification of the 
catarrhal processes by which the inflammatory activity is largely expended 



40 



DISEASES OF THE EESPIRATORY ORGAKS. 



upon the glandular follicles. Accumulation of the nasal mucus is favored 
by the destruction of the cilia of the epithelium. The prolonged contract- 
ing effect of inspissating nasal mucus promotes progressive atrophy of the 
soft tissues and bones. 

Symptoms.— There is usually entire loss of the sense of smell ; a feeling 
of fullness in the nose is sometimes complained of, the sensation resembling 
that produced by a foreign body. Neuralgia and dull frontal headache are 
often present. An annoying fetor, not an invariable occurrence, results 
from the decomposition of retained nasal secretions. Obstructed nasal 
respiration from accumulation or lodgment of crusts causes much discom- 
fort. Tenderness and extreme sensitiveness of the mucous membrane may 
follow the detachment of the incrustations. 

Differential Diagnosis. — The glazing and desiccation of the surface demon- 
strate the existence of dry catarrh; its chronicity will distinguish the affec- 
tion from the temporary dryness of an acute catarrhal inflammation. 
Accumulations of crusts, with the co-existing musty stench, are often associ- 
ated with the atrophic changes. In the advanced stages the unnatural 
roominess of the nares from general shrinkage of the soft and osseous 
structures is a distinguishing feature of the affection. 

Prognosis. — The disease does not perceptibly shorten life. Beneficial re- 
sults, or complete restoration of the glandular function, may be obtained by 
careful stimulation. An artificial supply of moisture relieves the dryness 
and promotes a return of the normal secretion. Antiseptic cleansing pre- 
vents decomposition, and removes a disagreeable feature of the disease. Loss 
of tissue from atrophy of the soft and solid structures is permanent. Be- 
lief of the dryness, nasal obstruction, offensive odor, and general discomfort 
is always possible. 

Treatment. — Thorough cleansing with alkaline solutions should be prac- 
tised to remove nasal incrustations. Dobell's solution or carbolized water 
rendered alkaline by the addition of soda or potash, as recommended for 
hypertrophic nasal catarrh, should be thrown into the nasal cavities by 
means of the post-nasal syringe. At first it maybe necessary to remove the 
crusts by mechanical means. Cleansing should be practised daily by the 
patient. Warner's douche may be used for this purpose. Accumulation 
and inspissation of the nasal mucus are effectually prevented. The painful 
spots sometimes produced by detachment of crusts are best treated by the 
application of iodoform. Fluid cosmoline or melted vaseline thrown into 
the nostril by an atomizer will prevent the reformation of catarrhal crusts. 
As the sensibility of the mucous membrane is largely obliterated by the 
atrophic changes, stimulating powder may be employed to provoke secre- 
tion, and thus promote the discharge of the accumulated debris. When 
there is marked general constitutional impairment, change of climate or 
occupation may be advisable, with the administration of tonic3 and 
alteratives. 



OZJENA. 



41 



OZ^EKA. 

{Fetid Nasal Catarrh.) 

The term Oz^na is applied to necrotic and ulcerative processes in the 
nose and its neighboring cavities, accompanied by fetor due to putrefaction. 

Morbid Anatomy. — The thick mucus, -dry crusts, and peculiar processes of 
atrophic catarrh are discoverable in catarrhal ozaena of the nasal cavity; 
muco-purulent secretions are imprisoned beneath the dried follicles of mu- 
cus adhering to the turbinated ridges and interspaces, and then undergo 
decomposition. When associated with the disease of the accessory cavities, 
the ethmoidal cells, the sphenoidal sinuses, and the antrum of Highmore, 
there is continually or intermittently a discharge of glutinous offensive 
muco-pus. In antral ozaena there usually exists a chronic catarrhal inflam- 
mation of the mucous membrane lining the maxillary sinus with a constant 
formation of muco-purulent matter. The tertiary ulcers of syphilitic 
ozaena progress rapidly, eroding the soft tissues, denuding the turbinated 
bones, and inducing necrosis. Their favorite situation is upon the carti- 
lage of the septum. Perforation of the nasal septum by syphilitic ulcera- 
tion is of common occurrence. In scrofulous ozaena the mucous membrane 
may be ulcerated, or an accessory cavity may be involved in an asthenic 
catarrhal inflammation ; when it is catarrhal in character, a peculiar bluish 
viscid discharge may be discovered oozing from the cavity or sinus 
involved. 

Etiology. — The ozaena of atrophic catarrh is due to the decomposition of 
secretions which adhere to the mucous membrane. When the ethmoidal 
cells or sphenoidal sinuses are involved, the offensive odor is due to de- 
composition of pent-up muco-purulent matter. Antral ozaena may origi- 
nate in the catarrhal inflammation set up by a tooth projecting into the 
antrum. Catarrh of the antrum may also result from the extension of in- 
flammation to it from the nares. Syphilitic ozagna may be caused by osteitis, 
or by fetid catarrh and decomposing debris of ulcers. It may be associated 
with disease of the pneumatic nasal cavities. Necrosed bone acts as an 
irritant, provoking and keeping up the fetid discharges. Scrofulous ozaena 
may originate in an ulcer or in catarrh of the accessory nasal cavities. 
Ozaena is seldom produced by the decomposition of retained secretions in 
hypertrophic nasal catarrh. 

Symptoms. — In the ozaena of atrophic catarrh, the patient is seldom 
disturbed by the odor, as he is unable to distinguish odors. When the 
disease implicates a cavity, the sufferer is usually painfully aware of the 
ozaenous taint. The detachment of incrustations may be followed by slight 
or alarming hemorrhage. Violent retching or vomiting may be caused by 
the passage of loosened crusts into the pharynx. The constant effort to 
free the nostril from incrustations proves extremely wearisome ; a dull 
headache is often associated with disease of the sinuses, its location being 
determined by the situation of the cavity. Ulcerative ozaena is seldom 



42 



DISEASES OF THE RESPIRATORY ORGANS. 



accompanied by acute pain. Occasional burning sensations and severe 
headache are its only painful symptoms. 

Differential Diagnosis. — The ozaena of atrophic catarrh is diagnosticated by 
the rules already given for the diagnosis of that affection. Failure to find 
a source for ozaena in the nasal cavity, discovery of the peculiar fetid dis- 
charge already described as trickling from the superior meatus, the condi- 
tion being usually unilateral, are evidences of the existence of ozaena of the 
sphenoidal sinus or ethmoid cells. Antral ozaena is easily recognized by 
the source of the discharge and the situation of the pain. Non-ulcerative 
strumous or syphilitic ozaena is usually confined to the accessory nasal 
cavities. The scrofulous diathesis and history or manifestations of syphilis 
determine its nature. In the ulcerative ozaena of syphilis the ulcers resem- 
ble similar lesions in other parts of the respiratory tract. Their edges are 
ragged, and the red areola encircling the ulcer fades away into the surround- 
ing normal or congested mucous membrane. There is often a puffiness and 
infiltration of the tissues about the sore. In the ulcerative ozaena of scrof- 
ula the edges of the ulcer are usually smooth and red, occasionally, how- 
ever, they are pale. The ulcer and areola are clearly defined in the pale 
anaemic membrane. Pale granulations, or a spongy mucous membrane, may 
surround the margin of the ulcer. Its chronicity, the enlarged cervical 
glands, cachexia, and general evidences of strumous diathesis, establish the 
nature of the ulcer. Perforation of the septum from constant removal of 
scabs, with consequent abrasion, should not be confounded with the ravages 
of specific disease. 

Prognosis. — The prognosis as regards life is almost always favorable. The 
conditions determining the course of atrophic nasal catarrh apply also to 
the ozaena complicating this affection. Scrofulous catarrhal ozaena of the 
sphenoidal sinuses and ethmoidal cells is dependent upon the general health, 
and may persist for months, or even years. Syphilitic non-ulcerative 
ozaena is more amenable to treatment than the scrofulous. Antral ozasna, 
due to simple catarrhal inflammation or the presence of irritants, responds 
to proper anti-syphilitic treatment. The cure or relief of syphilitic or 
scrofulous ulcerative ozaena depends upon the healing of these ulcers. 
When the disease depends upon the presence of dead or dying bone its 
removal will often produce a cure. 

Treatment. — The treatment recommended for an atrophic nasal catarrh 
relieves also the ozaena complicating this affection. When the disease is 
confined to the accessory cavities it is only possible to remove the discharges 
as they accumulate by means of Dobell's solution, or any of the antiseptic 
alkaline washes recommended for hypertrophic or atrophic nasal catarrh. 
The patient can accomplish much in this direction by faithfully using 
Warner's nasal douche. Careful applications of powder made with an Ely 
powder-blower prove beneficial. Its odor may be disguised by tincture of 
musk, tonga bean, or the aromatic essential oils. Antral catarrh due to a 
dead tooth, or misplaced filling, may require the removal of an upper molar 
and perforation of the alveolus. Superficial syphilitic ulcers when within 
reach are readily healed by local applications of chromic acid, or of nitrate 



ACUTE CATARRHAL LARYNGITIS. 



43 



of silver fused upon a probe. The same local treatment does not apply to 
the deep syphilitic ulcers. Iodoform frequently applied gives the best 
results in the treatment of this form. Local applications should be always 
preceded by careful cleansing by means of sprays or the syringe. Specific 
constitutional medication should be combined with the local treatment. It 
prevents the recurrence of the syphilitic lesions and materially hastens cica- 
trization. In the deep ulcers rapidly increased doses of iodide of potassium, 
with or without mercury, are required to facilitate healing. Local stimula- 
tion does not, as a rule, benefit scrofulous ulcers, on account of their low 
vitality ; the cleansing and iodoform treatment is preferable. Cod-liver oil 
emulsions, hypophosphites, iron, nutritious diet, with the usual hygienic 
observances, constitute the general treatment, The removal of dead or 
dying bone may hasten healing or complete the cure. 



DISEASES OF THE LARYNX. 

Laryngeal affections may be primary or secondary ; primary, when the 
larynx is first affected, and the affection is local; secondary, when the 
laryngeal disease occurs as a complication, and depends upon some morbid 
state of the general system. I shall consider them under the following 
heads : 

I. Acute Catarrhal Laryngitis. V. (Edema Glottidis. 

II. Chronic Catarrhal Laryngitis. VI. Croupous Laryngitis. 

III. Chronic Laryngitis of Phthisis. VII. Laryngeal Ulcers. 

IV. Chronic Laryngitis of Syphilis. VIII. Neiforoses of the Larynx. 

IX. Tumors of the Larynx. 

The most important to the general practitioner in this list are the inflam- 
mations. 

ACUTE CATARRHAL LARYNGITIS. 

Acute Catarrhal Laryngitis is an acute inflammation of the mucous 
membrane of the larynx, which gives only the products of a catarrhal 
inflammation. It may occur at any age, and be mild or severe in type ; 
the severity varies in proportion to the extent that the submucous areolar 
tissue of the larynx participates in the morbid processes. 

Morbid Anatomy. — The anatomical changes which take place in this 
affection are characterized by redness, swelling and softening of the laryn- 
geal mucous membrane ; its surface, at first dry, the function of the 
mucous glands being arrested, is soon coated with mucus which contains 
epithelial and pus-cells. When the deeper tissues are affected, the in- 
flammatory products accumulate beneath the mucous membrane, in its 
substance and upon its surface, causing tumefaction of the parts, which in 
this situation is attended with danger. On the other hand, when the in- 
flammatory process is superficial, and all the products are upon the surface 
of the membrane, there is little danger. At the post-mortem examination 
there is often less redness and swelling of the laryngeal membrane than were 
observed during life, owing to the richness of this mucous membrane in 



44 



DISEASES OE THE RESPIRATORY ORGANS. 



elastic tissue. The redness and swelling are due to hyperemia and infil- 
tration of the mucous membrane. The mucous follicles may be so en- 
larged as to be recognizable by the naked eye, and each may yield on pres- 
sure a drop of muco-pus. The mucus is their natural secretion greatly in- 
creased in amount, containing pus-cells and swollen epithelial cells. If the 
follicle continues to suppurate, it is destroyed, leaving a small depression 
or ulcer. This inflammation usually runs a rapid course, yet in some 
cases it becomes chronic. It may produce superficial erosions, it may also 
be accompanied by ecchymoses of the membrane, and an escape of blood in 
the secretions ; it is then said to be hemorrhagic, and the hemorrhage is 
due to rupture of capillary vessels. Again, in some cases it is limited to a 
portion of the larynx, more especially to the epiglottis ; then it is usually 
associated with inflammation of the mouth, fauces and pharynx. The 
danger in this form of laryngitis is due not only to the submucous inflam- 
mation, but also to the spasm of the glottis, which the infiltration causes, 
partly by reflex action, partly by direct irritation of the adductor muscles 
of the vocal cords. 

Etiology.— Badly nourished cachectic subjects, rather than the strong and 
healthy, are predisposed to acute catarrhal laryngitis ; those constantly ex- 
posed to changes of temperature in the open air are less liable to be affected 
with it than those who are rarely subjected to such exposures. There is 
also a peculiar vice of constitution that renders certain persons especially 
liable to catarrhal inflammation, and consequently predisposes them to 
attacks of catarrhal laryngitis. Among the exciting causes of this affection 
may be named chilling of the surface by exposure to wet and cold, par- 
ticularly that of the neck and feet. Mechanical violence to the larynx, in- 
halations of irritating vapors and acrid liquids may give rise to the most 
intense laryngeal catarrh. 

Laryngitis may also be developed secondarily during the course of the 
exanthematous fevers, typhus fever, diphtheria, syphilis, and phthisis; not 
infrequently it is the result of the extension of inflammation from parts 
adjacent to the larynx, as in tonsillitis, erysipelas, etc. Acute bronchitis is 
usually attended by a mild form of acute laryngeal catarrh. 

Symptoms— The symptoms that attend the development of acute ca- 
tarrhal laryngitis vary with the extent and severity of the inflammatory 
process ; it usually comes on insidiously, and a very mild laryngeal catarrh 
may suddenly become very severe. Usually at first there is soreness of the 
throat, accompanied by a sense of constriction, or a tickling sensation with 
a tendency to cough ; the larynx is tender on pressure, there is difficulty in 
swallowing, which becomes more and more marked as the disease pro- 
gresses ; to this is soon added difficulty of breathing. The character of the 
respiration varies with the seat of the inflammation. If it is confined ex- 
clusively to the upper portion of the larynx, as it often is at its onset, the 
difficulty will be with inspiration only, which will be prolonged and accom- 
panied with stridor ; if the lining membrane of the whole larynx is involved, 
and the calibre of the larynx becomes contracted from cedematous infiltra- 
tion and spasmodic approximation of the vocal cords, there will be difficulty 
with both inspiration and expiration, and both will be protracted and 



ACUTE CATARRHAL LARYNGITIS. 



40 



wheezing ; in severe cases the patient will be unable to lie down. There is 
a harsh stridulous cough, with (at first) little or no expectoration ; if there 
is any, it is tenacious ; later it may become thick, purulent and abundant. 
The voice is hoarse or is reduced to a whisper. These local symptoms are 
accompanied by a flushed face, a hot, dry skin, the temperature often rising 
to 105° F. The pulse is frequent and hard in character. In severe cases, as the 
disease advances, both acts of respiration become more and more labored, the 
cough more and more metallic in character, the patient's distress increases, 
symptoms of imperfect aeration of the blood are developed, the countenance 
becomes pale and anxious, or livid. During the exacerbations caused by 
spasm of the laryngeal muscles, suffocation seems imminent ; in the inter- 
vals the patient becomes drowsy, the vesicular murmur over both lungs is 
feeble or inaudible, the capillary circulation is obstructed, the lips and 
nails become blue, a cold perspiration breaks over the surface, the respira- 
tory sounds become gasping in character, and finally delirium and coma 
close the scene. 

As soon as the characteristic symptoms are manifest, a laryngoscopic 
examination will show the mucous membrane of the larynx to be of a 
bright red color ; if the case is severe, oedema soon appears, the parts 
being red, swollen and semi-transparent. The tumefaction will be most 
marked on the ventricular folds, which may entirely conceal from view 
the vocal bands ; this redness and tumefaction may extend into the 
trachea, or may be confined to the mucous membrane of the larynx and 
free borders of the epiglottis. Death may occur in a few hours or it may 
be delayed five or six days ; it is caused either by a complete closure of the 
rima glottidis from tumefaction of the mucous and submucous tissues, or 
the patient struggles on with obstructed respiration and dies from pulmon- 
ary or cerebral congestion and oedema. If death takes place suddenly, it is 
caused by the combined effects of cedematous swelling and spasm of the 
glottis. When fatal, its course is usually rapid and severe ; when recovery 
takes place, it is mild in character, and extends over a period of seven or 
eight days. 

Differential Diagnosis. — The affections which may be confounded with 
acute catarrh of the larynx, are croupous laryngitis, diphtheria, cedema of 
the larynx, spasmodic asthma, hysterical laryngeal spasm, and thoracic 
aneurism. In very young children it is often impossible to distinguish 
between catarrhal laryngitis and croupous laryngitis ; but when the laryn- 
goscope can be used, the presence or absence of false membrane decides the 
question. The history of the attack, the accompanying constitutional 
symptoms, and a careful laryngoscopic examination, will enable one readily 
to distinguish between the laryngeal symptoms of acute laryngitis and 
those of diphtheria, oedema glottidis, or laryngeal spasm ; while a physical 
examination of the thorax determines the existence or the non-existence of 
spasmodic asthma and thoracic aneurism. 

Prognosis. — Age is the most important element in prognosis. In young 
children this disease is always attended with danger ; in adults the danger 
depends upon the amount of oedema present. The tendency, even in 
severe cases, is to recovery. In those that tend to a fatal termination, 



40 



DISEASES OF THE RESPIRATORY ORGANS. 



when death is imminent it may be averted by the performance of tracheotomy. 
There is always danger that the inflammation will extend into the trachea, 
and lead to a bronchitis or pneumonia. 

Treatment. — When active febrile symptoms are present in the early 
stage of acute catarrhal laryngitis, occurring as a primary disease in a 
strong, robust adult, venesection to syncope may be of service ; bat if the 
symptoms which indicate imperfect aeration of the blood are present, or if 
the laryngitis is a secondary affection, venesection is not only useless but 
does positive harm. There is no reliable evidence that local depletion by 
leeches, the application of blisters, or the internal administration of an- 
timony or calomel, has any power to arrest the progress or alleviate any 
of the distressing symptoms of this disease. It has been claimed that when 
the disease involves but a small portion of the larynx, the direct applica- 
tion of a solution of nitrate of silver, eighty or even ninety grains to the 
ounce, to the inflamed portion, by means of a sponge, camel's-hair brush, 
or with a laryngeal nebulizer, speedily relieves the dyspnoea and ameli- 
orates the general symptoms. Few, however, have the requisite skill and 
experience in topical medication of the larynx to make such applications 
efficaciously, or at least to accomplish what is claimed for them. Most 
practitioners would do much more harm than good were they to attempt to 
make such applications. Externally, both hot and cold applications are 
recommended. The rubber or metallic coil is the most efficient means of 
employing either, and should be applied upon the earliest manifestation 
of the disease. Cold applications, when employed, are most efficacious at 
the onset of the inflammation, but my experience leads me to prefer hot 
applications throughout its entire course. 

For the successful management of this disease, a warm, moist, and uni- 
form temperature is essential ; the temperature of the apartment should 
never be allowed to fall below 76° F. When the submucous areolar tissue is 
either not at all or only slightly involved, vapor inhalations unquestionably 
give the greatest relief, and have greater power in arresting the inflamma- 
tory process than all other local measures ; they should be commenced 
early and perseveringly continued. Aconite, in \ ill doses, repeated every 
half hour until dryness of the throat is produced, is often of value in 
adults as well as with children. 

When the temperature reaches 103° F. at the onset, one or two full 
doses of quinine will be of service. If the inflammatory process is not 
arrested by the combined action of these remedies, oedema is almost sure 
to follow, and the parts should be freely scarified ; in the adult this may 
readily be done with a laryngeal lancet by the aid of the laryngoscope. 
Should this treatment fail or be impossible, and should the dyspnoea be of 
a threatening character, and the signs of imperfect aeration of the blood be 
well marked, tracheotomy must not be delayed. Intubation by O'Dwyer's 
method, or even the passage of a soft catheter through the larynx, may 
frequently be employed in place of the more serious operation with equally 
good results. Many lives have been lost by too long delaying operation. 
For the successful management of acute laryngitis, rest to the larynx is 
all important. 



SIMPLE CHRONIC CATARRHAL LARYNGITIS. 



47 



SIMPLE CHRONIC CATARRHAL LARYNGITIS. 

This is essentially a chronic inflammation of the lining membrane of the 
larynx, the submucous tissue being slightly involved. When once estab- 
lished its tendency is to remain stationary. Like the acute, it may be 
general or partial. 

Morbid Anatomy. — When the disease is fully developed the mucous sur- 
face of the larnynxis always more or less coated with mucus or pus. Its 
tissue is dark colored, sometimes of a grayish red or bluish hue, owing to 
previous ecchymosis ; it may be either softer or firmer than natural ; the 
mucous glands are large and prominent, the submucous tissue is thickened, 
and the vocal bands may either become relaxed or stilfened, and hence vi- 
brate less than in health. Paresis of certain laryngeal muscles may result 
from the thickening and infiltration. When the trachea is involved, the 
portion of the mucous membrane covering its rings is reddened, while 
the intermediate portions are of a dark gray color. 

Etiology. — This affection may occur as a primary disease, or as a sequela 
of a mild form of acute laryngitis ; not infrequently it is the result of the 
extension of a pharyngeal inflammation in those who constantly use the 
voice in public speaking or singing. It constitutes the chief morbid con- 
dition in what is termed " clergyman's sore-throat." It is frequently 
secondary to a chronic nasal catarrh — the catarrhal process extending from 
the nasal passages. The constant inhalation of irritating particles may be 
a cause of chronic laryngitis ; but it most frequently occurs as an accom- 
paniment of other affections, as syphilis, pulmonary phthisis, and laryngeal 
morbid growths. When it occurs, as it frequently does, in phthisical or 
syphilitic subjects, it is described as laryngeal phthisis, and syphilitic laryn- 
gitis. The variety which is the result of the extension of a follicular 
pharyngitis, is sometimes separately described as chronic glandular 
laryngitis, but it does not differ from simple laryngeal catarrh, except 
that in it the minute racemose glands are principally affected. The sudden 
development of the larynx in males which takes place at puberty is often 
attended by a mild form of chronic laryngeal catarrh. In every variety of 
chronic bronchitis, especially that occurring in old age, there is more or 
less chronic laryngeal catarrh, — in many instances the laryngeal catarrh is 
secondary to the bronchitis. 

Symptoms. — The symptoms of chronic catarrhal laryngitis are altogether 
local in character. The most characteristic are the changes which occur 
in the voice ; in some it is hoarse and husky, in other cases the patient is 
only able to speak in a husky whisper. The voice is most often reduced to 
a whisper in the dry variety of laryngeal catarrh. Accompanying or pre- 
ceding the vocal changes, there is a hoarse, stridulous cough, with more or 
less abundant muco-purulent, or purulent expectoration ; not infrequently 
the expectoration is streaked with blood, and of a fetid odor. Inspiration 
and expiration are more or less impeded, and are often accompanied by a 
whistling or stridulous sound, and moist rales can usually be heard over 



43 



DISEASES OF THE EESPIEATORY OEGANS. 



the larynx. There is often soreness and tenderness of the laryngeal carti- 
lages when pressed laterally or backward against the spine. In some cases, 
the act of swallowing fluids or solids is attended with no inconvenience ; 
in other cases it excites spasm of the glottis, and thus occasions fits of dis- 
tressing dyspnoea. If constitutional symptoms exist, they are due to sym- 
pathetic irritation, and are in no way characteristic of the disease. The 
principal danger is from chronic laryngeal oedema, but this is of exceed- 
ingly rare occurrence. The laryngoscopic appearances correspond to those 
changes already described under the head of morbid anatomy of the dis- 
ease. The laryngeal mucous membrane is of a deep red color, verging on 
purple. The change in color is most marked over the vocal cords and ary- 
tenoid cartilages ; sometimes the larynx has the appearance of being very 
much dilated, at other times it is apparently contracted. The mucous 
surface may be covered over with a muco-purulent secretion, or may pre- 
sent a dry and shining appearance ; the enlarged orifices of the glands may 
be seen as pale specks on the congested membrane, or as red circles stud- 
ding a pale membrane. In addition to these more common appearances, 
more or less extensive thickening and papillary excrescences are sometimes 
visible. 

Differential Diagnosis. — The diagnosis of chronic laryngitis is readily made; 
the changes in the voice at once direct the attention to the larynx, and 
the laryngoscope will determine the nature, extent and exact seat of the 
disease. From the general and local symptoms, chronic laryngitis may be 
confounded with laryngeal growths and nervous affections of the larynx, 
but a careful laryngoscopical examination will correct any error. Phthis- 
ical and syphilitic laryngitis may be distinguished from simple catarrhal 
laryngitis by the presence of ulcers, by a careful physical examination of 
rhe lungs, and by the history of the patient. If both phthisis and syphilis 
can be excluded, however extensive the disease, it must be regarded as of 
primary origin. 

Prognosis. — The prognosis in this affection depends on its pathological 
associations. All forms of simple chronic laryngitis, unless complicated, 
may be recovered from ; at least, it rarely, if ever, leads to a fatal termina- 
tion. It is always difficult, however, and sometimes impossible to cure 
chronic laryngitis in old people. 

Treatment. — The most efficient agents in the treatment of this variety of 
laryngitis are local applications, within the larynx, to the parts affected. 
These topical applications may be made at the time of a laryngoscopical 
examination, either by means of a sponge or camel's-hair brush carried 
within the larynx, by the inhalation of vapor impregnated with some vol- 
atile substance, or in the form of nebulized liquids. The most certain and 
most satisfactory method is the use of atomized liquids, applied by means 
of the laryngeal spray — the mechanical chilling produced by the spray adds 
to the efficiency of the astringent solutions. Sponges and brushes are apt 
to irritate, and produce hyperaemia of the larynx. When local applications 
are to be used for a long time, mild astringent solutions are preferred. 
A solution of alum, perchloride of iron, tannin, or the sulphate of zinc, 



CHRONIC CATARRH OF THE LARYNX IN PULMONARY TUBERCULOSIS. 49 

from one to twenty grains to the ounce of water, may be used. If the ap- 
plications are made directly to the diseased tissues, and sufficiently often, 
it matters very little what astringent solution is used. When the laryn- 
geal secretion is excessive, the local application of turpentine sometimes 
does good. For steam inhalations, a few drops of oil of creosote, oil of 
pine, or oil of juniper, added to half a pint of water at a temperature of 
150° F., may be employed. Neither the steam nor spray inhalations should 
be continued more than five minutes at a time ; they may be repeated three 
or four times during the twenty-four hours. A solution of carbolic acid 
(two grains to an ounce of water), either as a spray or as a steam inhala- 
tion, may be used with benefit in cases where the laryngeal secretion has a 
fetid odor. In such cases the nares should be carefully examined, and the 
passage of offensive nasal discharges into the larynx should be prevented. 
In addition to the local treatment, the patient must be removed from all 
sources of laryngeal irritation. The vocal organs must have perfect rest ; 
the patient, if possible, should change climate, removing to such as he finds 
best suited to his individual case ; as a rule, a warm, dry atmosphere best 
agrees with this class of patients. 

The constitutional treatment of each patient will be governed by his 
general condition, and the pathological relations of the laryngitis. The 
general hygiene of the patient should always be carefully regulated. 

CHRONIC CATARRH OF THE LARYNX IN PULMONARY TUBERCULOSIS* 

Simple catarrhal laryngitis associated with pulmonary phthisis is often 
modified by the phthisical cachexia. When the inflamed surface becomes 
the seat of tubercular development, and the secretions are found to contain 
bacilli, it is called laryngeal tuberculosis, or phthisis. 

Morbid Anatomy. — The laryngeal structure, sympathizing with the general 
impairment of nutrition, is pale in the earlier stage of the affection. As 
the inflammatory and tissue changes advance, the mucous membrane be- 
comes irregularly vascular and of a peculiar ashy-red hue, but its tissues 
become progressively thickened. A pear-shaped enlargement over the 
mucous membrane which covers the arytenoid cartilage is a characteristic 
feature of pronounced laryngeal phthisis. The epiglottis in the catarrhal 
stage of the affection is often enlarged and shaped like a turban. The sub- 
mucous tissues become infiltrated with small cells. These cells show a 
tendency to cluster and form cheesy centres, thus paving the way to the 
development of tubercular ulcers. (Edema from serous transudation within 
the loose mucous tissue often occurs. Later, localized abrasions occur 
where the tissues are in contact, or at points where the friable tissues are in 
constant motion. The ulcerative stage may become pronounced, and 
superficial sores of an ashy-gray hue occur at points most favorable for 
their development. These ulcers may enlarge by coalescence or individual 
extension until a large portion of the ventricular bands, vocal cords, and 
epiglottis becomes involved. They often advance in depth, descending the 
laryngeal skeleton and eroding the cartilages; the roughened structures are 



50 



DISEASES OF THE RESPIRATORY ORGANS. 



constantly covered with the tenacious mu co-purulent discharges which 
come from the lungs, or are excited by the intense local irritation. 

Etiology. — The phthisical peculiarity of the inflammation receives its 
impress from the development of tubercle. Constant hawking or cough- 
ing, provoked by the passage of the irritating discharges over the laryn- 
geal structure, and the constant movement of the parts, favor the develop- 
ment of the laryngeal complication. The general cachexia, with attendant 
impaired nutrition, modifies the nature and course of the catarrhal pro- 
cesses, and favors the development of tubercle. 

Symptoms. — The early subjective symptoms are generally those of a modi- 
fied chronic laryngitis, associated with constitutional manifestations of 
pulmonary phthisis. The respiration may he hurried or embarrassed. 
Hoarseness cr complete aphonia is produced by the structural changes, and 
the irritating discharges excite distressing paroxysms of coughing. An 
examination of the laryngeal secretions will reveal the presence of tuber- 
cle bacilli. Painful deglutition is induced by counter-pressure of the 
inflamed or thickened abraded mucous membrane, the disturbance of ele- 
vated ulcers, or the friction of food. A harassing nervous cough exists 
in the ulcerative stage of the affection. The patient hesitates to take food 
on account of the pain caused by the passage of the bolus. This hastens 
the general emaciation. 

Differential Diagnosis. — The peculiar pyriform thickening over the aryte- 
noid prominence distinguishes the hypertrophic from simple chronic 
catarrhal laryngitis. The ashy-gray hue, irregular vascularity, and gray 
infiltrated vocal cords can readily be contrasted with the bright inflamma- 
tory redness of the laryngeal structures seen in simple catarrhal laryngi- 
tis. The non-existence of ulcers in simple chronic laryngitis will also aid 
in differentiating between the two affections. The contour of the syphili- 
tic ulcer and its bright red areola and irregular margin are not easily mis- 
taken for the pale and peculiar thickened mucous membrane of laryngeal 
phthisis, and its irregular ashy-gray ulcers. The syphilitic ulcer, more- 
over, advances rapidly, but usually painlessly ; the phthisical ulcer pro- 
gresses slowly, and is accompanied with much pain. The presence of 
tubercle bacilli in the secretion which covers the laryngeal surface estab- 
lishes the diagnosis. 

Prognosis. — Healing of the ulcers is usually considered the cure of a 
laryngeal phthisis. This, however, will depend upon the site and size of 
the lesions. When superficial ulcers upon the ventricular bands, vocal 
cords, or arytenoid prominences are seen early, they are sometimes curable. 
Ulcerations of the epiglottis are incurable, and often the indirect cause of 
death. Erosions of the cartilages are always exceedingly troublesome, and 
generally lead to a fatal issue ; the extent of the pulmonary disease and the 
general cachexia modify the prognosis in laryngeal phthisis. Extensive 
hypertrophy of the laryngeal mucous membrane does not seriously influ- 
ence the prognosis. Judicious local and general treatment will afford 
relief in every case, and frequently postpone the fatal issue. 

Treatment. — Treatment should be both constitutional and local. The 
general treatment is determined by the laryngeal symptoms, the condition 



(EDEMA GLOTTIDTS. 



53 



of the patient, and the co-existing pulmonary disease. Cough may be 
quieted by the internal administration of bromide of sodium or solution of 
morphia (U. S. P.). Its relief removes a source of irritation which is con- 
stantly acting on the inflamed or ulcerated larynx, and by affording rest 
favors repair or retards the advance of the local disease. It also soothes 
the disturbed nervous system, and allows the patient to gain strength by 
undisturbed sleep. In connection with the constitutional and hygienic 
treatment of the accompanying pulmonary disease, great relief can be 
afforded and life prolonged by the following local management of the 
laryngeal ulcers. The surface of a phthisical ulcer should be thoroughly 
cleansed by means of an alkaline spray; — a one per cent, solution of the 
phosphate, or carbonate of soda, with glycerine and carbolic acid or thymol, 
is most serviceable. Finely pulverized iodoform should then be blown 
upon the ulcerated surfaces. When there is much pain Magendie's solu- 
tion, or, better, a 4^ solution of cocaine, may be sprayed upon the ulcer- 
ated or inflamed tissues. The laryngeal sponge or brush is always contra- 
mdicated. Tracheotomy to rest the larynx and lessen the suffering is 
sometimes justifiable. It is of doubtful curative value, and may hasten 
the impending crisis by accelerating the progress of the pulmonary lesions. 

CHRONIC CATARRHAL LARYNGITIS OF SYPHILIS. 

The course, symptoms, and appearance of chronic catarrhal laryngitis 
may be modified by constitutional syphilis. Constitutional infection may 
cause a syphilitic non-ulcerative laryngitis, as a secondary or tertiary mani- 
festation. In its advanced stage it is often complicated by ulceration. The 
vascularity of the mucous surface does not show the rapid variations seen 
in ordinary catarrhal laryngitis ; it is far more persistent. The arterial 
red of catarrhal laryngitis is replaced by a deep red or even a livid hue. 
The discomfort which it causes does not, as in simple laryngitis, correspond 
in severity with the intensity of the congestion. A syphilitic history and 
the disappearance of local manifestations under appropriate internal medi- 
cation aid in determining its character. The treatment consists in the 
application of tincture of iodine by means of sprays, brushes, or vaporizers, 
with or without the insufflation of iodoform ; simple applications of iodo- 
form by means of Ely's laryngeal powder-blower are often markedly bene- 
ficial. The parts should be thoroughly cleaned with alkaline sprays before 
each application. In all cases local and constitutional treatment should be 
combined. A rapid increase in the size of the dose of iodide of potassium 
is often required, to effect the desired changes. 

(EDEMA GLOTTIDIS. 

(Edema Glottidis is a term which has been used to indicate the 
occurrence of a dropsical effusion or inflammatory exudation into the areolar 
tissue beneath the laryngeal membrane above the vocal bands. Strictly 
speaking, it is not oedema of the glottis, but of the upper portion of the 
larynx. Its gravity, and the necessity of its prompt relief, make the early 



52 



DISEASES OE THE EESPIRATORY OEGAKS. 



recognition of its existence, and of fche pathological conditions which lead 
to its occurrence and attend its development, very important. 

Morbid Anatomy.— The effusion, which is almost always serous, takes 
place in the loose cellular tissue beneath the mucous membrane of the up- 
per part of the larynx, principally in the ary -epiglottic folds, and at the 
b'ise of the epiglottis ; as a consequence, these parts become prominent and 
the epiglottis swollen. On either side there may be a tumor an inch or 
more in diameter, projecting into the cavity of the larynx and pharynx ; 
in some cases these tumors touch each other, completely occluding the la- 
ryngeal cavity. The mucous membrane may be either red or pale. On 
pricking the tumors, a clear, or turbid, or even a purulent fluid may es- 
cape ; after which the parts previously distended collapse, and the mucous 
membrane is left wrinkled and folded. The effusion may occur wholly or 
principally on one side. Not infrequently after death, owing to the dis- 
appearance of the effusion, the wrinkled condition of the mucous mem- 
brane is all that is found, or, at least, there is much less effusion than 
might have been expected from the appearance of the parts during life. 

Etiology. — (Edema of the glottis rarely if ever occurs as a primary affec- 
tion, but is secondary to, or is a complication of, some local laryngeal dis- 
ease or constitutional disorder. Any inflammatory affection of the larynx 
or of the adjacent tissues may give rise to it, such as acute laryngitis (espe- 
cially that due to local irritation), erysipelas of the neck, deep-seated cer- 
vical abscesses, and acute tonsillitis. It occasionally occurs as a complica- 
tion of the laryngeal ulceration of typhus and typhoid fever, small-pox and 
scarlatina. Sometimes it is the immediate cause of death in the general 
dropsy of Bright's disease, and in the venous obstruction which attends 
some forms of cardiac disease and thoracic aneurism. 

Symptoms. — The prominent symptom of this affection is dyspnoea, and 
the difficulty in breathing is mainly confined to inspiration. No difficulty 
in swallowing is experienced, nor is there tenderness on pressure over the 
larynx. Fever and the other constitutional symptoms which attend acute 
laryngitis are absent. It is accompanied by paroxysms of extreme dyspnoea 
— suffocative breathing being usually the first indication of its occurrence ; 
there is also an uneasy sensation in the region of the larynx, and a constant 
inclination on the part of the patient to rid the upper part of the throat of 
some supposed secretion. If the index finger be carried below the epiglot- 
tis, cedematous tumors may be distinctly felt. Hoarseness or huskiness cf 
voice may not be present, unless laryngitis coexist. The laryngoscope re- 
veals two tense, smooth, rounded swellings immediately behind the epi- 
glottis ; these swellings, after meeting in the centre, with a sulcus between 
them, appear oval. The oedema is usually most marked at the ventricular 
folds, which explains the nature of the urgent dyspnoea. Whenever, dur- 
ing the progress of any disease in which oedema glottidis is liable to occur, 
there is the slightest difficulty in respiration, the difficulty being limited 
to inspiration, the possible occurrence of this complication should be re- 
membered. 

Differential Diagnosis. — The circumstances under which oedema glottidis 
is developed, the suddenness of its occurrence, the peculiar character of the 



ACUTE CROUPOUS LARYNGITIS. 



53 



respiration, indicating obstruction at the upper portion of the larynx, and 
the absence of febrile excitement, constitute a group of symptoms almost 
pathognomonic. When to these is added the presence of oedematous tu- 
mors at the upper portion of the larynx, the differential diagnosis between 
it and other laryngeal affections is easily made. 

Prognosis. — The tendency of this affection is to speedily destroy life, but 
in most instances death may be averted by prompt and efficient surgical 
interference. 

Treatment. — There is no time to be lost in fruitless medication. In ex- 
treme cases, laryngotomy or tracheotomy must be performed early. It is 
recommended, by some, to scarify the edges of the oedematous epiglottis or 
ventricular bands and ary-epiglottic folds, so as to give free exit to the 
effused fluid before resorting to these operations. This scarification can 
rarely be accomplished, except by an experienced hand, and, in extreme 
cases, the delay and danger which attend such an attempt are hardly justi- 
fiable. 

ACUTE CKOUPOUS LAKYXGITIS. 

{Membranous Croup.) 

Croupous inflammation of the larynx differs from catarrhal in the nat- 
ure of its inflammatory products. The inflammatory process may be 
limited to the larynx, or it may extend into the trachea ; and broncho-tra- 
cheitis so frequently accompanies it that the disease has received the name 
of cynanche'trachealis, but in all instances the tracheal inflammation is 
secondary to the laryngeal. Croupous laryngitis is a local inflammation. 

Morbid Anatomy. — When fully developed, there exists over a varying ex- 
tent of the mucous membrane a whitish, or yellowish-white, fibrinous 
layer, often spotted here and there with dots and lines. This membranous 
exudation may be limited to a few patches, or form a cylinder which may 
extend into the trachea and bronchi. At one time it is firm in its consist- 
ence, and tenaciously adheres to the subjacent membrane, while at another 
it is soft and easily separated from it. Its thickness varies ; sometimes it is 
scarcely perceptible, at others it may be a line or more in thickness. Its 
surface is smooth, it adheres firmly to the vocal cords and the upper part 
of the epiglottis. After the membrane is once formed, it may be cast off 
in the form of a cylinder, in bands, or shreds. Its separation is effected by 
the secretion of the follicles which have been obstructed, as well as by a 
serous exudation from the previously inflamed membrane. It may break 
up into threads, and be expectorated as such, or it may undergo a gran- 
ular, fatty, or, more rarely, a mucous degeneration, and so become a fluid 
resembling mucus, 

In its earlier stages, the mucous membrane of the larynx presents the 
same appearance as in catarrhal inflammation. When the false membrane 
has formed, it takes the place of the epithelium, and is situated on the ho- 
mogeneous boundary layer of the mucous membrane which exists in the 
greater part of the larynx. The tissue is pale, except when it is dotted 
with ecehymoses, which correspond to similar spots in the membranous 



54 



DISEASES OF THE RESPIRATORY ORGANS. 



exudation. The laryngeal membrane is somewhat swollen, and moister than 
normal. Generally, the submucous tissue is only slightly involved. A 
microscopic examination of this membranous exudation shows it to consist 
of a homogeneous, shining net-work, in the meshes of which are inclosed 
pus-cells, rarely epithelium ; it may be made up of alternate layers of fibrin 
and cells. As the membranous exudation is cast off, the epithelium is 
quickly replaced, and the laryngeal membrane returns to its normal condi- 
tion. Sometimes, after the mem- 
brane is thrown off, it is reproduced. 
The submucous tissue is more liable 
to be involved in adults than in chil- 
dren. Very frequently membranous 
pharyngitis precedes and is associated 
with croupous laryngitis. Pulmon- 
ary congestion, oedema, atelectasis, 
emphysema, and lobular pneumonia 
not infrequently occur as complica- 
tions in the course of this disease. 

Etiology. — Age is the most promi- 
nent predisposing cause. It is rare in 
adults (except from traumatic causes), 
or in very young infants. The time of 
its greatest liability is between the period of dentition and puberty. There 
is no evidence that its development is due to any specific atmospheric 
poison. Following Bretonneau, many authors have regarded croup as 
depending upon the same specific poison as diphtheria, but representing 
a milder grade of infection. I am unable to see that either pathological 
researches or clinical facts are sufficient to establish this position. Expos- 
ure to cold and moisture, with sudden alterations of temperature, are 
among its most frequent exciting causes. • It occurs more frequently dur- 
ing the winter and spring months. Delicate, weakly, and ill-nourished 
children, rather than the strong and healthy, are liable to it. It not infre- 
quently follows the sudden disappearance of eczematous eruptions on the 
head and face ; occasionally it follows measles, scarlatina, and variola, 
and sometimes complicates diphtheria ; and when diphtheria is prevailing 
it is often difficult to draw the line between them. 

Symptoms. — Acute croupous laryngitis usually begins with the ordinary 
symptoms of a simple cold ; at its commencement there is nothing to dis- 
tinguish it from an ordinary catarrh. If the throat is examined the whole 
visible mucous membrane will be found red and tumefied. Usually the 
first symptom that attracts attention is a slight hoarseness ; a little later the 
respiration becomes difficult, the expiration noisy, and it is accompanied 
by a high-pitched stridulous cough. The inspiration that immediately 
follows the cough is accompanied by a loud crowing noise. Although there 
is no pain or tenderness in handling the larnyx, there is some difficulty in 
swallowing, and the child frequently puts its hand to its throat as if to re- 
move some obstruction. With the first croupy paroxysm, however slight, 
the pulse is accelerated and becomes full and hard ; there is increased heat 




Fig. 12. 



Croupous Membrane from the Trachea. 

«, Section through the false membrane, 
b, Upper layer of mucous membrane, infiltrated 
■with pus-corpuscles (d t ). 
r, Filaments and granules of fibrin, 
d, Pus-corpuscles. After Zeigler. x 250. 



ACUTE CROUPOUS LARYNGITIS. 



55 



and redness of the surface, especially of the face, with injection of the 
conjunctival vessels ; the axillary temperature may range from 102° R to 
104° F. These febrile symptoms somewhat subside as the paroxysm passes 
off, to return, however, with greater intensity on the return of the next 
paroxysm. At the commencement of the attack the paroxysms of dyspnoea 
are more frequent and severe at night than during the day. 

As the disease advances the voice is entirely lost ; the patient speaks and 
cries in a whisper; the cough becomes more and more stridulous in charac- 
ter, without expectoration ; the head is thrown back ; the respiration grows 
more and more difficult, and with each inspiration there is contraction of 
the lower part of the chest and sinking in of the soft parts above the clav- 
icles. The vesicular murmur over both lungs is feeble or inaudible : with 
every inspiration the epigastrium, instead of projecting, is strongly de- 
pressed, and the outward movement of the lower ribs is arrested. Every 
muscle that can aid in expanding the chest is brought into violent action. 
During these laborious efforts at inspiration the nostrils are dilated. As the 
laryngeal obstruction increases, the paroxysms of dyspnoea become more 
urgent and without remission ; there is a restless tossing of the limbs, and 
the greatest terror is depicted on the face, which, at one time, is pale, at 
another livid; the pulse becomes rapid and feeble ; the temperature falls 
sometimes below the normal and the extremities become cold. Gradually, 
as the blood becomes imperfectly aerated, the patient becomes drowsy, at 
times rousing up and gasping for air, and springing from one place to an- 
other to find relief ; the lips and nails become blue, the respiration shorter 
and shorter, until at last, after a violent paroxysm of dyspnoea, the patient 
becomes unconscious and quietly ceases to breathe. The disease always at- 
tains its height by the end of the third day; death may occur within forty- 
eight hours after its commencement; its whole duration rarely exceeds five 
days. 

In accordance with its symptomatology, croupous laryngitis may be di- 
vided into three stages : a precursory or catarrhal stage, a stage of develop- 
ment, and a suffocative stage, or stage of collapse. The most important 
fact connected with its clinical history is, that in a large proportion of 
cases before the urgent symptoms come on, the membranous exudation can 
be seen on the tonsils. In most cases the membrane is first formed on the 
tonsils or in their immediate vicinity. As the membrane extends into the 
larynx there is loss of voice, a stridulous cough, difficult breathing, and the 
face is alternately flushed and pale. For a day or two, while the mem- 
brane is extending and becoming thicker, the patient remains in about the 
same condition, gradually growing weaker, the capillary circulation on the 
surface becoming more and more imperfect, the respiration more and more 
labored, the paroxysms of dyspnoea more and more frequent and severe, 
until there is little hope of recovery. Sometimes all the urgent symptoms 
are suddenly relieved, the patient coughs, and a stringy matter is expecto- 
rated, he struggles for a moment in a violent paroxysm of dyspnoea, and 
a perfect membranous cast of the larynx, and perhaps of the trachea, and 
larger bronchi is expectorated. Now he passes into a quiet sleep, and re- 
covery seems certain ; but still there is great danger — from the formation of 



56 



DISEASES OF THE RESPIRATORY ORGANS. 



a new membrane ; from the extension of the inflammation into the minute 
bronchial tubes, giving rise to capillary bronchitis and pneumonia ; and 
from the exhaustion that has occurred before the membrane was thrown off. 
A laryngoscopic examination is rarely possible in this class of patients. 

Differential Diagnosis. — The two affections of the larynx which are most 
liable to be confounded with this form of laryngitis, are simple catarrh of 
the larynx, called spasmodic or pseudo-croup, occurring in nervous subjects, 
and purely spasmodic affections of the larynx. In both, the laryngeal 
spasms give rise to croupy symptoms. In spasmodic croup or simple 
catarrh of the larynx, the croupous phenomena come on suddenly, the 
attack usually occurs at night, it is not preceded or accompanied by active 
febrile symptoms, there is no complete loss of voice, and there is absence of 
membranous exudation on the tonsils and epiglottis. All of these condi- 
tions are important diagnostic features of croupous laryngitis. Within 
twenty-four hours after the commencement of an attack of catarrhal croup, 
auscultation of the chest furnishes signs of incipient bronchial catarrh. 
Spasm of the glottis, which may give rise to croupy symptoms, is excited 
in infancy by a variety of causes. Among these are dental irritation, gas- 
tric irritation, enlargement of the thymus gland, giving rise to what is 
called thymic asthma, and undue excitability of the nervous system, the re- 
sult of hereditary predisposition. These laryngeal spasms may be recog- 
nized by the suddenness and violence of the attack, by the absence of the 
catarrhal and febrile symptoms, by the absence of alteration of the voice, 
and by the speedy and complete relief which immediately follows the spasm. 
Diphtheria involving the larynx, sometimes mistaken for croup, may be 
distinguished from it by the following characteristics : first, either diph- 
theria is epidemic, or there is a history of contagion ; second, the develop- 
ment of the throat symptoms is preceded or accompanied by constitu- 
tional disturbances ; third, the glands at the angle of the jaws are usually 
enlarged, and the laryngeal symptoms are at first not urgent ; fourth, 
the pharynx presents the characteristic diphtheritic appearance before any 
laryngeal symptoms are present. 

Prognosis. — There are no data from which to estimate the ratio of mortality 
in this disease ; unquestionably it is one of the most fatal diseases of child- 
hood. When the diagnosis is based upon the presence of the membranous 
exudation on the tonsils and epiglottis, recovery seldom occurs. The signs 
of a favorable termination are, diminution in the frequency and severity of 
the paroxysms of dyspnoea, with less distress in breathing during intervals, 
a gradual return of the voice, and a moist sound with the cough. If, on 
the other hand, the paroxysms of dyspnoea become more frequent and vio- 
lent, the restlessness and dyspnoea increase during the intervals, and the 
cough is less powerful and more stridulous, the blueness of the lips and 
nose more marked, and the patient becomes more and more drowsy, re- 
covery is scarcely possible. The younger the patient, the greater the danger. 
In fatal cases, the duration of the disease is from three to seven days. If 
recovery takes place, it is slow, weeks often elapsing before the voice re- 
turns, during all of which time the patient is subject to violent paroxysms 
of dyspnoea. 



ACUTE CROUPOUS LARYNGITIS. 



57 



Treatment. — I do not purpose to discuss the merits of the various plans of 
treatment which have been proposed for the management of membranous 
croup, for under every plan the disease has proved fatal in the majority of 
cases. Simple catarrh of the larynx is so liable to be mistaken for 
croupous, that it is difficult to estimate the real value of the different 
remedial agents which have been claimed to have a controlling power over 
it. Statements that certain plans followed, or agents employed, have been 
successful in the majority of cases arouse distrust of the diagnosis; the ex- 
istence of croup should be asserted only upon positive evidence cf the 
presence of the membranous exudation. With the written history of mem- 
branous croup before us there is no evidence that calomel, blood-letting, or 
antimony has any power either to arrest the progress of the inflammatory 
action or to prevent the membranous exudation. In the treatment of this 
affection it is of the first importance that the patient should be placed in a 
large, well- ventilated apartment, the temperature of which should be kept 
uniformly at 75° F. to 80° F., and the air rendered moist by steam. In 
the case of children, a tent maybe made over the bed by means of blankets, 
into which is made to pass a constant current of steam from a kettle con- 
taining boiling water. As soon as evidence of imperfect oxygenation appears, 
a continuous stream of oxygen gas should be carried into the tent, or ar- 
rangements should be made so that it will be constantly inhaled by the 
patient; sometimes, in addition to these means, lime vapor, produced by 
slacking large quantities of quicklime in the room, will be found of service. 
During the whole course of treatment external application of moist heat 
should be constantly maintained. This is best accomplished by a metal 
coil bound upon a thin flat sponge. Wheuever there are indications that 
loosened portions of membrane act as causes of dyspnoea, an emetic may 
be administered ; the sulphate of zinc acts most promptly and efficaciously. 
The frequent administration of emetics should be avoided, on account of 
their depressing influence. Topical applications are not to be resorted to 
in its treatment, as they intensify rather than relieve the laryngeal spasm, 
which plays so important a part in producing the paroxysms of dyspnoea, 
and there is no evidence that they have any control over the inflammatory 
process. It is all-important that this class of patients, from the onset of 
the disease, should receive a most nutritious diet ; and as failure of the 
vital powers becomes apparent, stimulants may be freely administered 
upon the same principles as govern all adynamic diseases. As regards 
internal medication, I have little confidence in any of the so-called 
specifics. After the formation of the membranous exudation, the vapor 
inhalation and the oxygen gas are the only means which afford any hope 
that the patient can be safely carried through the disease. In regard 
to the propriety of tracheotomy the opinion of the profession is divided. 
The statistics of this operation in this disease are not to be relied upon. 
The only question to settle is, Has one life been saved by it ? If this 
can be answered affirmatively, the operation is justifiable. It never 
should be resorted to with a promise even of relief : if there are evi- 
dences that the membranous formation has reached the bronchi, and 



58 



DISEASES OE THE RESPIRATORY ORGAN'S. 



even when the membrane has formed in the trachea, temporary relief 
from the dyspnoea is all that can be promised. The operation, to be 
successful, must be performed early, and not be delayed, as it usually 
is, until the patient is beyond hope of recovery. Its success also un- 
doubtedly depends much upon the manner of its performance and the 
subsequent management of the case. As in other obstructive condi- 
tions of the larynx, intubation may often be substituted with success, 
unless the fauces and posterior nares are implicated and filled with the 
exudation. 

ULCEES OF THE LARYNX. 

The remaining laryngeal affections come more directly within the prov- 
ince of the specialist, and only the most prominent points in their history 
will be considered. The different forms of laryngeal ulcerations are in* 
eluded under the following heads : the catarrhal, the follicular, variolous, 
typhous, phthisical, and syphilitic. The most common forms are those 
occurring in phthisis and syphilis. 

Morbid Anatomy. — Catarrhal ulcers are usually superficial, and at first 
may be either rounded or oval ; afterwards, as the loss of substance be- 
comes more extensive, they coalesce and have an irregular outline, The 
follicular ulcer, as a rule, is superficial, with a limited area of extension. 
It sometimes constitutes a serious complication of laryngeal phthisis. 
Though of common occurrence in the pharyngeal and faucial cavities, it is 
seldom seen in the larynx. These ulcers may be situated upon any portion 
of the laryngeal membrane ; when they are located upon the anterior or 
posterior ends of the vocal bands, they have a tendency to spread length- 
wise. 

Variolous Ulcers are the result of small -pox pustules on the laryngeal 
membrane. They commence by the formation of soft, non-umbilicated 
pustules, which after a little rupture and form a rounded ulcer, which 
readily heals. 

Typhous Ulcers are generally of large size, and deep, penetrating through 
the mucous membrane, and sometimes involving the cartilages. The 
edges of these ulcers are everted, and of a dark purple color ; their com- 
monest seat is the posterior wall of the larynx, and the edges of the epi- 
glottis. 

Phthisical Ulcers may be superficial or deep ; the most frequent seat is 
the inter-arytenoid commissure. They are complications of laryngeal 
phthisis. Tb*s deficient vascularity of the pale and thickened arytenoids 
favors the occurrence of these ulcers. They may have their inception in 
an inflammation of the follicles of the epiglottis or neighboring tissue, and 
spread by coalescence ; sometimes they produce deep destruction of tissue. 
The epiglottis is often eroded at its margin, and the cartilage may be ex- 
posed or perforated. Calcification, as well as necrosis of the laryngeal 
cartilages, occasionally follows phthisical ulceration. The necessary move- 



ULCERS OF THE LARYNX. 59 

ment of the arytenoid, and the irritant action of the pulmonary discharges, 
may induce ulceration of the vocal cords. 

Syphilitic Ulcers of the larynx are usually met with among the tertiary 
manifestations of syphilis, and rarely if ever occur as secondary lesions of 
the disease. These tertiary ulcers frequently begin on the epiglottis and 
spread rapidly ; they often involve the mucous membrane of the entire 
larynx, and cause great destruction of tissue. They have an irregular out- 
line, with everted edges and yellow hue, excavated base, and at times pre- 
sent a more or less gangrenous appearance. In some cases they extend to 
the pharynx. They may originate in the breaking down of syphilitic 
tubercle or gummata. They often heal at the point attacked, while the 
ulceration advances in other places. The scars which result from the 
healing of the ulcers have a tendency to contract and narrow the calibre 
of the larynx. The papillary growths which surround these ulcers are 
especially characteristic of their syphilitic origin. 

Etiology. — Catarrhal laryngeal ulcers are rarely the result of acute la- 
ryngeal catarrh, but, as has been mentioned, are of not infrequent occur- 
rence in chronic catarrhal laryngitis, especially that which accompanies 
pulmonary phthisis. The follicular variety generally results from the ex- 
tension of a follicular faucitis from the pharynx to the larynx, or at least 
the two are frequently associated. 

Variolous ulcers have their origin in the propagation of the exanthem 
from the mouth and pharynx. 

Typhous ulcers have their origin either in diphtheritic infiltration or im- 
perfect nutrition of the mucous membrane of the larynx. 

Syphilitic ulcers depend upon a specific constitutional poison acting in 
conjunction with a catarrhal inflammation of the mucous membrane of the 
larynx. 

Phthisical ulcers are always secondary to the development of tubercu- 
lar tissue, which usually appears in the form of gray nodules, and may 
develop about the base of any chronic ulcerative process. 

Symptoms. — All forms of laryngeal ulcers are attended by the general 
symptoms of chronic laryngeal catarrh. When a patient with a harsh, 
stridulous cough of long standing (the expectoration containing pure blood 
and laryngeal tissue), with hoarseness at times amounting to aphonia, 
complains of a burning, smarting, pricking sensation in the larynx, with 
tenderness on pressure, which 'is increased by speaking, and of difficult 
and painful deglutition, attended by a wavy laryngeal respiration, there is 
reason to suspect the existence of a laryngeal ulcer ; but a positive diagnosis 
cannot be made from these symptoms alone, as extensive ulceration may 
exist and all of these symptoms be wanting, and they may be present where 
there is only laryngeal catarrh without ulceration. The appearance of the 
posterior wall of the pharynx is always of great diagnostic importance. 
The use of the laryngoscope clears up all doubt as to the existence or non- 
existence of laryngeal ulcers. By a careful laryngoscopic examination, the 
existence, as well as the seat and extent of these ulcers may be determined. 



60 



DISEASES OF THE RESPIRATORY ORGANS. 



Haying determined their existence, the history of the patient and a careful 
auscultatory examination of the chest will enable one to decide their char- 
acter. 

Prognosis. — The prognosis depends entirely upon their character. The 
catarrhal, follicular, typhous, and variolous are usually readily recovered 
from ; while the phthisical and syphilitic rarely, the former perhaps never, 
entirely heal ; or, if healed, the destruction of the parts is so great that 
the remaining cicatrix permanently interferes with the functions of the 
larynx. 

Treatment. — The treatment of laryngeal ulcers has been considered un- 
der the heads of chronic laryngeal catarrh, phthisical and syphilitic lar- 
yngitis. Ulcers which arise independently of these conditions require no 
special treatment. 

NEUROSES OF THE LARYNX. 

The true neuroses which are met with in the larynx are due to defective 
innervation of the recurrent laryngeal nerve. They will be considered 
unier the following heads : — 

I. Recurrent Laryngeal Paralysis. II. Paralysis of the Abductors of 
theVocal Cords. III. Paralysis of the Adductors of the Vocal Cords. 
IV. Paralysis of the Tensors of the Vocal Cords. 

Each form of paralysis may be limited to one side, or may affect botl 
sides of the larynx. 

Morbid Anatomy. — Eecurrent laryngeal paralysis maybe unilateral or bi- 
lateral. All the muscles supplied by the recurrent laryngeal nerves are 
usually affected in this form of paralysis. There is no constant morbid 
change in the tissues which compose the larynx ; frequently, however, there 
is thickening of the laryngeal mucous membrane, and the vocal cords lose 
their pearly lustre ; such conditions are most likely to be met with in pul- 
monary phthisis. In the absence of appreciable morbid appearances, this 
paralysis is produced by insufficient or unequal supply of nerve force. In 
unilateral paralysis of the adductors, only one of the recurrent nerves is 
diseased, either primarily or secondarily, or an inflammatory degenerative 
process may have been established in the muscle involved. Bilateral paral- 
ysis of the adductors is caused by compression of both recurrent nerves by 
tumors, aneurisms of the aorta, innominata, or subclavian arteries, and by 
degenerative processes in the nerves. Pathological changes at the apices of 
the lungs, or in the lymph glands in contact with the nerves, may also give 
rise to it. In bilateral paralysis of the abductors of the vocal cords, or 
openers of the rima glottidis, there is generally advanced atrophy of the 
laryngeal muscles, which is evidently dependent upon interruption of nerve 
force, either from cerebral disease or local pressure on the vagi, or on both 
recurrent nerves. It is frequently associated with constitutional syphilis. 
Unilateral paralysis of the abductors is usually of central origin, and is rare. 
Unilateral paralysis of the vocal cords, of a functional nature, is a rare 



NEUROSES OE THE LARYNX. 



61 



affection. It is sometimes observed in cases of chronic lead or arsenical poi- 
soning. Bilateral functional paralysis is of common occurrence — it is met 
with most frequently in hysterical females. In unilateral paralysis of the 
abductors, local pressure by different kinds of tumors is most frequently 
met with, and the wasting of muscular tissue, which attends such pressure, 
is usually limited to one side. It is stated that paralysis of the tensor mus- 
cles of the yocal cords indicates changes in the spinal nerve. This condi- 
tion is not, as is frequently stated, that of functional disturbance. There 
may be organic lesions present, such as follow contusion or laceration of 
nerve tissue. Atrophy of the spinal accessory nerves, consecutive to com- 
pression in their passage through the foramen lacerum posterius, has occa- 
sionally been met with. 

Etiology, — The etiology and morbid anatomy of laryngeal paralysis cannot 
be separated. A common general cause of laryngeal paralysis is some local 
change in the mucous tissues of the larynx. Women rather than men are 
subject to it. Pressure on, or traction of, the pneumogastric or recurrent 
laryngeal nerves, by tumors, enlarged glands, and thoracic aneurisms, is a 
frequent cause of laryngeal paralysis. Diphtheria, typhus and malarial 
fevers and other acute blood diseases are occasionally followed by laryngeal 
paralysis ; under these circumstances the paralysis is undoubtedly due to 
the direct effects of the special poison of the disease upon the nerve centres. 
The action of certain metallic poisons, such as lead, arsenic, mercury, etc., 
upon the larynx, after months or years of exposure to their poisonous in- 
fluence, may cause it. Central diseases in the brain or upper portion of the 
spinal cord are sometimes its cause. Whenever there is bilateral paralysis 
of the abductors its cause may be found in some more or less defined lesion 
of the brain. Paralysis of the laryngeal muscles may occur as a late mani- 
festation of constitutional syphilis. In rare instances laryngeal paralysis 
may be due-to atrophy and degeneration of the laryngeal muscles, and conies 
on without anv assignable cause. Temporary laryngeal paralysis, occurring 
in connection with hysterical manifestations, has no cause save the erratic 
one of hysteria, appearing and disappearing without any apparent cause. 
Mechanical violence not infrequently causes paralysis of the tensors of the 
larynx, as when a blow is struck, or there is a fail on some projection ; it 
also may occur as a sequela of too loud, too frequent, and too prolonged 
exercise of the voice in public speaking. 

Symptoms. — The phenomena which attend the different forms of laryn- 
geal paralysis are for the most part local in character. In paralysis of the 
muscles supplied by the recurrent laryngeal nerve, the patient is voiceless 
and unable to cough. When this form of paralysis is of hysterical origin, 
the voice comes and goes most capriciously — now it is normal, and in a 
short time the patient may become completely aphonic without any ap- 
parent cause. A laryngoscopic examination of the larynx will show that dur- 
ing attempted phonation the vocal cords remain apart, midway between ex- 
treme abduction and adduction : they may be perfectly motionless. In 
unilateral recurrent laryngeal paralysis, the voice may be but slightly im- 
paired. In rare instances, it will be unchanged during ordinary conversa- 



62 



DISEASES OF THE RESPIRATORY ORGANS. 



tion, and will only be impaired when an endeavor is made to sound the 
higher notes in singing, or after some extraordinary, continued effort of the 
vocal organs. The sound produced during coughing, sneezing, and laugh- 
ing is usually much changed and weakened. The laryngoscope shows 
that one vocal band does not act when the patient attempts to speak or 
cough. As has already been stated, this form of paralysis is due to some 
cause acting directly on the nerve of the affected side. 

Bilateral paralysis of the abductors is often accompanied by decided 
hoarseness and huskiness of the voice, rarely by entire loss of the voice ; 
articulate speech is often almost normal, and then suddenly, as though the 
current of air were interrupted, the patient is unable to make himself 
understood, so feeble, so utterly lost, has his phonetic power become. The 
prominent symptom of this form of paralysis is dyspnoea, with noisy, strid- 
ulous inspiration, which is always more or less marked, but becomes greatly 
aggravated after violent exertion, or on deep inspiration. A laryngoscopic 
examination shows both vocal bands in juxtaposition, near the median line, 
and they do not separate when a full inspiration is made ; on the con- 
trary, a forced inspiration makes them approach even to touching, while a 

forced expiration separates them a 
little. In unilateral abductor par- 
alysis, the voice is shrill and dis- 
cordant, and dyspnoea is present 
only after physical exertion. Dur- 
ing inspiration the paralyzed band 
does not move, but its edge is con- 
cave. It frequently remains station- 
ary, near the median line, but usual- 
ly it remains in the median line 

Fig. 13. J 
Diagram showing position of the vocal bands in ab- on aCCOUnt Ot the Unopposed COn- 

far^gosXe * r P ara ^ is as seen with the traction of the abductors. The 
The dotted iin?x a and a' indicate the pomon of band seems shorter than normal, 

the band* in bilateral paralysis of the. abductors. „„A 11<51ia ll v prm oW pr l panPP^llv 
b and b' indicate the position in bilateral par aly- anu USUdliy IS congested, especially 

su of the adductors. after at t ac ks of dyspnoea. Gen- 

erally there is no difficulty in deglutition in any form of laryngeal paraly- 
sis. In those where the bands do not approximate sufficiently to guard 
the entrance to the larynx, there may be slight dyspnoea. 

Differential Diagnosis. — Laryngeal paralysis is easily recognized when a 
careful laryngoscopical examination of the larynx is made. The character 
of the respiration in paralysis of the abductors, and of that in paralysis of 
adductors, is usually sufficiently marked to distinguish the one from the 
other. In adductor paralysis the respiration is always performed with ease ; 
while, in paralysis of the abductors, dyspnoea and stridulous breathing are 
always present in a greater or less degree. In other forms of laryngeal par- 
alysis, the respiration is normal. 

Prognosis. — In those cases where paralysis of the vocal bands depends 
upon a morbid condition of the nerve centres, or is due to commission of 
the nerves by aneurisms or new formations, the prognosis is always grave. 




SPASMODIC AFFECTIONS OF THE LAEYXX. 



63 



On the other hand, it is favorable when it is due to functional causes, or 
originates in catarrhal inflammation of the mucous lining of the vocal or- 
gans. When there is paralysis of the adductors, usually the prognosis is 
favorable; while with paralysis of the abductors the patient is always in 
great danger. 

Treatment. — In recurrent laryngeal paralysis, where any method of treat- 
ment can be of service, the surest and best is the application of the electric 
current, galvanic or Faradic, one pole being placed over the thyroid or 
cricoid cartilage, and the other in contact with the vocal cords. These 
applications must be employed at regular intervals, and only for a short 
period at any time. As adjuvants, stimulating inhalations may be employed, 
such as ammonia, creosote, etc., and local applications of iron, nitrate of 
silver, etc. Whenever the abductor muscles have lost power, it becomes 
a question whether tracheotomy shall or shall not be performed ; if the 
dyspnoea becomes so intense as to be a source of immediate danger to the 
patient, tracheotomy should be performed without delay, for it affords 
the only chance of prolonging life. Eest of the voice is an all-important 
element of treatment, where there is deficient action of the muscles ; and, 
in obstinate cases, electricity, with the induced or galvanic current, may 
be used with advantage to the patient. In all forms of laryngeal paralysis, 
general treatment is indicated. 

SPASMODIC AFFECTIONS OF THE LAEYXX. 

The only spasmodic affection of the larynx which I shall consider, is the 
common form known as spasm of the glottis, or laryngismus stridulus, 
which is occasioned by temporary spasm of the adductors of the larynx ; 
this gives rise to temporary paroxysms of dyspnoea and stridulous breath- 
ing. 

Morbid Anatomy. — There are various opinions in regard to the patholog- 
ical nature of spasms of the glottis. According to some, there exists an 
altered or abnormal condition of the nerve centres — especially is this the 
case in children ; while other authorities recognize an excessive suscer> 
tibility of the glottic nerves to receive reflex impressions. "When an 
adult is affected, there is frequently some catarrhal or other inflammatory 
condition of the mucous membrane of the larynx, which acts as an effi- 
cient cause of the spasm ; in children, the mucous lining of the larynx 
is usually perfectly healthy. In adults, the brain is normal in appearance ; 
in children, serous effusion is frequently found in the ventricles and on the 
surface of the brain. Evidences of rickets are frequently apparent in the 
osseous system of children subject to laryngismus. The condition of the 
pneumogastric nerve has been variously reported by those who have writ- 
ten on this subject. Unquestionably, reflex irritation in the larynx may 
arise from a great variety of causes. 

Etiology. — There can be little doubt but that spasm of the glottis is 
usually due to a nerve impulse originating in some form of irritation and 
conveyed by the laryngeal nerves. The seat of the irritation may be in the 



64 



DISEASES OF THE RESPIRATORY ORGANS. 



brain, or at a point in the course of the nerves, or peripheral and reflex. 
Laryngeal spasm is most frequently met with in children, when indigestion, 
teething, and impressions of external cold are usually assigned as causes ; 
yet, in most cases of this class, cerebral irritation, due to some other cause, 
already exists. Scrofulous aud cachectic children are said to be especially 
subject to spasm of the glottis. In adults, it is observed in connection with 
hysterical manifestations, and is sometimes the result of pressure on the 
nerves ; it also occurs in connection with irritation from foreign bodies. 
It has been met with as a sequela of whooping-cough. 

Symptoms. — In children, the laryngeal spasm usually comes on at night, 
during sleep. The dyspnoea attending it is often intense, the respirations 
are stridulous and crowing in character, and the child presents the appear- 
ance of deficient oxygenation of the blood. It is sometimes attended by 
general convulsions, in which there is extreme contraction of the flexor 
muscles of the extremities; strabismus and involuntary discharge of faeces 
and urine are sometimes present. The spasm usually subsides suddenly, the 
recovery is complete, and is never accompanied or followed by fever. One of 
the characteristics of this affection is the tendency to recurrence of the at- 
tacks. Death from suffocation during the paroxysm may occur, but it is ex- 
ceedingly rare. In adults a spasmodic affection of the larynx is either hys- 
terical in its nature or it depends upon interrupted pressure along the course 
of the recurrent nerves. It gives rise to symptoms similar to those already 
described, except that the paroxysms are less severe and are more persistent. 

Differential Diagnosis. — The only disease liable to be mistaken for the 
one under consideration is croup, and its diagnosis has already been con- 
sidered under that head. 

Prognosis. — Those cases which depend upon reflex causes generally re- 
cover. The prognosis in every case will depend, however, upcn the vio- 
lence and frequency of the spasm, the age of the patient, and, above all, 
upon the cause of the spasm ; a spasm of the glottis depending upon un- 
interrupted pressure of an aneurism on the recurrent nerve, is not infre- 
quently the immediate cause of death. 

Treatment. — If spasm of the glottis is due to reflex irritation, the cause 
of the irritation should be immediately removed. In children, dentition 
or an overloaded stomach is most frequently the source of the irritation. 
In prolonged attacks, inhalation of ether or chloroform may be tried, or a 
hot bath, or an emetic may be promptly administered. During the inter- 
val between the paroxysms careful attention must be paid to the diet and 
general hygiene of the patient. If the spasms are severe and prolonged, 
and the patient seems to be sinking, the trachea must be opened and arti- 
ficial respiration resorted to. When laryngismus occurs in the adult, those 
means which have been proved beneficial for children may be employed for 
its relief. When laryngeal spasm occurs as an hysterical phenomenon, it 
must be treated in the same manner as any other hysterical symptom. If 
it occurs in connection with pressure upon any portion of the pneumogas- 
tric nerve, one must be prepared at any moment to perform tracheotomy 
for temporary relief. 



TUMOES OP THE LAEYXX. 



65 



TUMOBS OF THE LAKYXX 

Laryngeal growths may be divided into two classes, benign and malig- 
nant. 

Morbid Anatomy. — I shall only briefly consider the morbid anatomy of 
those laryngeal growths with which one should become familiar on account of 
their frequency ; other forms are more especially interesting on account of 
their rarity. Morbid growths, as they occur in the larynx, may have a broad 
base which attaches itself to the interior lining membrane of the larynx, 
or they may hang, as it were, into the interior of the larynx, from a narrow 
neck or pedicle. They may vary in size, shape, consistency, and number. 
They may fill up the cavity of the larynx so as to impair respiration, or 
they may be of such small size as to pass unnoticed. Three-fifths of all 
the benign growths which occur in the larynx are joapillomata ; where 
these growths are congenital, the proportion is even greater. These tumors 




Fig. 14. Fig. 15. 

Multiple Papilloma of the right Vocal Chord as seen with The Trachea laid open, showing the same 
the Laryngoscope. Tumor as seen in Fig. 8. 

grow rapidly ; sometimes they attain a considerable size in the space of a 
few months. For the most part, their structure is similar to that of the 
normal papillae. Their basic substance is formed of connective-tissue, 
which receives into its interior, vessels and nerves, while the surface is 
covered with a layer of epithelium. They have decidedly a villous appear- 
ance ; some of these growths contain spaces filled with colloid matter ; 
after removal, they are quite likely to recur. Relations have been traced 
between benign papillary growths and warty cancers. Some cases are 
related where papillomata have become softened, fatty and cheesy, and 
have been removed by coughing. 
5 



63 



DISEASES OF THE RESPIRATORY ORGANS. 



Fibromata are of less frequent occurrence than papillomata ; they grow- 
less rapidly, and are never congenital. These growths are composed of 
white fibres, diverging from, and interlacing one another in different direc- 
tions ; after removal they do not return. They are generally smooth, 
rounded, pedunculated and vascular. 

Fibro-cellular growths are composed of fibro-cellular tissue. They usually 
contain a serous fluid, are of slow growth, single, and after removal show 
no disposition to return. 

Cystic tumors are due to enlargement of the glands in the mucous mem- 
brane. They contain a white, sebaceous-like material, and have thick 
walls. This variety of tumor is less frequently met with than any of the 
other varieties. 

Glandular growths take their origin in the larynx, where the glands and 
follicles are most abundant. They sometimes attain considerable size. 

Carcinomatous growths in the larynx are of two varieties, epithelial and 
medullary. The epithelial is the more frequent. The medullary is not so 
liable to ulcerate as is the epithelial, but produces more displacement. 
Sometimes profuse hemorrhage occurs in connection with epithelial cancer 
of the larynx. 

Etiology of Laryngeal Growths. — The most frequent cause of laryngeal 
growths is unquestionably chronic or frequently recurring laryngitis. In 
some cases a more or less constant irritation of the vocal organs seems to 
give rise to their development, such as is met with among teachers, singers 
and public speakers. Around the ulcerations of syphilis and of laryngeal 
phthisis these growths are found. Those whose calling subjects them con- 
stantly to the inhalation of irritating vapors or dust, are especially liable 
to them. Non-malignant tumors of the larynx are always associated in 
their origin with local hyperemia. In malignant growths, in addition to 
the local changes, there are constitutional influences in operation which 
impart to them a specific character. They are sometimes congenital. 

Symptoms. — The symptoms which attend laryngeal growths are for the 
most part local in character, and these local symptoms will necessarily vary 
with the size, situation, and nature of these morbid growths, as well as with 
the size of the larynx. The development of these tumors is rarely accom- 
panied by pain, but sometimes there is a sense of uneasiness as though a 
foreign mass were in the larynx. Eespiration may be more or less interfered 
with, and there may be severe dyspnoea ; but usually it is present only after 
violent physical exertion, running, jumping, going up a long flight of 
stairs, etc. The breathing is sometimes stridulous in character, and fre- 
quent suffocative attacks due to spasm may come on. When the growth is 
above the glottis, all the difficulty in breathing is on inspiration ; the ex- 
piration is quite free. The voice is always more or less changed ; it is not 
only altered in quality and liable to sudden changes in intensity, but some- 
times it is completely lost. Cough is present in many cases ; it is usually 
due to accompanying laryngitis; not infrequently it is voluntarily excited 
by the desire on the part of the patient to get rid of the laryngeal obstruc- 
tion. In the expectoration, which is usually increased by coughing, frag- 



BRONCHITIS. 



67 



ments of the growth are sometimes found; as a rule there is nothing which 
can be considered as distinctive about it. Dysphagia is present in the ad- 
vanced stages of many laryngeal growths, especially when they are malig- 
nant. The most positive evidences of laryngeal growths are furnished by 
the laryngoscopic examinations. By moderately expert laryngoscopic exam- 
inations the seat, size, and, in some cases, the nature of the laryngeal 
growths will be readily determined. 

Differential Diagnosis. — The interference with the functions of the larynx 
will direct attention to this organ, and if the laryngoscope is used the ex- 
istence of these growths will rarely be overlooked; when seen it will hardly 
be possible to confound them with any other disease. The study of the 
histories of such cases as are recorded in laryngoscopic manuals will be of 
great assistance in making a differential diagnosis. 

Prognosis. — If the growth be pedunculated, of moderate size, and single, 
with ordinary condition of tolerance, the voice can, in many instances, be 
entirely restored. If the contrary condition exists, relief may be looked 
for, but never complete restoration of the voice. As to length of life, 
other things being equal, the prognosis is more favorable in adults than in 
children, for the reason that evulsion of the growth by the intra-laryngeal 
methods is more readily and certainly accomplished in the former than 
in the latter. Whenever these growths are cancerous in nature they ter- 
minate fatally. 

Treatment. — If a laryngeal growth is small, and does not interfere with 
the voice or respiration, the rule is to let it alone ; if, on the other hand, it 
is of considerable size, and is increasing rapidly, endangering life, operative 
measures, either intra- or extra-laryngeal, must be resorted to. These more 
properly fall within the province of the specialist than of the general prac- 
titioner. Whenever there is great obstruction to respiration, and suffoca- 
tion seems imminent, tracheotomy should be immediately performed, after 
which the intra-laryngeal methods of procedure may be resorted to. In 
malignant laryngeal growths, all remedial measures are only palliative. 

Ossification and calcareous infiltration of the cartilages of the larynx 
are met with in those cases where there has been chronic and frequently 
recurring laryngitis ; not infrequently the calcareous condition of the carti- 
lage, which is sometimes present in connection with chondritis or perichon- 
dritis, is preceded by its ossification. 

BEOXCHITIS. 

Bronchitis is essentially an inflammation of the mucous membrane of the 
larynx, trachea, and bronchial tubes, which may vary in extent, intensity, 
duration, and in the nature of its pathological products. Thus it may be 
limited to the larynx, trachea, and larger bronchi, or it may extend into 
the capillary tubes : it may be mild or severe in character, run a rapid 
course, or be indefinitely protracted. It may also be produced by a variety 
of causes, some external, some internal, some accidental, and others consti- 
tutional. It may be primary or secondary, — primary, when the result of 



08 



DISEASES OF THE RESPIRATORY ORGANS. 



exposure, or produced by the inhalation of irritating gases ; secondary, 
when it arises from constitutional vice, or from previously existing disease 
Again, it may occur as a complication during the course of other diseases, 
such as acute blood disease, pulmonary phthisis, pulmonary emphysema, 
and cardiac disease. It affects all ages and either sex. One attack predis- 
poses to a second. Bronchitis, clinically and pathologically, may be di- 
vided into the following varieties : — (1) Acute Catarrhal Bronchitis of the 
large tubes j (2) Acute Capillary Bronchitis ; (3) Chronic Catarrhal 
Bronchitis j (4) Fibrinous or Plastic Bronchitis ; and (5) Bronchiectasis. 

ACUTE CATARRHAL BRONCHITIS. 

This form of bronchial inflammation occurs at all ages. In childhood 
and old age it most frequently involves the smaller bronchi ; in adult 
life it involves the larger bronchi. It may be mild or severe in type. 

Morbid Anatomy. — The morbid anatomy of this variety of bronchitis does 




Fig. 16. 

Transverse Section of a Portion of a Medium- Si zed Bronchial Tube in Acute Catarrhal Bronchitis. 

a, New cells forming. 

b, Epithelium of mucous membrane. 

c, Desquamated cells (ci c 2 ). 

d, Mucus on epithelial surface. 

e, Opening of mucous gland. 
/, Attached* epithelium. 

g, Internal fibrous layer. 

h, i, Engorged vessels. 

k, Extra vasated red-blood corpuscles. 
I, Round cell infiltration, 
m, Hypertrophied glands, x 300. 

not differ essentially, whether it has its seat in the large or small bronchial 
tubes. In either case it rarely originates in the tubes themselves, but is the 
continuation of a similar process affecting the nasal, pharyngeal and laryngeal 



ACUTE CATAKRHAL BRONCHITIS. 



00 



raucous membrane, or is the extension to the smaller tubes of an inflammation 
commencing in the alveoli. As a rule, the simple variety does not advance 
beyond the larger bronchi ; when the smaller tubes are involved it is de- 
nominated capillary. In some cases the mucous membrane is swollen and 
reddened, either uniformly or in points or patches. Its surface may be 
roughened by the presence of enlarged papillae or granulations. It is usu- 
ally softer and moister than natural — occasionally ecchymoses are observed 
in it. The natural longitudinal rugge of the membrane are effaced, giving 
a smooth appearance to the reddened surface. The bronchi at first contain 
a clear transparent mucus, which, as the disease advances, becomes opaque, 
whitish, yellowish, or greenish. The change in the color of the secretion is 
owing to pus-cells contained in the fluid ; at the onset there are but few 
present. The presence of desquamated epithelium in the tubes after death 
is for the most part owing to the separation of the cells from the membrane 
between the time of death and the making of the autopsy. In a small pro- 
portion of cases, the only evidence of bronchitis which is found at the post- 
mortem is the presence of mucus or muco-pus in the tubes. Sometimes 
the tubes are more rigid than normal. These changes exist whether the 
larger or smaller tubes are involved. Generally, the tubes on both sides are 
equally affected. In the weak, the very young and the very old, or when 
there is some condition which prevents or enfeebles the cough, the mucus 
or muco-pus sometimes gravitates from the larger into the smaller tubes, 
and gives rise to yellow spots near the surface of the lung ; this is especially 
liable to occur in young, feeble children. 

There may be complications with acute bronchitis. The swollen mu- 
cous membrane, or the accumulation of mucus or muco-pus may produce 
a temporary air distention of the alveoli— a condition frequently met with 
at autopsies, and sometimes mistaken for vesicular emphysema. Fully 
developed emphysema, as well as atelectasis, may occur as the result of 
these bronchial obstructions. Atelectasis is specially liable to occur in 
young children. In these patches of collapsed lung, or as the result of 
the extension of inflammation from the bronchi to the alveoli, lobular 
pneumonia is not infrequently developed as a complication. This is rare 
in the acute bronchitis of the adult, but frequent in children. Pulmonary 
congestion and oedema are not infrequent complications of general capil- 
lary bronchitis. Temporary bronchial dilatation often occurs in children, 
when the disease affects the smaller tubes, and lasts more than a week. 

Etiology. — The most marked predisposing causes of acute bronchial ca- 
tarrh are infancy and old age, indulgence in enervating habits, or debility 
from any cause, constitutional diseases, chronic pulmonary affections, the 
breathing of impure air in badly ventilated apartments, and sudden changes 
in temperature. It is comparatively rare in continuously hot or cold cli- 
mates. In our climate it prevails most in the spring and fall. The disease, 
when primary, is either due to some sudden atmospheric change, to some 
morbific agent in the atmosphere, or to the action of cold on the surface of 
the body when imperfectly protected, causing a chilling of the surface. It 
occurs secondarily in connection with blood-poisoning, as in measles, ty- 



70 



DISEASES OF THE RESPIRATORY ORGANS. 



phoid and typhus fevers, gout, rheumatism, etc. In the course of other 
pulmonary affections, and in chronic cardiac diseases, it is of quite frequent 
occurrence. It may be produced traumatically by the inhalation of irritat- 
ing gases, particles of dust, etc., which act directly upon the mucous 
membrane. Those who live in the open air are less liable to it than those 
living in-doors. At times bronchitis prevails epidemically, associated with 
influenza and due to the action of some unknown atmospheric influence. 

Symptoms. — A common "cold" may be regarded as a bronchitis of the 
larger tubes. This simple form of bronchial catarrh does not extend below 
the second division of the bronchi, but expends itself on the larynx, trachea, 
and large bronchi. Its invasion is commonly marked by coryza, lachryma- 
tion, sore throat and slight hoarseness, with chilliness scarcely amounting 
to rigor. The occurrence of the coryza, with an uneasy sensation in the 
frontal sinuses, gradually passing from the nasal passages to the larynx and 
trachea, is diagnostic of its primary character. The pulse is slightly in- 
creased in force and frequency, there is aching in the back and limbs, but the 
general febrile symptoms are usually mild ; in very young and weakly chil- 
dren convulsions may occur. As the bronchial inflammation becomes fully 
established, more or less pain and discomfort are felt behind the sternum ; 
there is a sense of tickling, rawness and soreness at the upper portion of the 
chest, which amounts to actual pain on coughing ; the respirations are 
somewhat increased in frequency, and there is a sensation of constriction 
with oppressed breathing which may be somewhat laborious, but there is 
no evident dyspnoea. The cough, an essential feature of the disease, at 
first is dry and hacking, sometimes incessant, especially on lying down, and 
on waking after a long sleep ; it may be paroxysmal in character. After 
one or two days the cough becomes loose, and is attended with an expec- 
toration of frothy mucus, of a yel- 
lowish color and a saline taste ; 
gradually this becomes mucopuru- 
lent and even purulent. As soon as 
the expectoration becomes free the 
patient is relieved. The disease 
lasts from four or five days to two 
or three weeks, and ends in complete 
recovery or in chronic bronchitis. 

Physical Signs. — In slight attacks 
of acute bronchial catarrh of the 
larger tubes, there may be no physi- 
cal signs to indicate its existence. 
The severer forms are attended by 
easily recognized physical signs. 
As a rule, inspection and palpation 
give negative results. The percus- 
sion sounds are normal, unless there is a very considerable accumulation of 
mucus in the bronchial tubes ; in such cases, the normal resonance is dimin- 
ished posteriorly in the infra-scapular region. On auscultation over the 



Sibilant 



Subcrepitant rales 




Diagram illustrating 



Fig. 17. 

the Physical Signs of Bronchitis. 



ACUTE CATARRHAL BRONCHITIS. 



71 



affected tubes, the respiratory murmur is feeble, temporarily suppressed, or 
sonorous in character. In the dry stage, sibilant and sonorous rales may 
be heard on both sides over the whole chest, more distinctly posteriorly. In 
the stage of secretion with the sibilant and sonorous rales, moist rales, large 
and small in size, are heard on both sides of the chest. These rales are in- 
constant, coming and going, and changing their situation ; after a violent 
fit of coughing, they may entirely disappear for a time. When they are 
abundant and very loud, they often altogether mask the respiratory mur- 
mur. When the secretion is watery, they have a "rattling" sound. In 
some cases, secretion takes place so rapidly that moist rales are heard from 
the first. Vocal resonance in bronchitis is normal. 

Differential Diagnosis. — It is hardly possible to confound bronchitis of the 
large tubes with any other pulmonary affection. The absence of lancina- 
ting pains in either side, the bronchial character of the cough and expec- 
toration, the coryza and hoarseness which precede the attack, are usually 
sufficient to distinguish it from pneumonia and pleurisy ; besides, its 
physical signs, if properly appreciated, render the diagnosis easy and 
positive in all cases. The early stage of whooping-cough may be con- 
founded with it, until the characteristic cough is heard. 

Prognosis. — This form of bronchitis, unless it occurs in the very young, 
or very old and feeble, never directly destroys life. It usually terminates 
by resolution in from three to four days to two or three weeks ; some- 
times it becomes chronic : in such cases the inflammation is likely to 
extend into some of the smaller tubes, giving rise to circumscribed capillary 
bronchitis. 

Treatment. — In the majority of cases, this form of bronchitis is easily 
managed. In mild attacks the patient is not sufficiently ill to consult a 
physician ; it is simply regarded as a severe cold. At the onset, while the 
coryza is present, it may generally be arrested by a Dover's or Tully's pow- 
der and a warm bath at night, followed in the morning by a brisk saline 
purge — in the case of children by a full dose of castor oil. The patient 
should remain in a warm, moist, equable temperature for a day or two. 
gr. xx. of quinine or of salicylic acid acts oftentimes as an abortive in 
adults. If this plan has not been resorted to, or has not proved successful, 
then moderate but continued action of the skin and kidneys should be in- 
duced by the administration of mild diaphoretics and diuretics, the patient 
remaining in a warm, even temperature. In the early stage of the disease, 
especially in the case of children, great benefit is often derived from steam 
inhalations. Counter-irritation, by means of cups and mustard sinapisms, 
to the upper part of the chest, is of great service in its late as well as in its 
early stages. If the disease shows a tendency to pass into the chronic 
stage, or to extend into the smaller tubes, from eight to ten grains of 
the sulphate of quinine should be daily administered ; in children, cod- 
liver oil with lime-water should be given. A succession of small blisters 
applied to the posterior portion of the chest will be of service after the 
acute stage is past. When simple bronchitis occurs in those of a gouty 
or rheumatic diathesis, colchicum must be given in connection with alkalies. 



72 



DISEASES OF THE KESPIJRATOKY ORGANS. 



ACUTE CAPILLAEY BEONCHITIS. 

When acute catarrhal inflammation invades the small-sized bronchia] 
tubes, it is termed capillary bronchitis. It is also known as "catarrhus 
senilis/' bastard pleurisy, and suffocative catarrh. In most instances, this 
form is an extension of simple bronchitis, whose characteristic symptoms 
have preceded ; but sometimes the smaller as well as the larger bronchial 
tubes are affected, or the smaller bronchi may be the primary seat of the 
inflammatory process. General capillary bronchitis is much more fre- 
quently met with in infancy and old age than during any other periods of 
life. If the inflammation is limited, and only a few of the smaller tubes 
are involved, it is called localized capillary bronchitis ; but when the bron- 
chial inflammation is intense, and diffused over the lining membrane of 
all the bronchial tubes, it is termed general capillary bronchitis. In the 
symptoms which attend its development, and in its tendency to destroy 
life, it differs very much from bronchitis of the larger tubes. The morbid 
anatomy of this form of bronchitis has been already sufficiently described; 
but its symptomatology, prognosis, and treatment require separate consid- 
eration. The causes which give rise to capillary bronchitis are similar to 
those which have been named in connection with the etiology of simple 
bronchitis, except in those instances where it occurs as a secondary affection. 
The danger from acute catarrhal inflammation of the smaller tubes in pa- 
tients with Bright's disease, typhus fever, measles, and the chronic bron- 
chitis of old age, should never be lost sight of. Some of the worst cases 
are met with in connection with emphysema of the lungs. 

Symptoms. — The milder types of this form of bronchitis are usually pre- 
ceded by inflammation of the larger tubes, and the symptoms of invasion 
are not marked. In fact, the capillary element of the disease might not be 
recognized, were it not for its physical signs, and difficult or labored respi- 
ration. On the other hand, the severe forms may be ushered in by distinct 
chills, high febrile excitement, and great dyspnoea. The patient is unable 
to lie down on account of the difficulty of breathing, and the countenance 
is anxious and flushed. Paroxysmal orthopnoea is not uncommon. The 
respirations are accelerated, reaching 60 and 70 in a minute, attended by 
great muscular effort. The pulse is feeble, beating from 100 to 130 in a 
minute. The axillary temperature is raised to 103° R, but as the disease 
advances it may fall to 100° F., although the pulse and respiration remain 
frequent. The patient, at the commencement of the attack, has an inces- 
sant hacking cough, which is often so violent as to compel him to sit up, 
bend forward, and hold his sides. At first, there is little if any expectora- 
tion ; if expectoration is present, it is a thick, tenacious mucus ; later, it 
becomes more abundant and less tenacious. So viscid and tough is the ex- 
pectorated material, that cast-like masses of the bronchioles maybe formed. 
When some of the sputa is put in water, the froth floats and is connected 
by filaments with the heavier masses underneath the surface. The cough 
may be accompanied by a rattling sound in the trachea. There is great 



ACUTE CAPILLARY BRONCHITIS. 



73 



exhaustion. If the disease progresses, all the phenomena of deficient oxy- 
genation are developed. The face betokens great distress and has a livid 
aspect, the lips become blue, and there is blueness of the finger-ends, "with 
fulness of the jugnlar veins. The respiratory acts become more and more 
labored and imperfect, the expectoration becomes more and more abun- 
dant, and the matter expectorated thin, frothy, and less tenacious. There 
is great restlessness, with signs of impending suffocation, and the surface 
of the body is covered with a cold, clammy sweat. As death approaches, 
the pulse becomes small and thready, the respiratory efforts are less violent 
and less frequent, muttering delirium comes on, or the patient lies in a 
state of partial coma, both cough and expectoration cease, and he dies 
asphyxiated. These symptoms vary somewhat with the age and peculiari- 
ties of the individual affected, and with the diseases which it may com- 
plicate. In aged persons, or in those who are constitutionally weak from 
any cause, the fever is very apt to take on an adynamic type. When it 
occurs in connection with acute blood diseases, it is likely to come on very 
insidiously, without any of its usual symptoms being prominent. 

Physical Signs. — In addition to the signs belonging to simple bronchitis, 
the percussion sound in the early part of the disease may be somewhat 
exaggerated in the infraclavicular regions, the percussion resonance may 
be diminished on account of the attendant pulmonary cedema, and the 
accumulation of morbid products in the small bronchi. While resonance 
is diminished in the lower portions, the superior portions of the lung may 
give an emphysematous percussion note. 

Auscultation. — If the bronchitis is extensive, the vesicular murmur over 
both lungs is feeble or suppressed, and the inspiration may be masked by 
high-pitched, hissing, sibilant rales ; as the disease advances the subcrepi- 
tant distinctive rale of capillary bronchitis is heard all over the chest, but es- 
pecially in the infra- scapular region. (See Fig. 17.) If the subcrepitant rales 
are abundant and are heard over the whole chest, they indicate very positively 
the existence of a general capillary bronchitis. These rales may be present 
over circumscribed spaces posteriorly, as the result of the gravitation of the 
fluid secretion from the larger into the smaller tubes. If they are confined 
to the apex or base of one lung, with resonance on percussion, they indicate 
the existence of a localized capillary bronchitis. 

Differential Diagnosis. — Capillary bronchitis may be confounded with pneu- 
monia, pulmonary cedema, and phthisis. It differs from simple Ironchi- 
tis in the higher temperature, greater frequency of the respiration, the ex- 
treme dvspncea, the interference with the general capillary circulation, and the 
presence of the hissing, sibilant, and subcrepitant rales. It is distinguished 
from pneumonia by the absence of pain in the side, prolonged initial chill, 
and the characteristic pneumonic sputa, by the greater frequency and labor 
of respiration, and the more intense dyspnoea, by its lower temperature, by 
the normal or exaggerated resonance on percussion, by the presence of the 
subcrepitant rales on loth sides of the chest, and by the absence of bronchial 
breathing and of increase in the vocal fremitus. The points of differential 
diagnosis between capillary bronchitis and phthisis will be considered 



74 



DISEASES OF THE RESPIRATORY ORGAKS. 



under the latter head. The existence of the physical signs of capillary 
bronchitis at the apex of one lung, accompanied by evidence of pulmon- 
ary consolidation at that point, always leads to the suspicion of incipient 
phthisis. The physical signs, pyrexia, and history of the patient will suf- 
fice to distinguish it from asthma. 

Prognosis.— General capillary bronchitis is a disease attended with great 
danger, especially when it occurs in infancy or old age, or when it super- 
venes upon some grave organic disease, as phthisis, Bright's, heart disease, 
and acute blood diseases. When it occurs in persons suffering from pul- 
monary emphysema, although for a time the symptoms are urgent, it rarely 
proves fatal. It usually lasts from three to five days ; but when very exten- 
sive may prove fatal in twelve hours. Among the unfavorable symptoms 
may be named great difficulty of expectoration, shallow breathing, cessa- 
tion of cough, urgent dyspnoea with evidences of incipient asphyxia, and 
the presence of adynamic symptoms. In this disease, death results from 
asphyxia caused by imperfect oxygenation of the blood. 

Treatment. — All the so-called antiphlogistic remedies lessen, if they do 
not destroy, the chances of recovery. From the commencement of the 
attack, the treatment must be supporting. In general capillary bronchitis, 
the patient must be kept in bed, the surface of the body covered with flan- 
nel, the temperature of the apartment must range from 75° to 80° F. and the 
air must be moistened with steam. Children should be placed in the steam 
tent, as advised in the treatment of membranous croup. Dry cups should 
be applied over the whole surface of the chest, after which it should be 
covered with an oil-silk jacket. The inhalation of steam usually increases 
the bronchial secretion, facilitates expectoration, and for a time, at least, 
relieves the difficult breathing. If symptoms of imperfect oxygenation 
are developed, the inhalation of oxygen gas in connection with the steam 
will often afford the most marked relief. The internal administration of 
muriate of ammonia, or chlorate of potash in five or ten grain doses every 
two hours to the adult (two grains may be given to a child two years of 
age), often seems to have a controlling influence over the inflammatory 
processes, Iodide of potassium is of benefit in children threatened with 
atelectasis and lobular pneumonia. The so-called expectorants are of little 
service. Sometimes, when suffocation is imminent and the power of ex- 
pectoration is entirely lost, stimulating emetics will be found of service, 
especially in very young children ; the action of the emetic seems to sup- 
ply the want of voluntary power to expectorate, and it dislodges the accu- 
mulated secretion in the bronchial tubes ; care must be taken not to repeat 
emesis so often as to produce exhaustion. 

In the advanced stage of the disease, when the pulse becomes small and 
thready, quinine and stimulants must be freely administered. The chief 
object of treatment in this disease is to sustain the life of the patient until 
the inflammatory process has passed through its different stages. As re- 
gards the use of stimulants, there is no disease (especially of childhood) in 
which their judicious use is so markedly beneficial. They should be 
commenced early, and given in sufficiently large quantities to overcome the 



CHRONIC CATARRHAL BRONCHITIS. 



75 



signs of exhaustion, which are present very early. To allay spasm of the 
bronchial tubes, which is occasionally present in this form of bronchitis, 
and gives rise to the most distressing paroxysms of dyspnoea, full doses of 
hydrocyanic acid may be given, and this is often followed by most marked 
relief. Opium should never be given, for by its action the power of expec- 
toration is often diminished, and it favors the dangerous accumulation of 
inflammatory products in the bronchial tubes. Each case should be stud- 
ied by itself, with attention to the constitutional conditions under which 
it occurs, and the treatment should be so modified as to meet the indica- 
tions. The general management of capillary bronchitis associated with 
Bright's disease is very different from that of capillary bronchitis occur- 
ring in a person previously healthy. During the whole course of the dis- 
ease when this complication is present the patient should receive the largest 
possible amount of concentrated nutrition — the yolk of eggs and milk are 
generally well borne by this class of patients. Precaution must be taken 
against the slightest exposure to changes in temperature during convales- 
cence. 

There are certain peculiarities which attend the capillary bronchitis of 
young children. It differs from the bronchitis of adults in the greater 
liability to extension of the bronchial inflammation to the alveoli, with 
consequent lobular pneumonia; also, in the liability to the occurrence of 
atelectasis or collapse of the lobules, the result of the plugging up of the 
small bronchi by accumulation of secretion in them, with intense swelling 
of the mucous membrane. The occurrence of lobular atelectasis cannot 
be determined with certainty either by the rational or physical signs. It 
may be suspected in young children whenever physical signs indicative of 
extensive capillary bronchitis are associated with extreme dyspnoea and evi- 
dence of defective oxygenation of the blood, the physical signs and other 
symptoms of broncho-pneumonia being absent. The development of lobu- 
lar pneumonia is certain to follow lobular atelectasis, if the life of the pa- 
tient is sufficiently prolonged after the occurrence of the latter. In the 
treatment of bronchitis of young children, the liability to these complica- 
tions should always be borne in mind. • 

CHEONIC CATAEEHAL BEONCHITIS. 

This is a very common disease, and results from any cause which excites 
and keeps up a low grade of inflammation of the bronchial mucous mem- 
brane. It is usually a disease of adult life. One of its chief characteristics 
is its tendency to recurrence ; the attacks increase in severity and duration 
at each return, until the individual is rarely free from it. Chronic bronchitis 
may he primary or secondary. Primary, when it is the result of exposure 
to wet or cold, or when it is excited by the daily inhalation of dust, vapors, 
or other irritating substances. Secondary, when due to some constitutional 
vice, as gout, rheumatism, syphilis, etc. ; or some local affection, as cardiac 
or renal disease. It may occur as a complication of other pulmonary affec- 
tions, as phthisis, pulmonary emphysema, etc. 



76 



DISEASES OF THE EESPIRATOEY OEGANS. 




Morbid Anatomy. — As in acute bronchitis, any portion of the bronchial 
and tracheal membrane may be the seat of the inflammatory action. Thus 
it may be limited to the large bronchi, or it may extend into the capillary 
tubes. Usually, the inflamed membrane has a slaty, reddish blue, or even 
a violet color. In the more chronic cases, its tissue is frequently hyper- 
trophied, its glands are enlarged and prominent, and their ducts so in- 
creased in size that their mouths are readily visible. The mucus secreted 
may be in transparent gelatinous masses and small in quantity, it may be 
muco-purulent, or a serous fluid may be exuded in great abundance. As a 
- - ...... : :!>J: . rather infrequent occurrence, the 

— , - r - surface of the membrane presents an 

«. 'fo^-V^i^v^^^ « uneven appearance, clue to the pres- 
^^SHbSK ence of little villosities covered by 
^^^p^^3i normal epithelium ; occasionally fol- 
f^^'^r'^ licular ulcerations are met with. 
-S^^T^^^ >sd^J^^>< ' These papillary excrescences and 
I "■ / r -f" ' ulcerations are usually arranged lon- 

^ ^ i ^ '* gitudinally. In the early stage, the 

' - \ * - # V - other coats of the bronchial tubes 

& v - may be weak or yielding; later, an 

' ~>>%,^\ > -- r increase in connective-tissue takes 

- place, leading to thickening and in- 

Fig. is. duration. The cartilages are SOme- 

Transverse Ete^on^^^Wril in Chronic Ws norma]j at other times hyper- 

a, Epithelium covered with mucus. trophied, and at times calcified. In 

o, Infernal elastic coat. 1 7 . 

c, Muscular layer. Round cell infiltration seen in the posterior Wall of the trachea and 

0/16 2)l(lC€. • 

d, Submucous tissue containing r hyper trophied carti- the larger bronchi, Separation of the 

lage, increased connective-tissue, enlarged glands -\ i i ji 

and vessels, x ^50. muscular fibres, and relaxation 01 

the bronchial wall occur, with a protrusion of the mucous membrane 
through fissures in its middle coat. These diverticuli may involve a large 
or small extent of the posterior bronchial wall. The submucous coat shows 
increase in connective-tissue. In very old subjects the ultimate bronchi 
may be changed intg calcified cylinders, each with a minute canal running 
through it. 

In very chronic cases, where there has been a puriform secretion for a 
long time, the bronchial mucous membrane not infrequently presents 
slight, or no apparent alteration. The results of chronic bronchitis are 
dilatation and stenosis of the bronchial tubes, an accumulation of secre- 
tion in a state of cheesy degeneration more or less obstructing their 
calibre, pulmonary emphysema, and induration of lung tissue adjacent 
to the inflamed bronchi, Ulcerations of the bronchial membrane rarely 
occur ; if present they are slight and superficial, and for the most part 
are found in the bronchitis which accompanies phthisis. In old age 
deep ulcers may be formed, and fistulous communications may be estab- 
lished with the oesophagus, aorta, pleural cavity, large blood-vessels, pul- 
monary parenchyma, or, very rarely, externally. In tertiary syphilis, 
chronic bronchitis may be accompanied by gummy tumors of the mucous 



CHEOXIC CATARRHAL BRONCHITIS. 



77 



membrane of the tracliea and primary bronchi, or by a fibrous indnration 
which leads to stenosis. 

Fetid Bronchitis. — An excessively fetid odor of the breach and of the 
matter expectorated in the course of a chronic bronchitis, may find no ex- 
planation after death, except decomposition of the accumulated bronchial 
secretion. This decomposition usually takes place in bronchial dilatations ; 
it may arise independently of any bronchial dilatation. It is claimed that 
germs, usually atmospheric, enter, and, lodging in a cavity, cause putres- 
cence. This decomposition of the secretion may exert no special injurious 
infLiienee, or it may give rise to gangrene of the bronchial mucous mem- 
brane, and may thus involve the adjacent lung tissue, causing more or less 
extensive gangrene of the lungs. About the tubes the characteristic 
changes of peribronchitis are nearly always found ; these changes are best 
marked at the periphery of the lung. The changes that take place in the 
small bronchi, in that form of bronchial catarrh -which accompanies 
phthisis, will be considered under the head of phthisis. 

Etiology. — The most interesting part of the history of chronic catarrhal 
bronchitis is its etiology. TVhen primary, it arises almost always from ex- 
ternal causes ; snch as exposure to cold and wet, the inhalation of dust or 
unwholesome air. It is unquestionably the exception for chronic bronchi- 
tis to be developed from exposure to what are termed the ordinary causes 
of "taking cold," without some special predisposition, snch as long-contin- 
ued mechanical irritation of the bronchial membrane, constitutional vice, 
or some previously existing organic disease. Acute bronchitis may fre- 
quently be the result of some temporary exposure, but if it becomes chronic, 
there will almost invariably be found to exist a predisposing cause. Bron- 
chial irritation may exist, perhaps for years, as the result of some mechan- 
ical irritation (as in the case of stone-cutters, grain -he avers, etc.), and not 
particularly inconvenience the individual, until an acute catarrh is devel- 
oped from exposure ; this invariably becomes chronic, and sooner or later 
leads to the development of broncho-pneumonia, and a condition called 
knife-grinders' or stone-cutters' phthisis follows. 

Secondary chronic bronchitis, or that which arises from some previously 
existing acquired or congenital dyscrasia, is of more frequent occurrence. 
An hereditary tendency to gout frequently manifests itself in a form of 
chronic bronchitis. Sometimes in the same individual attacks of bronchitis 
and gout alternate. In some instances the gouty diathesis only produces a 
strong predisposition to bronchitis, which requires for its development some 
external exciting cause much slighter than would joroduce the disease in 
health ; in other instances, there is for a long time a slight bronchial ca- 
tarrh, which, as life advances, slowly merges into chronic. Xot infre= 
quently chronic bronchitis occurs in connection with psoriasis and eczema, 
and these affections alternate one with the other ; as one disappears the other 
manifests itself ; under such circumstances it seems evident that these dif- 
ferent affections are manifestations of the same constitutional vice. Pul- 
monary emphysema is produced in many instances by chronic bronchitis ; 
sometimes, however, it occurs independently of it, and then it is a strong 



78 



DISEASES OF THE RESPIEATOEY OEGAKS. 



predisposing cause to the development of the latter. Disease of the left, 
side of the heart predisposes to bronchitis* which is sub-acute in character 
and. chronic in duration. Chronic bronchitis is very often associated with 
asthma. Chronic alcoholismus is one of its frequent causes. 

Symptoms. — The symptoms of this form of bronchitis vary with the con- 
stitutional and local causes under the influence of which it is developed. 
There are, however, certain prominent characteristics common to all varie- 
ties, the most constant of which are cough and expectoration. The pecu- 
liarity of the cough, and the quantity and quality of the matter expectorated, 
determine to a great extent the character and severity of the bronchitis. 
In some cases the cough is slight, the expectoration moderate in quantity, 
and muco-purulent in character; this occurs in the mildest variety — a 
variety which comes on in the winter and disappears, or is mitigated, in 
summer. After a time it becomes permanent, and is liable to exacerbations 
in cold, damp weather. It is the simplest form of chronic bronchial 
catarrh. In another class of cases the cough is violent and more constant, 
severest in the morning — the expectoration is either tenacious and scanty, 
or thin, semi-transparent and abundant ; it is sometimes streaked with 
blood, and frequently is difficult to expectorate. So severe is the cough that 
vomiting is very commonly induced, the contents of the stomach and 
bronchi being simultaneously expelled. The matter expectorated varies in 
color from an ashy-yellow to a deep green ; it is slightly aerated, and not 
infrequently sinks in water. Its odor varies : sometimes it is sweet and 
nauseous ; at other times it has a fetor similar to that of gangrene of the 
lungs. The microscope shows it to be composed of granular matter, broken 
down epithelial and pus-cells, and sometimes blood-globules and small fila- 
ments of bronchial tissue. Some cases of this form of bronchitis are at- 
tended by loss of flesh, fever, and night sweats. It occurs most frequently 
in strumous, broken-down subjects, especially those given to alcoholic 
excess. More or less extensive bronchial dilatations are usually present in 
this variety of bronchitis. 

Again, there is a class of cases in which the cough is exceedingly 
troublesome and paroxysmal in character — the expectoration is scanty, 
consisting of small, rounded, semi-transparent masses of tough mucus. 
This variety is met with almost exclusively in connection with pul- 
monary emphysema, gout, spasmodic asthma and irritant inhalations, 
and has received the name of " dry catarrh. " There is also a variety 
of chronic bronchitis, not infrequently met with in old people, especially 
in connection with heart disease, in which the cough is paroxysmal, and 
often violent, and the paroxysms are attended by a peculiar flux from the 
bronchi. The expectoration often amounts to four or five pints in twenty- 
four hours, and is either watery and transparent, or gelatinous and ropy, 
resembling an emulsion of white-of-egg and water. The patient often finds 
great relief after a paroxysm of coughing and expectoration. In some cases 
this variety of bronchitis is accompanied by loss of strength and flesh ; it 
has received the name bronchorrhoea. In some cases of simple chronic 
bronchitis the sputa are moulded in the form of the smaller tubes. Blood 



CHRONIC CATARRHAL BRONCHITIS. 



TO 



in the sputa indicates superficial ulceration. A brownish fluid expectora- 
tion is sometimes present ; and in this are fatty granules and crystals oi 
cholesterin and margarin. In all these varieties there is dyspnoea and 
labored respiration — the respiration is much more accelerated in other 
chronic pulmonary affections than in bronchitis, but it is never so labored. 
The pulse in a purely chronic bronchitis does not exceed the normal fre- 
quency, and on this account it may readily be distinguished from pneu- 
monia and phthisis ; besides, in chronic bronchitis the temperature is rarely 
much above the normal, excepting in those cases which are accompanied by 
a fetid expectoration. A little uneasiness or soreness is often felt behind 
the sternum, which is increased by violent coughing ; but pain in the side 
is rarely present. Individuals with any form of chronic bronchitis are un- 
able to sustain prolonged physical exertion without great exhaustion, and 
they are markedly affected by atmospheric changes. 

Physical Signs. — These are very nearly the same as in acute bronchitis. 

Inspection shows labored respiration with diminished expansion on inspi- 
ration. The chest may appear more convex than normal. 

Palpation. — Vocal fremitus varies : if the bronchial walls of the larger 
tubes are thickened, it is exaggerated ; if the tubes are obstructed, or much 
dilated, it is diminished or absent. In the simple forms of chronic bron- 
chitis the vocal fremitus is normal. 

The percussion sound rarely differs from that in health : if the accumu- 
lation of a thick secretion gives rise to obstruction in some of the bronchi, 
then localized temporary dulness on percussion is the result. 

On auscultation, the vesicular murmur is more or less deficient over the 
whole chest, and the respiratory sound is coarse, loud, and harsh, with 
prolonged expiration. After free expectoration, it will often be audible at 
points where it had been inaudible a moment before ; it is accompanied, 
and sometimes entirely masked, by rales of every variety, but chiefly sono- 
rous and sibilant. Large and small mucous rales are present in those cases 
in which there is abundant liquid secretion. These rales are constantly 
varying in size and character — at times they may be altogether absent ; 
they are altered in character and position by coughing and by full inspira- 
tion. Vocal resonance may be normal, diminished, or slightly exaggerated. 
Large and persistent gurgles in the lower portion of the lung suggest the 
existence of bronchiectasis. 

Differential Diagnosis. — The diagnosis of chronic bronchitis is rarely at- 
tended with difficulty, except in connection with pulmonary phthisis. It 
may be distinguished from pleuritic effusions, not only by the cough and 
expectoration which attend it, but by the continuance of vocal fremitus, 
and the existence of resonance on percussion. From pneumonic consolida- 
tion, by the absence of bronchial breathing, of rusty expectoration, 
accelerated breathing, and high pulse-rate and temperature. In those 
cases of chronic bronchitis in which the general health suffers, ema- 
ciation takes place and bronchial dilatation occurs. The bronchitis 
sometimes so closely simulates phthisis in its rational and physical signs, 
that the differential diagnosis is exceedingly difficult ; the points of 



80 



DISEASES OF THE RESPIRATORY ORGANS. 



difference will be more fully considered under the head of pulmonarv 
phthisis. 

Prognosis. — This disease rarely, if ever, directly destroys life ; but when 
it occurs in the old and feeble, it is always attended with danger, on ac- 
count of the frequent occurrence of acute attacks involving the small bron- 
chi. Any pulmonary affection associated with chronic bronchitis rendery 
the condition of the patient more serious, on account of the liability to 
bronchial obstruction from the accumulation of the secretion in the bron- 
chial tubes. It is very apt to lead to the development of pulmonary em- 
physema, pulmonary collapse, dilated bronchi, and fibrous phthisis. It is 
rarely recovered from when it occurs in those past middle life. Hepatic 
congestion, abdominal dropsy, and general anasarca are frequent attend- 
ants cf chronic bronchitis. Seventy-five per cent, of such cases are compli- 
cated by the presence of small, granular kidney. 

Treatment.-— The one important fact to be borne in mind in the treat- 
ment of this affection is, that it rarely occurs as a primary disease, but is 
due to some constitutional disorder. The patient must be removed from 
every possible source of bronchial irritation, and be protected from expos- 
ure to sudden changes of temperature ; flannels should be worn next the 
skin, and if a suitable climate cannot be obtained, the patient must keep 
in-doors during bad weather, in well-ventilated apartments, the tempera- 
ture of which should range from 65° to 70° F. Night air and. cold 
winds must be avoided. The region best adapted to patients affected with 
any of the forms of bronchitis, is one with a moderately warm, dry atmos- 
phere, protected from cold winds, and of moderately high altitude. In cases 
that are attended by emaciation, a long sea-voy age is often of the greatest 
benefit. The diet at all times should be most nutritious. As regards the 
use of stimulants, no definite statement can be made, but, as a rule, mod- 
erate stimulation is of service. 

In no disease is a careful study of each individual case more important. 
The immediate and remote cause of the affection must, if possible, be 
determined. If the bronchitis is the result of an irritant inhalation, 
removal from exposure to this is of the greatest importance. If cardiac 
disease exist, which keeps up the bronchial affection by inducing hyper- 
emia of the mucous membrane, the treatment should be directed to 
the cardiac affection, and, if possible, the heart's action regulated. If 
a gouty or rheumatic diathesis exist, the use of colchicum and alkalies 
is indicated. Steam inhalations of hyoscyamua, conium, or stramonium 
are often of great service in gouty bronchitis. When pulmonary emphy- 
sema is associated with, or is the apparent cause of the bronchitis, the 
internal administration of iodide of potassium will be followed by most 
marked relief. Dilute nitric acid, and the ethereal extract of the acetate 
of iron are beneficial. In general anaemia accompanying bronchitis, prepa- 
rations of iron are indicated ; in fact, in the majority of cases of chronic 
bronchitis, a general tonic plan of treatment is attended by the most 
marked benefit. Quinine, mineral acids, bitter vegetable infusions com- 
bined with iron, often prove of great service. Bronchial catarrh, alternat- 



BRONCHIECTASIS. 



81 



Ing with chronic skin affections, yields most readily to preparations of 
arsenic and sulphate of zinc. 

The treatment of the immediate symptoms must depend upon the quan- 
tity of the expectoration, the degree of difficulty which attends its dis- 
charge, and the presence or absence of any spasmodic action of the 
bronchial tubes. When the bronchial secretions are excessive in quantity, 
steam inhalations of tar, creosote, copaiba, and naphtha are often of 
great service in limiting their formation ; the vapor of iodine, muriate 
of ammonia, and the different balsams are also of service in accomplish- 
ing the same purpose. These remedies may be given internally at the 
same time. When the power of expectoration is deficient, owing to the 
adhesive character of the expectoration, stimulating expectorants are 
indicated, such as senega, serpentaria, camphor, tincture of benzoin, 
combined with such alkalies as carbonate of potash and soda. In those 
cases where the bronchial membrane is extremely irritable, the secretions 
scanty, and the cough attended by violent paroxysms, narcotics and seda- 
tives should be administered in full doses ; opium, hydrocyanic acid, hy- 
oscyamus, belladonna, and conium are the most trustworthy agents of this 
class. Where there is much spasm of the bronchi, shown by the breath- 
ing and cough, a few drops of ether or chloroform may be inhaled ; when 
the tendency to the spasm is great, the narcotics and sedatives already re- 
ferred to should be administered. Tincture of cannabis indica acts well 
in some of those cases. In all varieties of chronic bronchitis, localized 
counter-irritation over the seat of the most extensive bronchial changes 
may sometimes be employed with benefit, such as may be produced by dry 
cups, sinapisms, blisters, croton-oil, and turpentine. It is never necessary 
or desirable to abstract blood, either locally or generally. Occasionally, 
emetics may be employed with benefit, when the bronchial secretion accu- 
mulates in the larger tubes and cannot be expectorated. The close con- 
nection of chronic bronchitis with dilatation of the bronchi renders 
it necessary to consider briefly some of the prominent features of the 
latter. 

BRONCHIECTASIS. 

Bronchiectasis, or dilatation of the bronchial tubes, is closely connected 
with chronic bronchitis. 1 

Morbid Anatomy. — It may be general or partial. When partial, it is 
called saccular or ampullar. The dilatation may be cylindrical, fusiform, 
or sacculated. When dilatations are connected together by tubes of normal 
calibre, the condition is distinguished as the " moniliform " dilatation of 
Cruveilhier. In bronchiectatic cavities, the result of chronic bronchitis, 
the walls are hypertrophied, the mucous membrane is thickened, and may 
be covered over with small papillary outgrowths. The submucous tissue 
is hypertrophied and loses to a great extent its elastic fibres, and the mu- 



6 



1 First described by Laennec. 



82 



DISEASES OF THE RESPIRATORY ORGANS. 




Diagram illustrating forms of dilatation 

of the Bronchi. 
A- " Moniliform" dilatation— the tube 

between the enlargements being of 

normal size. 

B. "Sacciform" dilatation— several of 
the ampullar enlargements connecting. 

C. Formation of a Cyst — by atrophy of 
the connectiug tube. 



cous glands are atrophied. The muscular fibres are often dissociated. 1 
Bronchiectasis is rarely met with independent of some stenosis ; we often 
find alternate stenosis and dilatation. On the tracheal side these bronchial 
dilatations usually communicate with a slightly enlarged bronchial tube ; 

but, on the peripheral side, the continuity 
of the tube is almost or entirely lost by 
narrowing or actual obliteration. Cystic 
cavities may be found ; these are isolated 
bronchial dilatations, whose supplying bron- 
chus has become permanently obstructed. 
Pus, muco-pus, crystals of margarin, fibres 
of lung-tissue, and even chalky debris 
have been found in these cavities. The 
lung tissue close to the bronchiectases is 
altered in various ways ; there may be fibroid 
induration, emphysema, lobular pneumonia, 
and atrophy. The contents of a bronchiec- 
tatic cavity may decompose and, ulceration 
occurring, gangrene or abscess of the lung 
may result; but neither gangrene nor abscess 
occurs with bronchial dilatation as often 
as collapse and fibroid thickening. The 
small bronchi, and the bronchi in the lower 
lobes, are the parts most often involved in bronchiectasis. 

Etiology. — Chronic bronchitis is the most frequent cause. Atelectasis, 
lobular collapse, fibroid induration, and old pleuritic thickenings also 
cause it. Phthisical processes are nearly always accompanied by more or 
less bronchial dilatation. 

Symptoms. — Many of the symptoms are referred to under the head of 
"fetid bronchitis" An abundant, fetid, purulent, and often nummular 
expectoration, frequent and paroxysmal cough, a very fetid breath, some 
emaciation, occasional profuse haemoptysis, and not infrequently night 
sweats, associated with the symptoms of chronic bronchitis, are the character- 
istics of bronchiectasis. The pulse is accelerated, and there is hectic fever 
during its advanced stage. 

Physical Signs. — Inspection shows retraction, prolonged expiratory motion, 
with diminished expansion on the affected side, or of the whole of the chest 
if both sides are involved. 

Palpation. — There is increased vocal fremitus. 

Percussion elicits dulness if the dilatation is filled, or if it is sur- 
rounded by consolidated lung. There will be extra resonance if the dilata- 
tion is empty and superficial, and there maybe a cracked-pot resonance if 
the dilatation is very large, surrounded by fibrous tissue,and near the surface. 

Auscultation. — The respiratory sounds maybe harsh, blowing, bronchial, 
cavernous, or amphoric, according to the seat, size, and condition of the 
dilatation. Large and small gurgles are often heard. 



1 In children these bronchiectases not infrequently disappear when the bronchitis which caused them 
disappears. 



FIBRINOUS BEOXCHITIS. 



83 



Its differential diagnosis will be considered in connection with phthisis. 
This condition cannot be cured. It may exist for many years without ma- 
terially impairing the general health. Death may be caused by gangrene, 
abscess, exhaustion, or some complication. 

Treatment — Its treatment is that of chronic catarrhal bronchitis (q. v). 
It is benefited, by the daily use of antiseptic sprays of creosote, carbolic 
acid, etc.; by a residence in a moderately high, warm and dry locality; by 
a carefully regulated, nourishing diet, and a proper hygiene ; and in most 
instances by tonics in addition to cod-liver oil. 

FIBRINOUS BRONCHITIS. 

Under this head, will be considered croupous, pseado-membranous, or 
plastic inflammation of the bronchial mucous membrane, as it occurs inde- 
pendently of laryngeal croup on the one hand, and of croupous pneumonia 
on the other, or of that form of catarrhal bronchitis during the course of 
which a few membranous flakes are expectorated. This disease may pursue 
either an acute or chronic course. Both forms are rare ; the acute is the 
more infrequent. 

Morbid Anatomy.— It differs from catarrhal bronchitis in the character of 
the exudation, as plastic material is poured out into the tubes in the form 
of casts, which are either soiid or hollow, according as the small or large 
tubes are affected. In the chronic form, the membranous exudation occurs 
over a circumscribed portion of the bronchial membrane ; in the acute, it 
is distributed over a greater portion of the bronchi. The membrane may 
be firmly adherent or loosely attached to the mucous surface. These casts 
are of a whitish color, sometimes dotted over with blood-spots. Microscop- 
ically, they consist of fibri Hated fibrin, abundant granular matter, oil- 
globules, exudation corpuscles, and fusiform ovoid cells. They always 
consist of concentric laminae. Acetic acid causes them to swell. In some 
cases no membrane exists ; the bronchial membrane is pale and congested. 

Etiology. — There is no known special exciting or predisposing cause to this 
disease — it is supposed to be due to some diathetic state. It is most fre- 
quently met with in young adults, and occurs more frequently in females than 
in males, and in those of feeble, delicate constitutions, rather than in those 
who are strong and healthy. It has been seen associated with asthma and 
emphysema. The strumous and phthisical are markedly predisposed to it. 

Symptoms. — The acute form is usually preceded by catarrhal symptoms 
of short duration. It is attended by fever, by dyspnoea (often severe), by 
a dry, hoarse, ringing cough (not as stridulous as in croup), and by a sense 
of constriction and oppression across the chest. After severe paroxysms of 
coughing, either fragments of membrane, or membranous casts or cylin- 
ders are expectorated, usually in small masses. The membranous expecto- 
ration, in rare instances, is wanting, and occasionally not even cough is 
present. There are no symptoms of laryngeal obstruction. When the dis- 
ease pi ogresses toward a fatal termination, the dyspnoea rapidly increases 
in severity, and is finally superseded by those phenomena which precede 
death by asphyxia. 



84 



DISEASES OF THE RESPIRATORY ORGANS. 




TJie chronic form is generally preceded by catarrhal bronchitis, which 
sometimes has lasted for a long time; severe haemoptysis may have preceded 
its development. Not infrequently, in pulmonary phthisis, where haemop- 
tysis has occurred, casts of bronchial tubes are expectorated, which are 
nothing more than decolorized blood-clots. The history of the chronic 
form of plastic bronchitis is rarely a continuous one, but is made up of in- 
tervals of health and paroxysms of disease ; during the latter, expectora- 
tion of membrane in fragments or casts occurs. Their removal is often pre- 
ceded by fits of severe coughing, and by paroxysms 
of dyspnoea of variable intensity, lasting usually a 
few hours, sometimes a day or more ; at other 
times, simple sneezing effects their removal. Gen- 
erally, along with the membrane, there is catarrhal 
expectoration, in which small portions of mem- 
brane may be hidden. In about one-third of the 
cases, haemoptysis (generally slight) has either pre- 
ceded or accompanied the membranous expectora- 
tion. The membranous exudation, if it comes from 
the large bronchi, is in the form of casts ; if from 
the small, it is in the form of cylinders. Occasion- 
ally, there is mucus or blood in the interior of the 
casts, while streaks of blood are often present on 
the exterior. The casts are of variable thickness 
and length — usually two or three inches long, 
laminated, and of a whitish or grayish color. 
Microscopically, they are composed of a structureless mass, more or 
less fibrous in character, in which cells are imbedded, more particularly 
pus cells. During the interval between the paroxysms, in uncompli- 
cated plastic bronchitis, the general health is good and fever is not present. 

Physical Signs. — These depend upon the obstruction produced by the 
membrane, sometimes upon the vibration of a portion of it, and on coinci- 
dent catarrh. When the bronchial tubes are obstructed, there is feebleness 
or absence of the respiratory murmur, — in the chronic form, over a limited 
portion of the chest, in the acute, over a large extent. At the same time, 
the percussion note may be normal, extra resonant or dull ; the latter ex- 
isting when collapse of the lung has taken place, disappearing, it may be, 
immediately after membranous expectoration, while the respiratory mur- 
mur regains its normal character, thus masking the exact seat of the dis- 
ease. Flapping and rubbing sounds have been described as a result of vi- 
bration of the membrane. Dry and moist rales are also usually present, due 
either to the narrowing of the tubes, or to coincident bronchial catarrh. 

Differential Diagnosis. — This form of bronchitis may be mistaken for acute 
catarrhal bronchitis, pneumonia, or pleurisy. The history of the case, the 
character of the paroxysm, the membranous expectoration, and the accom- 
panying physical signs, will generally enable one to make the diagnosis of 
plastic bronchitis ; without the membranous expectoration, however, the dif- 
erential diagnosis between acute croupous and acute catarrhal bronchitis 



Fig. 20. 

Mould of bronchial twigs 
expectorated in a case of 
Plastic Bronchitis. One- 
half the original size. 



BRONCHIAL ASTHMA. 



85 



cannot be made. The absence of the symptoms which usually attend pneu- 
monia and pleurisy serves to exclude them from the question of diagnosis. 

Prognosis. — With the acute form, more than one-half die ; with the 
chronic form, if death occurs, it is due to some complication ; so that, in 
uncomplicated cases of chronic plastic bronchitis the prognosis as re- 
gards life is good ; but the disease, having once occurred, is very apt to 
return. The duration of the disease varies. In the fatal cases, when the 
disease is acute, it lasts from three to ten days ; in those cases that recover, 
it lasts from ten to fourteen days. In the chronic form, the paroxysms 
usually last ten or twelve days, and recur, at longer or shorter intervals, for 
months or years. Complete recovery is rare. Croupous bronchitis is very 
likely to lead to pneumonia and pulmonary phthisis. 

Treatment. — The acute form is to be treated the same as croupous laryn- 
gitis. In the chronic form, during the paroxysm, alkaline steam inhala- 
tions should be resorted to, with the hope of removing the membrane as 
quickly as possible. The patient should be kept in a warm, equable 
temperature. During the interval, the general system should be invigorat- 
ed in every possible way, and all exposure to the causes of bronchial irri- 
tation should be avoided, The internal administration of iodide of potas- 
sium has been highly recommended ; quinine, iron, and cod-liver oil are 
often called for. If the paroxysms continue to recur, a change to a warm 
climate, or a long sea voyage must be tried. There is no known remedy o' : 
plan of treatment which promises a cure in this disease. 

BKONCHIAL ASTHMA. 

This is a spasmodic affection of the bronchial tubes, which gives rise to 
dyspnoea of a paroxysmal character. The spasmodic contractions may be 
regarded as due to a neurosis which depends upon the existence of a peculiar 
diathesis. Some muscular spasm or contraction of the circular muscular 
fibres of the bronchial tubes is the essential element of the asthmatic parox- 
ysm ; and the consequent narrowing of the tubes is a necessary mechanical 
result. Bronchial catarrh, when present, may precede the paroxysm, or it 
may not come on until its close. Although bronchitis plays an important 
part in the development of asthma, it only acts as an exciting cause, as there 
must exist a special neurotic condition, without which the paroxysm would 
not occur. This neurosis undoubtedly has its seat in the vasomotor 
system, and in some instances — notably cases of hay asthma — appears to 
result in paralysis rather than spasm of the bronchial and vascular walls. 

Etiology. — Unquestionably, the primary cause of asthma is some consti- 
tutional idiosyncrasy, which is frequently hereditary. Heredity is traced 
in about forty per cent. It is a diathetic disease, and, like all such dis- 
eases, may be readily transmitted from parent to offspring. It is believed 
by some to be connected with a gouty or rheumatic diathesis. No period 
of life is exempt from it; I have seen a well-marked paroxysm of asthma 
in an infant six weeks old, born of an asthmatic mother. 

The exciting causes of the asthmatic paroxysms may be grouped into 
three classes : 



86 



DISEASES OF THE RESPIRATORY ORGANS. 



First. — Those cases in which the bronchial spasm is produced by some 
material respired which acts directly on the bronchial mucous membrane. 
In this class are included all those cases of asthma in which the paroxysms 
are excited by irritating inhalations, such as ipecacuanha powder, many 
chemical vapors, smoke, dust, fog, emanations from newly mown hay, 
stables, roses, sulphur matches, burning sealing-wax, certain atmos- 
pheric conditions, and the emanations from certain animals, cats, horses, 
etc., etc. A pure mountain air excites it in some, and relieves it in others. 
Asthmatics present remarkable peculiarities as to the conditions of atmos- 
phere which suit them best. Second. — Those cases which are of more dis- 
tinct reflex origin. In this class are included those in which the asthmatic 
paroxysms follow errors in diet, an overloaded rectum, uterine irritation, 
the sudden application of cold to the surface, the irritation of an enlarged 
prostate gland, or of hemorrhoidal tumors. Chronic inflammations and 
obstructive diseases of the nasal cavities are frequent causes of reflex asth- 
matic paroxysms, which may develop into a permanent asthma. Third. — 
Those cases which occur as complications, or in connection with bronchitis, 
heart disease, or emphysema, and are most likely to occur after fatigue and 
physical exertion. Bronchial catarrh is one of its most frequent causes. 

Each individual subject to asthma is susceptible only to his own peculiar 
exciting cause. The retrocession of gout and rheumatism, syphilis, renal 
diseases, disappearance of chronic skin eruptions, the stoppage of an habit- 
ual discharge, or the healing of old ulcers may be followed by asthmatic 
paroxysms. Certain organic diseases of the brain induce it. Angina, neu- 
ralgia, gastralgia and asthma often alternate. That form of asthma termed 
hay asthma, which is produced by emanations from newly mown hay, 01 
other vegetable emanations, is always preceded or accompanied by coryza 
and bronchitis ; persons may have the coryza and bronchitis for years with- 
out having the asthmatic paroxysm, yet the paroxysms are certain to come 
sooner or later, and differ in no respect from other asthmatic paroxysms. 

Symptoms. — An attack of asthma may or may not be preceded by precur- 
sory symptoms ; the majority of those suffering from asthma know when 
the attack is coming on, by some peculiar symptom which they alone rec- 
ognize. There may be languor, drowsiness, depression of spirits, or the 
opposite condition, abnormal buoyancy of spirits. Often a large amount 
of 4 'hysterical " urine is passed before the attack, or there may be wakeful- 
ness, headache, itching of the chin, etc. Ordinarily, the individual goes 
to bed as well as usual, and quietly falls asleep ; after an hour or two, while 
he is still asleep, the characteristic wheezing commences, and soon he is 
awakened by a most distressing attack of dyspnoea. He feels as if his chest 
were compressed, and he were about to be suffocated ; sits up in bed and rests 
his elbows on his knees, and with fixed head, elevated shoulders and mouth 
open, labors for breath. There may be immoderate sneezing, attended by 
running at the nose. There may be flatulent distention of the abdomen. 
His face becomes red, turgid or livid, his eyes prominent, his surface cov- 
ered with perspiration ; he springs out of bed, and hastens to an open win- 
dow in search of air ; respiration is noisy and wheezing, the inspirations 
are short and jerking, while the expirations are prolonged, and terminate 



BROXCHIAL ASTHMA. 



87 



with a sudden effort at expulsion. The number of respirations varies from 
sixteen to thirty a minute. All the auxiliary muscles of respiration are 
brought into play ; yet the chest remains almost motionless. The labor 
may be so great that the patient is in a dripping perspiration. The mouth 
is wide open, the nostrils are dilated, the cervical and facial veins are tur- 
gid. If the bronchial spasm is prolonged, the surface temperature falls be- 
low the normal, the extremities become cold, blue and shrunken, and the 
patient seems to be dying. The pulse during the paroxysm is small, rapid, 
thready, and feeble in proportion to the intensity of the dyspnoea. The 
duration of the paroxysm varies ; at one time it lasts only a few minutes, 
at another an hour or two, in rare instances it may continue two or three 
days without intermission. 

As the paroxysm passes off, the patient begins to cough and expecto- 
rate ; in some patients the expectoration consists of a few small, rounded 
masses like pearls of mucus, and contains neither pus nor watery con- 
stituents ; in others it is profuse and watery. The expectoration occurs 
after the bronchial spasm has ceased ; it does not cause its cessation ; 
and even when the attack begins " dry," there is some expectoration at 
the end of the paroxysm. Occasionally in severe attacks, there are 
blood-streaks m the sputa, and sometimes quite profuse hemorrhage occurs. 
The paroxysm, recurs after intervals of varying length ; some experience 
an attack only annually, others monthly, and others only when sub- 
jected to their own peculiar exciting cause. Less violent attacks mav 
last five to six days. During the interval, if the asthma is not due to any 
organic disease, the condition of the asthmatic subject varies ; some are 
perfectly well ; others constantly have a sense of thoracic constriction, 
which renders the breathing somewhat labored, especially during active 
exercise. Some suffer severely from a bronchial or nasal catarrh. When 
the catarrhal element predominates, the asthmatic paroxysms are excited 
by slight exposure. The longer the attack, the less abrupt its cessation 
and more profuse the sputa. Immediately after a paroxysm, there is usu- 
ally a feeling of exhaustion, aching and " soreness, 55 which passes off in a 
few hours, and the individual experiences a sense of relief, and has for a 
time an almost certain immunity from a repetition of the attack. Some 
claim that the urine exhibits a remarkable diminution in chloride of so- 
dium and urea just after an attack, while later both return to the normal. 1 
Analysis of expired air shows oxygen to be almost wholly replaced by car- 
bonic acid, which may be eleven per cent, above the normal quantity. 

Physical Signs. — During the paroxysm inspection shows labored respira- 
tion, while the upper part of the chest is almost motionless, and the 
muscles of the neck rigid; the inferior costal and abdominal respiration is 
labored, the act of inspiration is slower than in health, and expiration is 
more active and violent, and also longer than normal. Vocal fremitus and 
vocal resonance are normal. The percussion sound is slightly exaggerated. 
On auscultation the respiratory murmur is jerking and irregular ; some- 
times it is exaggerated, at other times it is suppressed. Sibilant and sono- 



1 Sidney Ringer. 



88 DISEASES OF THE RESPIRATORY ORGAN'S. 

rous rales of a high-pitched, hissing and wheezing character are diffused 
over the whole chest, often loud enough to be heard at a distance from the 
patient. These are best marked over and between the scapulas. The 
respiratory murmur is very faint or absent, especially in the old and where 
expiration is prolonged and low pitched. All sounds are loudest during 
expiration. The rale sounds are often musical. These rales are constantly 
changing their character and site, disappearing at one point and making 
their appearance at another. At the close of the paroxysm some moist 
rales may be heard ; or if bronchial catarrh exists then the sounds will be 
moist throughout. 

Differential Diagnosis. — Spasmodic asthma will rarely be confounded with 
any other disease, if its rational and physical signs are properly appreciated. 
The phenomena of a paroxysm are quite distinctive, while the physical 
signs are unmistakable. The affections with which there is a possibility of 
its being confounded are spasmodic affections of the larynx, acute capillary 
bronchitis, angina pectoris, hydrothorax, pulmonary oedema and congestion 
and emphysema. It is easily distinguished from laryngeal affections by the 
absence of the change in the voice which is so characteristic of laryngeal 
spasm, and by the presence of auscultatory signs never heard in spasm of the 
glottis. It is distinguished from bronchitis by the slowness of respiration, 
by the absence of subcrepitant rales and pyrexia, and by the suddenness of 
its advent. In angina pectoris there are no sibilant and sonorous rales. 
Angina pectoris is accompanied by lancinating pain — absent in asthma 
— and there are no attendant physical lung symptoms. In hydrothorax 
there is no resonance on percussion over the entire thorax, no succussion, 
and no change in the line of dulness. In pulmonary oedema there is 
dulness ; in asthma extra resonance. Liquid, bubbling, stationary rales 
are heard in oedema ; in asthma the rales are dry and constantly change 
position and character. There is profuse watery expectoration in oedema, 
absent in asthma. Asthmatic dyspnoea and cardiac dyspnoea are some- 
times confounded ; in some respects they resemble each other — both are 
paroxysmal, both are intense, and both generally occur at night. There 
is little wheezing in cardiac dyspnoea. In both, the respiration maybe per- 
fectly normal between the attacks, but a careful physical examination will 
enable one to determine whether the dyspnoea is asthmatic or cardiac. 

Emphysema has a vesiculo-tympanitic percussion note, not present in 
asthma. Prolonged low-pitched expirations exist in emphysema; in asthma 
the expirations are never low pitched. The barrel-shaped chest and change 
in the position of the heart are absent in asthma, and are notable signs of 
emphysema. The two conditions are often found together. In croup the 
dyspnoea is inspiratory ; in asthma it is expiratory. The condition most 
likely to be mistaken for asthma, in old age, is latent pericarditis with 
effusion. Spasmodic dyspnoea often accompanies it ; but it is marked by 
a feeble, often an irregular pulse, diminished cardiac impulse, obscure 
heart sounds and increase in precordial dulness, and there are no rales 
present. 

Prognosis. — Death rarely, if ever, occurs from uncomplicated asthma. 
Asthmatic patients are frequently long-lived, which may be accounted for by 



BRONCHIAL ASTHMA. 



8 9 



the fact that they are compelled to observe the most rigid hygiene in order 
to avoid their asthmatic attacks. The fact that a person has had one 
asthmatic attack, is presumptive evidence that he will have another. The 
prognosis, as to recovery, is hopeful in proportion to the youth of the 
patient. If the attacks only come on at long intervals arid are not severe 
and prolonged ; if during the intervals the patient is well and there is no 
organic disease; if the paroxysms can be traced to some obvious cause which 
may be avoided, the prognosis as to the complete recovery is good. At first, 
the attacks are violent and exhausting ; then they lose their periodical 
character and run together, as it were, so that the patient is never wholly 
free from asthmatic dyspnoea. The periodicity varies from one year to one 
month. Emphysema, chronic passive pulmonary hyperemia, right car- 
diac hypertrophy and dilatation, and chronic bronchitis are among its 
complications. 

Treatment. — There are two things to be considered in the treatment of 
this affection, viz., the relief of the paroxysms and the prevention of their 
recurrence. The first thing is to ascertain the exciting cause of the 
paroxysm, and, if it is still in operation, to remove it if possible. If the 
paroxysm is dependent on an overloaded stomach, an emetic should be ad- 
ministered; if upon a loaded rectum, an enema should be given; if smoke, 
dust, or any animal or vegetable emanation is the cause of the attack, it 
must be removed. " Eose fever " and " hay fever " are only relieved by 
removal from places where there are roses or hay. If, in a certain locality, 
the attacks of asthma are of frequent occurrence, the patient should re- 
move to one where he is free from asthmatic paroxysms. Ebt infrequently 
the removal of the exciting cause will be all that is necessary for the relief 
of the patient. If the exciting cause cannot be removed, or if its removal 
is not followed by relief of the paroxysm, free ventilation should be secured, 
and the patient should be placed in a position in which respiration may be 
carried on with as little mechanical impediment as possible. Curtains and 
obstructions to the free entrance of the air should be removed from the 
room. Usually the best position during an attack is the sitting posture — 
in a chair which will give support to the arms and so elevate the shoulders. 
Some old people are relieved by sitting before a hot open fire in a close 
room. 

Having placed the patient under the most favorable circumstances for the 
relief of the paroxysm, the next thing is to select those remedial agents 
best adapted to the case. This selection will be very much influenced by 
the patient's own experience and idiosyncrasy. The great majority of 
asthmatics know the remedies that will give them relief. The remedies 
that give relief to asthmatics maybe divided into three classes: depressants, 
sedatives, and stimulants. Among the leading depressants are antimony, 
ipecacuanha, tobacco, and lobelia. Ipecacuanha is to be given in quanti- 
ties/^ sufficient to produce nausea, and tobacco till it begins to sicken. 
If a patient has been previously relieved by the use of depressants, it is well 
to inquire which one of this class he made use of. The relief obtained by 
this class of remedies is by bringing the asthmatic into a condition of com- 



00 



DISEASES OF THE RESPIRATORY ORGAN'S. 



plete relaxation. Sometimes this may be accomplished by the administra- 
tion of one full dose of ipecacuanha. 

Sedatives seem to act in two ways : some act locally on the nervous 
supply of the lungs, but the majority give relief by their action on the 
general nervous system. Those which experience has shown to be most 
efficacious in arresting the asthmatic spasm are stramonium, chloroform, 
belladonna, conium, assafoetida, the bromides, ether, opium, cannabis 
indica, hyoscyamus, and the fumes of burning nitre paper. Smoking 
stramonium often relieves when the internal use of the extract is inert. 
The datura tatula is by many regarded as more efficacious than the datura 
stramonium. Smoking tobacco often relieves a paroxysm. Some will be 
promptly relieved by the inhalation of the fumes of stramonium leaves ; 
others by the inhalation of chloroform. Perhaps there is no agent in this 
class that will so speedily and completely relieve the spasm as chloro- 
form ; but the relief is only temporary ; so soon as the stupefying effects 
have passed away the paroxysm generally returns with increased violence. 

Ether is safer to inhale than chloroform, and has no such after-effects. 
A combination of the two is often efficacious. Trousseau advocates inhala- 
tion of vapor of ammonia. Many asthmatics find immediate but temporary 
relief by spraying the naso-pharyngeal passages with a four per cent, solu- 
tion of cocaine. This measure is especially valuable in " hay asthma." 
Quebracho has proved efficacious in a few instances. Recently grindelia 
robusta has been strongly advocated. In this class of remedial agents, that 
which I have used most successfully is opium given in full doses — small 
doses are unavailing. One half a grain of the sulphate of morphia should 
be administered at once. I prefer its hypodermic use. Atropine may be 
combined with the morphia ; there are cases which are quickly relieved by 
this combination, which are not relieved by the use of either of these drugs 
alone. Conium, hyoscyamus and belladonna act much less certainly. 
They should be tried, however. Nitrite of amyl is not so successful as its 
physiological action would indicate. Iodide of ethyl is advocated by some. 1 
Fumes of nitre paper is one of the oldest and best remedies. The paper is 
prepared by dipping filter or blotting paper in a solution of saltpetre. 
How it acts is not well understood ; certainly not by relieving the bronchial 
irritation, for, as a rule, the patient is not relieved if bronchitis is asso- 
ciated with the asthma. When this remedy is employed it is necessary 
that the apartment occupied by the patient should be filled with its fumes. 
If it acts favorably it will do so quickly, and its administration must not 
be prolonged if relief is not promptly obtained. 

Among stimulants, the two principal remedies are coffee and alcohol. 
Coffee is the more efficacious. It should be taken strong without 
milk or sugar, and as hot as it can be swallowed ; it should always be 
taken on an empty stomach. Not infrequently a paroxysm of asthma 
can be warded off by taking two or three cups of strong coffee imme- 
diately upon the accession of the first asthmatic symptom. Alcohol 
is another stimulant which experience has led me to regard very highly. 
It is of little importance what alcoholic stimulant is employed, but it 



i Gazette Medical de Paris. 1878, p. 69. 



BRONCHIAL HEMORRHAGE. 



91 



must be taken hot and strong, that is, as a "hot toddy," and in suffi- 
ciently large doses for the patient to feel its intoxicating effects. As a 
rule asthmatic patients will bear large quantities of alcoholic stimulants 
without becoming intoxicated. By whichever class of remedial agents the 
patient is relieved, after a time the remedy will fail or cease to have the 
desired effect. The three most reliable remedies are ipecacuanha as a de- 
pressant, opium as a sedative, and coffee as a stimulant. Compressed air I 
have never found to give the relief promised by its advocates ; nor does 
inhalation of*oxygen allay the paroxysms as a rule. Certain mineral springs 
are beneficial for asthmatics ; the most noted are Cauterets, Mont-Dor e, 
and Eaux Bonnes. Faulkner paints the track of the pneumogastric in 
the neck with iodine and claims remarkable results. Nitro-glycerine and 
pilocarpin have both been used. 1 In the intervals the treatment is hygi- 
enic ; no known remedies can prevent the return of the paroxysms, whereas 
the observance of certain hygienic rules may often prevent or delay their 
return, It is claimed by good observers that the removal of nasal obstruc- 
tions, as deviated septa, turbinated and mucous hypertrophies, etc., is fol- 
lowed by marked or even permanent relief from the asthmatic paroxysms. 
When skin diseases alternate with attacks of asthma, arsenical preparations 
are beneficial. Where the cause is undiscoverable, many state that iodide 
of potassium not only prevents or delays an impending attack, but even 
effects a permanent cure. Asthmatic patients are usually dyspeptic ; and 
it is a noticeable fact that in such cases, as long as they exercise proper 
care as to diet, they are free from asthmatic attacks. This is not to be 
overlooked in the management of asthmatics between the paroxysms. A 
change of residence is all-important in cases dependent for their develop- 
ment upon certain atmospheric causes. There is no definite rule for this 
change ; each one must decide for himself, finding by experience the place 
in which he is free from his attacks. If the patient is anaemic and poorly 
nourished, cod-liver oil and iron must be administered during the interval. 
I have quite a number of asthmatics under observation who, by taking- 
daily from gr. xv. to gr. xx. of the sulphate of quinine, can prevent parox- 
ysms of asthma. As soon as the daily use of the quinine is discontinued, 
the asthmatic symptoms begin to manifest themselves, and soon culminate 
in a paroxysm. Helmholtz found relief by injecting into the nostrils a 
solution of quinia when he suffered from "hay fever." The diet, espe- 
cially in old age, should be strictly regulated, ¥o fats, no water within 
one hour before dinner or supper, or till three hours after — these should 
be laws never to be broken. Flannel must be worn next the skin. Exer- 
cise should be constant, but moderate. Should the chest development be 
defective, however, active gymnastic exercise is then to be advised. 

HAEMOPTYSIS. 2 

In the majority of instances, when blood is expectorated in considerable 
quantities, the source of the hemorrhage is the bronchial mucous membrane. 



1 British Medical Journal, Vol. I. 1880. p. 900. 

2 Haemoptysis means spitting of pure blood only : i. e., the rusty blood-stained sputa of pneumonia do 
not constitute an haemoptysis. 



92 



DISEASES OF THE RESPIRATORY ORGANS. 



Spitting of blood occurs in pulmonary congestion, pulmonary apoplexy, 
and in the inflammatory processes affecting the lungs and bronchi ; but 
hemorrhage from the bronchial tubes is by far the most frequent cause of 
blood-spitting or hcemoptysis ; and when blood comes from the bronchial 
tubes the hemorrhage is properly called bronchorrliagia. 

Morbid Anatomy. — If the bronchial mucous membrane is examined soon 
after or during a bronchial hemorrhage, at the seat of the hemorrhage it 
will be found swollen, relaxed, bleeding on slight pressure, and of a uni- 
formly dark-red color, with here and there spots of ecchymosis. The lungs 
are pale but are marked by bright pink spots, corresponding to the air-cells 
into which blood has been inhaled. If the examination is made some time 
after the bleeding, the bronchial membrane -will either present a pale and 
bloodless appearance, or no traces of the seat of the hemorrhage can be 
found. If the examination is made during or soon after the hemorrhage, 
the bronchi may be found more or less completely filled at points with 
blood-clots ; these clots are usually exsanguinated. The healthy portions 
of the lungs are inflated. In haemoptysis occurring in advanced phthisis 
there will either be aneurism of a pulmonary vessel in a cavity, or ulcera- 
tion of an exposed vessel. In the early stage of phthisis, tubercle will be 
found in the walls of the small vessels. If the blood has been forced from 
the bronchi into the air-cells, small, red, dense nodules will be found 
scattered through the lung-substance, very closely resembling, in their 
gross appearance, pulmonary infarction. 

Etiology. — Ulceration of the bronchial mucous membrane is rarely a 
source of bronchial hemorrhage ; and seldom does an aneurism open into a 
bronchus. The two prominent causes of bronchial hemorrhage are : first, 
over-distention of the capillaries of the bronchial mucous membrane ; 
secondly, weakness of the capillary walls of the bronchial membrane. Such 
weakness of the walls of the capillaries may be an hereditary or an acquired 
condition. In both cases there is probably rupture, which may escape 
detection at the autopsy. The tendency to bronchial hemorrhage from 
weakened capillaries is much stronger between the ages of fourteen and 
thirty, especially in young, delicate persons born of phthisical parents, than 
at any other time. There is also a strong disposition to this form of hem- 
orrhage in those who are already suffering from developed phthisis, or 
who have an acquired phthisical diathesis. Usually in these cases the 
direct cause of the hemorrhage is a sudden distention of the weakened 
bronchial capillaries from violent physical exertion, or from certain peculiar 
atmospheric influences. In rare instances it occurs without any appreciable 
cause. That form of bronchial catarrh which precedes or attends the devel- 
opment of phthisis is very frequently preceded or attended by bronchial 
hemorrhage. Here, probably, the exciting cause of the hemorrhage is act- 
ive hyperemia of the bronchial membrane. Bronchial hemorrhage may 
be induced by the inhalation of irritating gases or vapors and by the rare- 
fied air of high elevations ; in both of these instances the hemorrhage fol- 
lows over-distention of the capillary vessels of the bronchial membrane. 



1 Rindfleisch thinks that when phthisis follows haemoptysis the hemorrhage is due to ''vascular tuber- 
cular infiltration. 1 ' 



BRONCHIAL HEMORRHAGE. 



93 



Any form of obstructive heart disease that leads to passive hyperemia of the 
lungs will predispose to bronchial hemorrhage. Intense active hyper- 
emia will also cause it. The violent coughing of bronchitis, pertussis and 
pneumonia oftentimes induces it. It may follow suppression of any habit- 
ual discharge, and is then called " vicarious bronchorrhagia." 

Symptoms. — The symptoms which attend a bronchial hemorrhage vary 
with the profuseness of the hemorrhage. If the quantity of blood expec- 
torated is very small no symptoms will be developed except the spitting of 
the blood, which is of a bright red color. It is not often, however, that 
the symptoms that attend a bronchial hemorrhage are so trivial, for these 
hemorrhages are usually profuse. All bronchial hemorrhages are attended 
by the spitting of bright red, frothy, arterial blood. A very profuse bron- 
chial hemorrhage may come on suddenly without any warning, but usually 
the patient has had some previous indication of its occurrence, such as a 
sense of constriction at the upper portion of the chest, or a sense of uneasi- 
ness during inspiration, which he cannot account for. Those who have had 
haemoptysis may suffer prodromata, such as headache, dizziness, palpitation, 
increased pulse-tension and a general constriction about the chest. Cough 
may or may not precede the hemorrhage. Usually the patient feels as if 
some fluid had suddenly commenced trickling under the sternum, and he 
notices an unusual sweetish taste in the mouth. He spits and finds that 
the fluid is blood, although there may have been no cough previous to the 
hemorrhage. Xow he feels more or less bronchial irritation, which is fol- 
lowed by a cough. Loud moist rales are heard, more or less blood is expec- 
torated, short intervals occur between the fits of coughing, and in this way 
blood may continue to be expectorated for several days, or the expectoration 
may continue only for a few hours. 

The amount of blood expectorated varies ; sometimes, when the hem- 
orrhage is profuse, the whole quantity may reach a pound or more ; at 
other times not more than an ounce or two is expectorated. During the 
occurrence of the hemorrhage the countenance of the patient assumes an 
anxious expression ; he becomes tremulous and often faints. This, how- 
ever, is not owing wholly to the loss of blood, but is probably due to 
the shock to the nervous system from the sight of blood and knowledge 
of the fact that a hemorrhage from the lungs has taken place. The pulse 
becomes rapid and tense, and, unless the bleeding is profuse, the face 
is red. The temperature during the bleeding is usually depressed, but 
soon returns to the normal. If the temperature rises to 103° or 104° F. 
during: or immediately following, it is a verv certain indication that the 
haemoptysis is the ushering-in symptom of acute tubercular pneumonia. 
All these symptoms may be present when the individual has not lost more 
than half a pound of blood. Hemorrhage from the lungs weakens a patient 
more than an equal amount of hemorrhage from any other organ of the body. 
After the profuse expectoration of blood has ceased, the patient goes on 
coughing for a few days, expectorating small, dark, coagulated masses of 
blood or blood-streaked sputa. Sometimes bronchial hemorrhage is so pro- 
fuse that the blood spouts out of the mouth and nose. This is followed by 
nausea and vomiting of blood, but it is worthy of notice that the nausea and 



04 



DISEASES OF THE RESPIRATORY ORGANS. 



bloody vomiting follow and do not precede the hemorrhage. Death may 
occur from suffocation in these cases. Rapid and profuse (but now-phthisi- 
cal) hemoptysis should lead to the suspicion of the rupture of an aneurism. 
Attacks of bronchial hemorrhage are rarely single ; usually for a week or 
two they recur at intervals. At length the patient becomes pale and 
feeble, then recovery gradually takes place, so that in a few weeks he may 
feel better than before the hemorrhage. This is the most favorable termi- 
nation that can be hoped for, except in those cases in which the hemor- 
rhage is comparatively insignificant. It is important to remember that 
attacks of bronchial hemorrhage, however profuse, are generally recovered 
from in spite of extreme prostration and tendency to syncope which some- 
times attend their occurrence. When the recovery from a bronchial 
hemorrhage is not speedy it is quite likely to be followed by more or less 
febrile excitement, the temperature rising, perhaps, to 101° F., the pulse 
becoming accelerated and feeble. The patient becomes paler and weaker, 
has almost complete loss of appetite, and is troubled with a hacking cough, 
almost constant, which is accompanied by a tenacious, scanty, muco-pur- 
ulent expectoration. The respiration is hurried, and there is dyspnoea 
on slight exertion. Under these circumstances the bronchial hemorrhage 
is followed by broncho-pneumonia, which, in the majority of cases, within 
a few weeks goes on to more or less complete resolution, and the patient, 
by means of change of air and proper hygiene, may finally recover. There 
is another class of cases in which the hemorrhage is followed by still more 
active febrile symptoms, the temperature rises higher, the pulse is more 
rapid and feeble, emaciation follows, usually accompanied by profuse night 
sweats, and the patient dies of acute phthisis within a few months after the 
first hemorrhage. Previous to the hemorrhage he has good health, and 
there were no physical evidences of disease of the lungs or bronchi. (This 
subject is more fully considered under the head of Acute Phthisis.) 

A physical examination of the chest during a bronchial hemorrhage usu- 
ally gives negative results. On auscultation nothing abnormal is found, 
with the exception of a few large and small moist bronchial rales. It is not 
well to disturb the patient by frequent examinations of the chest. 

Differential Diagnosis. — There are four conditions which may be con- 
founded with bronchial hemorrhage, namely, epistaxis, pulmonary apo* 
plexy, hcematemesis, and aneurisms rupturing into the air-passages. 

Epistaxis is very easily distinguished from bronchial hemorrhage, for the 
nose-bleed occurs before the apparent bronchial hemorrhage, and the blood 
is always coagulated and dark-colored. It is not attended or followed by a 
cough, and blood can always be detected in the nostrils, posterior nares, or 
pharynx. The characteristics of the haemoptysis w r hich occurs in connection 
with pulm onary apoplexy will be considered under that head. The diagnosis 
between these two forms of haemoptysis rests upon the character and quan- 
tity of the blood expectorated, and the existence or non-existence of cardiac 
disease or pyaemia ; and here a physical examination is of great importance. 

Hmmatemesis is to be distinguished from bronchial hemorrhage by the 
fact that the blood in hasmatemesis is always coagulated and grumous, of 
a dark red color, and vomiting precedes or accompanies the hemorrhage. 



BRONCHIAL HEMORRHAGE. 



05 



In bronchial hemorrhage if nausea and vomiting are present they follow the 
spitting of arterial blood ; and haematemesis is not accompanied or followed 
by a cough. The gurgling in the bronchi, loose cough, and bright frothy 
appearance of the blood are never met with in haematemesis. Blood is 
alkaline when from the lungs, and acid from the stomach. " Spurious 
haemoptysis" (bleeding from gums, pharynx, etc., as from bad teeth) may 
be confounded with bronchorrhagia, but an examination of the mouth soon 
reveals the true state of affairs. When an aneurism ruptures into a bron- 
chial tube, the hemorrhage is generally profuse, and it is soon followed by 
death. The long history of aneurism which precedes the rupture, as well 
as the physical signs, which at least will have led to the suspicion of 
aneurism, are in most instances sufficient to enable one to determine the 
nature of the hemorrhage. 

Prognosis. — Bronchial hemorrhage rarely proves immediately fatal, or 
directly endangers life. The prognosis as to final result is always unfavor- 
able ; it is in a large proportion of cases either the precursor of phthisis, 
or a sign that phthisis already exists. It certainly always demands serious 
consideration. The prognosis is much more favorable when the hemor- 
rhage is due to the excessive action of the heart, or bronchial hyperemia 
induced by the inhalation of irritating substances or gases than when it 
occurs without any apparent exciting cause. Should haemoptysis be suffi- 
cient to induce anaemia, the latter condition is very obstinate and persist- 
ent, more so than when it follows other hemorrhages. 

Treatment. — Absolute rest in a cool room is of the greatest importance. 
The patient should be placed in bed and not allowed to sit up, turn over, 
or even speak above a whisper. If the cough continues and is constant, or 
induces the hemorrhage, it must be quieted by full doses of opium. Ergot, 
tannin, gallic acid, acetate of lead, spirits of turpentine, persulphate of 
iron, or common salt may be administered ; the balsams, copaiba or sweet 
spirits of nitre, maybe given, if their administration will quiet the anxiety 
of the patient or friends. It has never seemed to me that styptics or astrin- 
gents have any control over bronchial hemorrhages, but aconite and opium 
are the two remedies upon which I rely. When the pulse is full and strong, 
I use the aconite ; when it is weak, I employ morphia hypodermatically. 
The application of ice bags to the surface of the chest may be resorted to in 
extreme cases, but it must be carefully done, for the reason that patients to 
whom ice bags are applied are exceedingly liable to have broncho-pneumonia 
follow their attacks of bronchial hemorrhage. Dry cupping over the surface 
of the chest is of service whenever the hemorrhage is preceded or attended 
by marked pulmonary hyperemia. Patients with haemoptysis should be 
urged to eat ice and drink freely of cold drinks. In all cases it is impor- 
tant to keep the patient under observation until all bronchial irritation pro- 
duced by the presence of blood in the bronchial tubes has subsided. If 
there is tendency to a return of the hemorrhage, everything likely to bring- 
on an attack must be carefully avoided, and the nutrition of the patient 
must be improved by the administration of iron combined with a most 
nutritious but non-stimulating diet. Moderate exercise should be taken 
daily in the open air, and all mental and physical exertion should be avoided. 



96 



DISEASES OF THE RESPIRATORY ORGANS. 



DISEASES OF THE 

I shall consider the diseases of tl 
heads : 

I. Acute Lobar Pneumonia. 
II. Lobular Pneumonia. 

III. Interstitial Pneumonia. 

IV. Pulmonary Hyperemia. 

V. Pulmonary (Edema. 

VI. Pulmonary Infarction. 
VII. Pulmonary Apoplexy. 

VIII. Pulmonary Gangrene. 



LUNGS AND PLEURA. 

e lungs and pleura under the following 

IX. Pulmonary Ancemia. 
X. Pulmonary Collapse. 
XI. Pulmonary Emphysema. 

XII. Morbid growths in the Lung 

and Pleura. 

XIII. Parasitic Diseases. {Hydatids.) 

XIV. Pleurisy. 

XV. Pulmonary Tuberculosis. 



ACUTE LOBAR PNEUMONIA. 



Acute Lobar or croupous pneumonia or pneumonitis is an acute general 
disease characterized by an inflammation of the vesicular structure of the 
lungs, with an exudation into the alveoli which renders them impermeable 

to air : a condition called 
" hepatization." A single 
lobe, the whole of a lung or 
both lungs may be simulta- 
neously involved. 

Morbid Anatomy. — Ana- 
tomically as well as clinical- 
ly, lobar pneumonia may be 
divided into three stages. 
First : a stage of congestion 
or engorgement. Second: a 
stage of consolidation or red 
hepatization. Third : a stage 
of gray hepatization. Arte- 
rial injection preceding en- 
gorgement cannot be demon- 
strated. Some have called 
this injection the "dry stage'' 
of pneumonia. 

Stage of Congestion or 
Engorgement— In this stage 
the portion of lung involved 
in the pneumonic process 
does not collapse when the 
thoracic cavity is opened ; it has a firmer feel than normal, and is more 
or less distended ; its resiliency is lost ; it crepitates less than normal ; 




Fig. 21. 



Section of Lung showing a single Alveolus in the first Stage of 
Lobar Pneumonia. 

A, A. Wall of alveolus. 

B, B. Distended, varicose and tortuous capillaries. 

C, C. Alveolar epithelial cells. 

Z>, D. Blood globules in cavity of the alveolus, x 300. 



ACUTE LOBAR PNEUMONIA. 



97 




Fig. 22. 

Section of Lung in the second Stage of Lobar Pneumonia. 

The pulmonary alveoli are seen filled ivith Pus corpuscles (A, A), changed Epithelial cells (B, B), 
jibrillated Fibrin (C, C), and red Blood globules {D, D). x 250. 

and often pits on pressure. It is not wholly airless, for air can be pressed 
from one part to another. It is somewhat friable ; its color is a dark 
brownish red, often purple; and its weight and specific gravity are 
increased. 




Fig. 23. 

"Vertical Section of the Lung and Pleura in the Second Stage of Pie mo-Pneumonia. 

a. Plastic exudation on thickened pleura. 

b. Thickened pleura. 

c. Dilated blood-vessels in pleura. 

d. Loose epithelial cells. ^ 
The alveoli contain red blood corpuscles (e), pus cells (g), changed epithelial cells (/), and fionllatea fiorin 

(i). The blood-vessels (h) in the alveolar walls are seen filled with red corpuscles, x 2o0. 
7 



08 



DISEASES OF THE RESPIRATORY ORGANS. 



On section a thin, frothy, blood-stained serum exudes. Sometimes 
it flows freely on pressure; it may be tenacious. When alcohol is 
added to the fluid it coagulates iuto a granular and amorphous mass. 
Dark blood flows from the distended capillaries. Occasionally, just under 
the pleura and between the air sacs, there are small spots of extrav- 
asation. 

On microscopical examination of a thin section of the affected lung tis- 
sue the lumen of the alveoli will be found diminished by the distended, 
varicose and tortuous capillaries. Early in the disease some of the air- 
sacs may be collapsed from pressure. The alveolar epithelium is swollen 
and granular. In the air-cells are exfoliated epithelial cells, a few pus cells, 
red globules and serum. 1 At the autopsy it is sometimes difficult to distin- 
guish the stage of pneumonic congestion from pulmonary oedema and con- 
gestion. In the latter the fluid in the alveoli is serum and contains no 
cell elements. When a stream of water flows over the cut surface of a 
pneumonic lung the color remains ; in oedema and congestion it dis- 
appears. 

Stage of Red Hepatization. — This stage receives its name from the color 
of the lung and its resemblance, when cut, to liver-tissue. The affected 
portion has a dark liver or mahogany color, and is mottled, the mottling 
becoming more marked as the stage advances. The volume of the affected 
lung is increased; so much so that it often bears the impress of the ribs. 
It is solid, firmer, and heavier than normal. Pressure does not indent, but 
tears it ; it is friable, easily torn, and its torn surfaces have a granular 
appearance. Its specific gravity is increased. It is airless, and there is 
entire absence of crepitation. Artificial inflation is impossible. 

On section the cut surface has a granular appearance ; the granules 
correspond to plugs of inflammatory exudation, which fill the air-cells 
and the small bronchi. Tom surfaces show the granulations better than 
cut surfaces. The granules can be lifted out by means of a fine needle. 
When cut a dirty red viscid fluid slowly oozes from the surface, or it may 
only appear after twelve or twenty-four hours' exposure to the air. This 
may be scraped from the cut surface. A piece of the inflamed lung quick- 
ly sinks in water. Small spots of extravasation are sometimes seen. When 
a stream of water is poured over the cut surface the color changes from a 
maroon to a gray or a yellow-gray. 

On microscopical examination the alveoli are found filled with a solid exu- 
dation composed of a network of fibrillated fibrin, in whose meshes are pus- 
cells, red globules, micrococci, and changed epithelial cells. The latter are 
in various forms — round, oval, quadrangular, triangular, or irregular — and 
have received different names, according to the views entertained by differ- 



1 It is still a disputed question whether the bronchial or pulmonary vessels are the chief source of the 
pneumonic exudation. The lung-tissue is nourished by the bronchial arteries, while the pulmonary ves- 
sels are the medium for the interchange of gases. Hence it is claimed that only the bronchial vessels are 
implicated. Virchow has shown that pneumonic processes can be established when large branches of the 
pulmonary artery are plugged; yet he admits that the pulmonary capillaries have, secondarily, much to do 
with the exudation. Again, it is claimed that early in the disease the parts supplied ny the bronchial 
vessels are not injected as they would be were they alone at fault. Probably both sets of vessels are 
involved. 



ACUTE LOBAR PNEUMONIA. 



99 



ent observers in regard to their origin. At first these cells contain fibrinous 
material, but later they become granular, and then fat globules accumulate 
in them. They may become discolored from imbibition of hsematin. The 
whole contents of an alveolus now present a more or less round form. The 
interstitial connective-tissue between the lobules may be infiltrated with 
pus and fibrin ; the pulmonary pleura is always coated with fibrin if the 
surface of the lung is involved; and if the pleurisy precedes the pneu- 
monia, or if it is extensive and an abundant plastic exudation covers the 




by camera lucida.) 

pleura over the inflamed portion of the lung, it receives the name of pleuro- 
pneumonia. The anatomical changes within the lung are, however, 
unmodified by the more extensive pleurisy, although it undoubtedly delays 
the processes of pneumonic resolution in the third stage. The red blood 
globules give the color to the lung. This stage may last from twenty-four 
hours to several days. 

Gray Hepatization. — In the early part of this stage the lung remains of 
the same consistency as in the second stage. There is no sharp transition 
from red to gray hepatization. The mottling gradually becomes more 



100 



DISEASES OF THE RESPIRATORY ORGANS. 



marked, so that the affected portion becomes " marbled/' or has a "gran- 
ite" look. The surface is gray. The consistency becomes less and less 
until the tissue is a mere pulp, readily breaking down on pressure. The 
change in color is due to pressure on the blood-vessels, to the decoloration 
of the red blood globules, and to the fatty and granular change in the 
inflammatory products. The weight, friability, and density of the lung 
are increased. 

On section the surface presents a uniformly dirty gray appearance. A red- 
dish gray or dirty white puriform fluid flows either spontaneously or on slight 
pressure from the cut surface. The " granular " look of the second stage has 
disappeared or is indistinct. The amount of the accompanying oedema va- 
ries; when it is excessive a large quantity of serum exudes, and the tissue 
does not break down so readily as in other forms of gray hepatization. 

On microscopical examination the alveoli are found filled with numerous 
round, mono-nucleated cells and micrococci ; the intercellular fibres that 
bound the elements together have become granular. The alveoli are filled 
with a fluid or semi-fluid mass, in which numbers of discrete oil globules 
and protein granules are freely mingled. The contents of the alveoli are 
shrunken, and between them and the alveolar wall is a layer of fluid, so 
that, in a thin section, the contents of an air-sac are readily lifted out by 
a camePs-hair brush. The pleura over the affected portion is covered 
with a thin plastic exudation. 

Lobar pneumonia may terminate : (1), in resolution (recovery) ; (2), 
suppuration (purulent infiltration) ; (3), abscess; (4), gangrene; or (5), 
chronic pneumonia. 

During resolution the lung is moist, lighter than during hepatization, 
has a yellow or a yellow-green color, and shows a marked loss of elasticity. 
On section it is now granular, of a yellow-gray hue, and a tenacious puriform 
fluid readily escapes when the section is pressed. Some oedema may still 
remain. Microscopically the vessels are seen to have returned to their normal 
calibre ; the alveolar epithelium is restored, the cells in the alveoli are 
degenerated and broken down into a detritus. The coloring matter of the 
blood gives origin to the pigment so plentifully scattered throughout the 
liquefied mass. The contents are either expectorated or absorbed ; and the 
lung returns to its normal condition. 

When purulent infiltration or suppuration occurs, the surface of the lung 
becomes yellow, its substance is soft, friable, moist, and it feels " miry," as 
if an abscess were being pressed. On section a diffluent purulent fluid ex- 
udes from the cut surface. The yellow color is due to the cells that are 
undergoing fatty change and to the anaemia resulting from over-distention 
of aveoli with pus. Microscopically the pus cells are seen to crowd the 
alveoli and to infiltrate the inter-alveolar tissue. This infiltration may, 
by its presence, interfere with the nutrition of the lung tissue, and the 
alveolar walls may become thin, indistinct and rupture. 

Abscess may follow purulent infiltration, a small anfractuous cavity be- 
ing formed by the rupture of several alveolar septa. These abscesses vary 
in size from that of a pea to one which may occupy an entire lobe. They 



ACUTE LOBAR PNEUMOKIA. 



101 



may have a thick well-defined wall. Their interior is crossed by shreds 
of broken-down tissue. They increase either by peripheral growth or by 
fusion of several small abscesses. Their most common seat is in the 
lower lobes. These abscesses may be obliterated by a process of granula- 
tion and cicatrization. In such cases the abscesses are small, and com= 
municate with a bronchus which allows a free discharge of their contents ; 
or they may be encapsulated in firm cicatricial tissue, their contents sub- 
sequently undergoing cheesy and then calcareous changes. They may open 
into the pleural cavity (causing pyo-pneumothorax), or into the pericar- 
dium. External fistulous openings have occurred. 

Gangrene occurs in about two per cent, of all cases. It is liable to occur 
when there is great constitutional weakness, and in chronic alcoholismus or 
in septicaemia. It may be circumscribed or diffused. The gangrenous 
portion consists of a dirty pulpy debris, 
sometimes without the " gangrenous 
fetor." When the part becomes dif- 
fluent a cavity is formed and shreds 
of gangrenous lung tissue are found 
in a fetid fluid. About this there is 
a zone of gray hepatized friable tissue, 
which in turn is bounded by normal 
lung tissue. In diffused gangrene, 
the cavities are large and shreds of 
tissue and vascular bands cross from 
side to side, and the cavity swarms 
with bacteria. Sloughing of the 
pleura may follow such a process. 

Chronic pneumonia may be a result 
of lobar pneumonia, when resolution 
is delayed and an interstitial inflam- 
matory process is established during 
the stage of gray hepatization. The 
peculiarly hard and cedematous con- 
dition that sometimes marks gray 
hepatization is, by some, regarded as an intermediate stage between croupous 
and interstitial pneumonia. Finally, the alveolar contents in the third stage 
may undergo subsequent cheesy changes. Whether this occurs independent 
of tubercle is doubtful. This is sometimes called cheesy infiltration as 
opposed to tubercular infiltration. 

In childhood, except before the second year, croupous pneumonia is rare. 
Double pneumonia is, however, more frequent than in adult life. The 
morbid appearances are the same as in adults. In old age the changes are 
somewhat different ; the process usually begins in the upper lobes. In the 
stage of engorgement crepitation is absent; and in the second stage the lung 
is blue or nearly black. A section shows granules that are much larger 
than in adult He. " Granulations " are very often absent in senile pneu- 
monia. Gangrene is far more frequently a termination of lobar pneumonia 




Fig. 25. 
Purulent Infiltration. 

Section of Lung showing a single alveolus. 

A. Alveolar toall, largely infiltrated. 

B. Transverse section of a small artery with infill- 

tration of its walls. 

C. Epithelial cells of alveolar wall. 

D. Capillaries of wall of the air-vesicle. 

E. Pus corpvsctes. 

The alveolar cavity is filled with pus corpuscles, 
granular fibrin, and a few large nucleated cells. 
x 250. 



102 



DISEASES OE THE RESPIRATORY ORGANS. 



in old age than at any other period. The highly rarefied state of the lungs 
at this time of life seems to favor the development of the small abscesses so 
common in the aged. 

The most frequent seat of lobar pneumonia is the lower lobe of the right 
lung ; the next most frequent seat is the lower lobe of the left lung ; then 
the upper lobe of the right, the middle lobe of this lung being least fre- 
quently involved. 

Double pneumonia has been variously estimated as occurring in from 5 
to 15 per cent, of cases. Even in epidemics it rarely ranges above 12 to 15 
per cent. Double pneumonia is more frequent in the senile than in the 
adult period of life. 

The stage of congestion lasts from one to three days ; red hepatiza- 
tion from three to seven days ; and gray hepatization from two to thirteen 
days. In old age the stages merge rapidly into each other; abscess 
of the lung may occur within 36 or 48 hours after the onset. Red hepa- 
tization is not infrequently reached within the first six or eight hours 
in the aged. The changes in the pulmonary pleura over a pneumonic 
lung are quite characteristic. An uneven, thin, downy-looking layer of 
plastic exudation covers its surface. This plastic layer may conceal the 
liver-brown color of the pneumonic lung. As the third stage is reached 
the opposing surfaces of the pleura may become agglutinated. The pleurit- 
ic changes follow very closely those which occur within the lung. The 
cells in the pleuritic exudation are mainly pus. The pleuritic membrane 
is opaque, congested and ecchymotic. It may become so thick as to give a 
dull note on percussion after resolution is reached. The right heart is 
dilated ; and immediately after death both ventricles may contain clots. 
The pulmonary vessels going to the involved part may contain thrombi. 

Pericarditis is so frequent that it must be regarded as more than a coin- 
cidence or complication. The liver and spleen are congested. The splenic 
changes resemble those which occur in fevers. The lymphatics of the 
lung are choked with fibrin and blood corpuscles. The deeper lymphatics 
contain products identical with those in the pulmonary alveoli. In the 
lymphatic vessels and in the bronchial glands there is always some evidence 
of inflammation. 

G astro -intestinal catarrh is sometimes present ; and may be attended 
by hemorrhage. The vessels of the brain are more or less engorged. Men- 
ingitis is a not infrequent complication of pneumonia. 

Etiology. — Among the predisposing causes age ranks first. There are 
three periods in life in which the liability to pneumonia is greatest : early 
childhood ; 20 to 40 ; and after 60. Though catarrhal pneumonia is 
very frequent in children, 1 the statement that lobar pneumonia is rare at 
that period is not correct. From reliable data it appears that lobar pneu- 
monia is five times more frequent in the first two years of life than in the 
whole succeeding eighteen. Nine-tenths of all deaths after the sixty-fifth 
year are caused by lobar pneumonia. 



1 Vogel. Kinderkr. s. 222. 



ACUTE LOBAR PNEUMONIA. 103 

Sex. In early life (before the third year) both sexes are equally at- 
tacked. Between twenty and forty, when the condition of the sexes is 
most diverse, the proportion of males to females attacked is 3 or 2 to 1. 
After sixty, when the condition of the sexes again is similar, there is little 
disproportion ; but always in favor of males. Whenever women work, or are 
exposed, as men, the disease makes no discrimination as to sex. The puer- 
peral state does not seem to increase the predisposition to pneumonia; but 
it is more apt to occur at the time of the catamenia. 

The general bodily condition at and before the pneumonic seizure has but 
little predisposing influence. It is a question whether the strong or the weak 
are of tenest attacked. Convalescents from acute and severe illness, habitual 
alcohol drinkers and those who are " malarious " are far more liable to pneu- 
monia than those who are free from such conditions. Enervating habits, 
poverty, dyscrasia (cancer and chronic nervous diseases especially) and anti- 
hygienic surroundings are predisposing causes. Diphtheria, measles, erysipe- 
las, small-pox and the other acute infectious diseases must be regarded as pre- 
disposing causes. Chronic and acute uraemia and all diseases which arise 
from the retention of excrementitious products are powerful predisposing 
causes. Chronic blood diseases act in like manner. Long-continued passive 
pulmonary hyperemia — e. g. y from heart disease or from hypostasis — leads to 
pneumonia. The pneumonia that frequently occurs during acute articular 
rheumatism has been regarded by some as " metastatic from the joints." A 
more rational view is that it is due to the blood changes which are part of the 
rheumatic fever. One attack of pneumonia predisposes to others ; twenty- 
eight attacks have been noted in one individual. When pneumonia follows 
a severe blow or injury to the chest or shock from any traumatic cause, the 
. injury or shock must be looked on as a predisposing cause. In the aged 
lobar pneumonia has developed as soon as four hours after fracture in the 
hip joint. Cold does not affect the pneumonia rate except in the old. 
March and April statistics usually exhibit the highest pneumonia rate. A 
continuously low or high temperature has much less influence than a 
changeable temperature. Its etiology shows that it is a disease predisposed 
to by all things that depress the vital powers. Children and the aged are 
greatly depressed by the intense cold of winter and the chilling winds of 
March and April. In Europe it is often called the " May epidemic.'' 

Pneumonia is unknown in the Polar regions ; it is common along the 
coast of the Mediterranean Sea. Elevation above the sea seems to predis- 
pose to it both in hot and cold climates. North and east winds favor its 
development. Rainy seasons do not influence the pneumonia rate to any 
appreciable degree ; nor do damp or marshy districts. But both have a 
marked influence over bronchitis and other local pulmonary diseases. It is 
a well-established fact that pneumonia occurs oftener among the poor than 
among the rich, the private soldiers than their officers, the sailor on shore 
oftener than on ship, the soldier oftener than the civilian at the same mili- 
tary post. All this is explained by the better hygienic surroundings of the 
one class as compared with the other. The less the resistance capable of 
being opposed to some (unknown) pneumonic influence, the more strongly 



104 



DISEASES OF THE EESPIRATORY ORGANS. 



predisposed is the individual. Every increase in population in a district 
increases the pneumonia rate. 1 In New York City from 1840 to 1858 the 
mortality rate of pneumonia was 5.85 per cent. From 1859 to 1877 it was 
6.2 per cent. 

The question now meets us : is pneumonia a specific constitutional dis- 
ease, an acute infectious disease, or a local inflammation ? 

The following facts tend to prove that it is not a local 7nalady. All kinds 
of solid and gaseous inhalations and traumatism have failed to produce lobar 
pneumonia. 2 They always induced lobular and not lobar pneumonia. Sec- 
tion of the vagi produces hepatization, but not croupous pneumonic con- 
solidation. Cold does not influence the prevalence of pneumonia as it 
would were it a local disease {e.g., bronchitis). Wet and cold increase a 
bronchitis but not a pneumonia rate. Lobar pneumonia is more prevalent 
in our Southern than in our Northern States. Epidemics in the West 
Indies were more devastating than those in Iceland. On our continent 
the prevalence of pneumonia increases from pole to equator. All acute 
general diseases increase with the population ; pneumonia does this. Sta- 
tistics show pneumonia to be more frequent in New York City now than 
twenty years ago. 3 While cold has something to do with its development, 
the exciting effect of cold cannot be accepted. Again, there is no relation 
between the amount of lung involved and the intensity of the symptoms. 4 
In local inflammations the reverse of this is true. No second chill occurs 
when another lobe, part, or the other lung is attacked. 5 Prodromata some- 
times occur in pneumonia. But the absence of regular and constant pro- 
dromata, the absence of a (known) period of incubation, of a typical tem- 
perature range, and of characteristic surface phenomena, the fact that the 
disease is not contagious — these are the reasons advanced by those who re- 
gard it as a local, not a general disease. The resemblances of pneumonia 
to acute general diseases are : distinct initiatory chill, an orderly pyrexia, 
a rather typical course, L e., a day of abrupt crisis, a definite duration, and 
the symptoms following in regular sequence. There is a peculiar facies ; 
an occasional herpetic eruption ; nephritis is not rare ; the cerebral symp- 
toms resemble those of the exanthems ; there are sweats and sudamina ; 
and its mode of commencement — coma in the old and convulsions in the 
young — indicate that it is an acute general disease. Etiologically it is often 
developed under conditions similar to those which attend the development 
of diphtheria and cerebro-spinal meningitis ; atmospheric conditions 
are acknowledged factors in its causation. English writers describe a 
" sewer-gas pneumonia." There have been epidemics of pneumonia in 
garrisons and aboard ship where there was overcrowding, bad hygiene, 

1 Hirsch says: " The amount of mean fluctuation in the mortality from pneumonia is in inverse ratio to 
the density of the population." 

*Virchow's Aj-chiv,Bd. LXXX. Heidenhaln, Silyl. K. K. Akad zuWien,867. Reilz, Gendrin, Hist. Anat. 
des Infiam 

3 iV. Y. Med. Record : Article on Causes of Death in Acute Pneumonia.— Loomis. 

4 " The local inflammation * * * offers no sort of parallelism to the accompanying fever."— 

Sturqes. 

5 " Small consolidations with high fever and severe constitutional symptoms, and extensive infiltration? 
with a comparatively slight fever— this is the rule, not the exception. "- Ziemssen's Cycl. Vol. 5, p. 146. 



ACUTE LOBAE PNEUMONIA. 



105 



etc., etc. 1 There is a "pythogenic " pneumonia arising under miasmatic 
influences which is contagious. 2 The epidemic form of pneumonia at cer- 
tain times bears the distinct characteristics of a specific infectious disease. 3 
Miasmatic and zymotic pneumonia are names indicative of a supposed 
origin. We have abortive cases of pneumonia, just as we have abortive 
typhoid and cerebro-spinal meningitis. Again, the names sthenic, asthenic, 
malignant, icteric, etc., etc., indicate varieties similar to those found in 
fevers and acute general diseases. Pneumonia is allied to acute general 
diseases by the fact that certain complications occur with more or less 
regularity — lesions in the peri- and endocardium and albuminuria — and 
that abortion is usually induced when it attacks pregnant women. It has 
visceral and blood changes very like those of fevers. Pneumonia is some- 
times a disease of intra-uterine life. No local disease occurs in the foetus, 
but fevers frequently do. 

The success of modern methods of treatment based on this belief bears 
evidence to its being a general (self-limiting) acute febrile disease. The 
nature and action of the poison that may be supposed to cause pneumonia 
are indicated by the following facts : — hyperinosis does not seem capable 
of causing pneumonia : fibrin increases as hepatization advances and does 
not ante-date it or the pyrexia. 4 Its resemblance to the acute general diseases 
is mainly in its nervous phenomena, and the complications which render 
pneumonia dangerous are those which diminish the nerve supply or weaken 
the muscle-power of the heart. 

While pneumonia is thus admitted to be a general constitutional disease 
with local manifestations, undoubtedly depending upon a specific cause, 
that specific element is at present not satisfactorily determined. Various 
micrococci have been described as the exciting cause of the disease. To my 
mind the proofs of the invariable etiological relation of any one are insuffi- 
cient. It seems more probable that under certain predisposing conditions 
several micro-organisms may become the exciting cause of a pneumonia. 

Symptoms. — Subjective or rational symptoms. The invasion, in about 
one fourth of the cases, is preceded by prodromata. & In old age they are 
more frequent than in adult life (60 per cent.). They rarely occur in chil- 
dren. For a day or longer there may be malaise, anorexia, headache, dull 
pains in the limbs, back, and lumbar region, vertigo, epistaxis, and slight 
diarrhoea, or there may be slight jaundice, flashes of heat, and rigors. Fly- 
ing pains in the limbs and chest are common in old age. Rise in tempera- 
ture is sometimes a prodrome. In Bellevue Hospital, in 1877, a patient for 
two or three days preceding the initial chill had a temperature of 102°-103° 

1 In the U. S. Sanitary Commission Memoirs Dr. Russel reports : "The surgeons on duty with the 
regiments in the barracks (Benton, Mo.) report that men occupying the same bunks with those affected 
were very much more liable to be attacked than those more remote. Some of the most intelligent sur- 
geons believed that it was actually contagious." 

2 Dublin Med. Journal, Vol. I. 1874. 

3 Berliner Klinische Wochenschrift, 1879, No. 878.— Kuhn. 

4 Pneumonia resembl >s quinsy and acute articular rheumatism. Trousseau finds a resemblance be- 
tween erysipelas and p.ieumonia. Sturges places it in a " middle class " between specific diseases and 
local inflammations. Cohnheim calls it a miasmatic contagious disease. The idea of its being a specific 
general disease dates from the eighteenth century. Nov. Theo. Morg. 1786, Strackins. 

6 Grisolle found them in about 25 per cent, of his cases. Fox found them in 28 per cent. 



106 



DISEASES OF THE RESPIRATORY ORGANS. 



F. In epidemics, febrile symptoms and diarrhoea are common. 1 In most 
cases the invasion is sudden, and the disease is ushered in by a distinct chill. 2 

Generally the patient is seized with a chill in the night. This chill is 
intense and prolonged, more so than in any other disease except pyaemia 
and malarial fever. It lasts from one half an hour to three hours. Its 
abruptness and violence are characteristic. In children, headache, nausea, 
vomiting, delirium and convulsions may usher in the disease, its onset 
resembling that of an exanthem ; when these do not occur in all their in- 
tensity, the child is restless or stupid, and there are thirst and anorexia, 
increasing towards night. Again, a child may awake in the middle of the 
night with a burning skin, bounding pulse, flushed face and hacking cough. 
When, in children, the pneumonia is ushered in by convulsions followed 
by a loss of consciousness, the consolidation is usually at the apex. 

A distinct chill is less frequent in the pneumonia of old age ; yet when an 
old person has a marked chill pneumonia may always be suspected ; although 
less frequent it is more diagnostic than in adults. A protracted fit of shiv- 
ering and pain in the side are the two initial symptoms in about 50 per 
cent, of the cases of acute sthenic senile pneumonia. In the other half of 
the cases the onset is attended by slight increase in the frequency, and 
irregularity of the respirations, slight pyrexia, short hacking cough, and a 
feeling of great exhaustion. Intense weakness may be the only symptom. 
Nausea, vomiting, diarrhoea and collapse, or a semi-comatose condition, not 
infrequently usher in a senile lobar pneumonia. In a very few eases, stu- 
por, coma, and disturbance of intellect may be the only early noticeable 
symptoms, and they may persist during the whole course of the disease. 
The initial chill (whenever occurring) is rarely repeated. 

With the initial symptoms there is a rapid rise in temperature accom- 
panied by pain in the side, which is aggravated by coughing and by deep 
inspiration. The breathing is accelerated, there is dyspnoea, cough, expecto- 
ration, the countenance is flushed and anxious, there is headache, loss of 
appetite, and intense thirst. The urine is scanty and dark. The bowels are 
constipated. The tongue is heavily coated. The symptoms increase until 
the day of crisis, when they either suddenly remit and the patient breaks 
out in a profuse sweat, or they subside by lysis. The defervescence is usually 
reached between the fifth and ninth day. 

The following is an analysis of the prominent objective symptoms of 
pneumonia : 

The respiration is more constantly increased in frequency in pneu- 
monia than in any other acute disease, and varies from 30 to 80 per min- 
ute. Usually, in acute diseases, the respirations increase with the pulse 
rate ; in lobar pneumonia the ratio between pulse and respiration is early 
perverted. The respiration may be 80 per minute and the pulse rate not 
more than 100. The acceleration is not in proportion to the amount of 
lung involved, and it does not depend on the pain in the chest or the py- 
rexia. It is panting, not "catching," in character. It may or may not be 

1 London Lancet, 1878, Vol. II. 

2 77-80-92 per cent, are the figures given by Fox, Louis, Huss, Grisolle and Lebert as representing tbe 
frequency of the initiatory chill. 



ACUTE LOBAK PNEUMONIA. 



107 



accompanied by dyspnoea. In children accelerated breathing is more 
marked than in adults. The discrepancy between the pulse and respiration 
is not as marked as in adults ; in the former the pulse may range between 
150 and 160, and in the latter between 80 and 90. Expansion of the nos- 
trils is an early symptom in the pneumonia of children. In old age expi- 
ration is sri-l Ion, the whole act is " panting. '' The average number of respi- 
rations per minute is 22, and the duration of inspiration is to that of expi- 
ration as G to 9. It is rarely accompanied by dyspnoea. An exaggeration 
of (normal) senile "catching breathing" is one of the most frequent forms 
of abnormal respiration in senile pneumonia. 

Dyspnoea, although frequent, is. by no means constant. It does not de- 
pend upon the amount of lung involved, since double pneumonia may 
be accompanied by less dyspnoea than when only a single lobe is involved. 
It is often so great that the patient is unable to lie down. The greatest 
dyspnoea occurs where there is marked nervous prostration. In " second- 
ary " and complicated pneumonia the dyspnoea is greater than in primary 
uncomplicated pneumonia ; it is panting, not labored. In children, dysp- 
noea is most marked when the apex of the lung is involved. In old age 
dyspnoea is so infrequent that even with respiration at 70 they do not 
complain of difficult breathing. When a patient over seventy years who is 
asthmatic, or who has chronic bronchitis, develops a pneumonia, the dysp- 
noea that may have accompanied the previous condition diminishes. He 
simply feels exhausted, and usually dies suddenly. 

Pain follows the chill ; it is situated underneath the nipple of the af- 
fected side. It is sharp and stabbing, often located over the pneumonic 
spot, and is intensified by coughing, sneezing and deep inspirations. In 
central pneumonia there is no pain ; it is the pleurisy that causes it. Pneu- 
monia itself is a painless disease. Pain in the affected side rarely continues 
beyond the third or fourth day. If it continues beyond the eighth day it 
is evidence of pleuro-pneumonia. It is present in 85 per cent, of all cases. 
In old age pain is never severe. It is rather a dull, uneasy feeling referred 
to the whole chest or to the abdomen. 

Cough is present in over 90 per cent, of the cases. It comes on within 
twenty-four hours after the advent of the disease. At first it is short, 
"hacking "in character. It may entirely cease just before a fatal issue. 
It is more constant in children than in adults; it is sometimes parox- 
ysmal. Old people with pneumonia often have no cough. When present 
it may be so slight as to escape the notice of both patient and physician. 
Should bronchitis or asthma have preceded the pneumonia, the cough 
diminishes, and may wholly disappear on the advent of the latter. The 
expectoration is characteristic. In the first forty-eight hours of the dis 
ease it is simply frothy mucus. Then it becomes semi-transparent, viscid, 
gelatinous and tenacious, but never opaque. So tenacious is it that the 
cup containing it may be inverted without spilling the mass. It can be 
drawn out between the thumb and finger into thin strings. This tenacity 
in great part causes the difficulty of expectoration. Its color varies. About 
the second day the "brick-dust" or "rusty" sputa may be observed. 
This color is due to the presence of blood. The sputa may be creamy and 



108 



DISEASES OF THE RESPIRATORY ORGANS. 



yellow, or of a very dark or prune-juice color ; the latter is indicative of a 
depraved blood state, and occurs especially in alcoholic subjects. As death 
approaches, the sputa become scanty, less tenacious, more diffluent, and 
often of a greenish hue. Greenish sputa may occur in the middle of the 
pneumonia and during resolution, and in "bilious pneumonia." When res- 
olution occurs the sputum becomes abundant, and of a yellow, creamy color. 
There may be no sputum throughout ; or it may not appear until the 
sixth or even the twelfth day. The sputum may remain brick-dust till 
the ninth or tenth day. In pneumonia of the apex and in that compli- 
cating acute articular rheumatism the sputa are often entirely wanting. 
In children sputa are usually absent ; but brick-dust masses may be de- 
tected in the matters vomited. In senile pneumonia expectoration is never 
an early symptom, and is liable to cease suddenly during any period of 
the disease. Busty sputa are present in about 33 per cent, only of such 
cases ; frothy or "catarrhal" sputa are the rule. A chocolate-looking 
serous sputum, appearing soon after the onset of a pneumonia, shows a 
depraved condition and indicates "typhoid pneumonia." Examined under 
the microscope the sputum is found to contain swollen spheroidal red and 
white blood discs, minute fat spherules and the other elements described 
under morbid anatomy. 1 In about 75 per cent, of cases there will be found 
in the sputa (when floated in water) casts of the alveoli and bronchioles. 
The chemical constituents of the sputa are albumen and mucin. Tyrosin 
and sugar are sometimes found in it. There are two explanations of the 

acid reaction of the sputa : Verdeil 
thought it due to excess of pneumic 
acid ; Bamberger claims that it is due 
to deficiency in alkaline phosphates. 2 
Early in pneumonia there is an increase 
in the chloride of sodium in the serum, 
and it has been thought that, from the 
rapid and excessive cell-transformation 
in the lung, chloride of sodium is at- 
tracted to that organ. 3 The expired air 
in pneumonia is colder than normal, 
and there is a diminution in the amount 
of carbonic acid excreted. 

The temperature-range of a typical 
case of lobar pneumonia indicates that 
it belongs to a remittent or sub-remit- 
tent type, rather than to the class of feb- 
rile disorders marked by a continuously 

high temperature. Rarely, it is inter- 
Temperature Record in a case of Acute Lobar , . mi , , t 

Pneumonia, ending in Recovery. mittent. Ine temperature rises sua- 

1 Dr. Walshe affirms that pus cells are not found in the brick-dust sputum. 

2 Catarrhal sputa contain 10 to 14 per cent, of alkaline phosphates : pneumonic sputa none. In catarrh, 
soda is to potash as 31 to 20 : in pneumonia, 15 to 41. There is 5 per cent, more sulphuric acid in pneu- 
monic sputa than in catarrhal. 

3 In one case where there was no chloride of sodium in the urine, 10 per cent, of the solid material ot 
the sputa consisted of that salt. 



2, 



4. 



6, 



105 
104 
103 
102 
101 
WO' 



-ft- 



ACUTE LOBAR PNEUMONIA. 



109 



denly daring the initial chill, and in two to three hours after it may range 
from 102° to 105° F. After the first twenty-four hours the temperature is 
subject to morning and evening exacerbations and remissions ; but the 
morning temperature is rarely 2° F. lower than the evening — the difference 
in the sub-remittent type may amount to only J° or 1° F. At midnight a 
second exacerbation may occur, but not so marked as that occurring early in 
the evening. Rarely, remissions 
occur in the evening and exacerba- 
tions in the morning. The tem- 
perature is usually highest on the 
evening of the third clay. In some 
cases the maximum is not reached 
till a few hours before the crisis. 
Just before death the tempera- 
ture may rise very high, even to 
109J- 0 F. If, after the fourth day, 
a marked remission is followed by 
a high temperature, it indicates 
either an extension of the pneu- 
monia, or the occurrence of some 
active complication. If, in a mild 
pneumonia, the temperature sud- 
denly rises, it indicates a grave 
complication. The sudden fall of 
temperature on the fifth or sixth 
day indicates a crisis, and the beginning of convalescence : it may occur in 
the morning or after the evening exacerbation. In a typical case it is usual 
to find the temperature on the morning of the fifth, sixth, or seventh day 
two or more degrees lower than on the preceding night. Then it falls 
gradually until a normal, often a subnormal temperature is reached. The 
crisis may show itself by successively increasing remissions, while the tem- 
perature during the exacerbations rises to the same height as before. It is 
usual for the remission to be exaggerated just before the crisis ; again, 
the fever may reach its highest point just before the final fall. When 
the temperature declines gradually ("lysis"), a normal point is usu- 
ally reached by the ninth day, sometimes not until the twelfth or 
fourteenth. A protracted, slow fall is met with oftenest in the weak, 
debilitated, and in those who have been bled or depressed by treatment. 
A continuously high temperature after the tenth day indicates purulent 
infiltration. (See Fig. 25.) Pneumonia at the apex has the highest 
temperature range. The fifth and seventh are the days of crisis in the 
majority of uncomplicated cases. Of 867 cases, 677 ended before the 
eighth day. Neither the height of the fever nor the amount of lung in- 
volved influences the day of crisis. In bilious pneumonia occurring in mi- 
asmatic regions, the temperature is paroxysmal. In children the tempera- 
ture rises very rapidly, sometimes reaching 106° in the first twelve hours, 
The highest recorded temperatures are in the pneumonias of children. The 
critical fall is remarkable, the temperature quite often reaching 2° to 2 J° 




110 



DISEASES OF THE KESPIRATORY ORGANS. 



below normal. This low temperature may continue two or three days. In 
old age it is mainly by the temperature that the exact time of invasion is 
determined. The rectal temperature may be 103° to 104° on the first days, 
and then continue at the initial point for three or four days, with morning 
and evening oscillations of a degree or The temperature does not be- 

gin to rise until several hours after the chill, if the chill occur. (See Fig 
21. 

The pulse varies with the severity, extent and stage of the pneumonia. 
In mild cases it ranges from 90 to 120 ; if it continues above 120 the case is 

severe. The pulse is soft 



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and full at the onset. 
Later it becomes small 
and feeble. In severe 
cases, and when the ner- 
vous system is markedly 
implicated, it is rapid, 
small and feeble, and may 
be 130 to 140 or 160 at 
the onset. High temper- 
ature is usually accom- 
panied by a rapid pulse, 
and vice versa. When the 
critical fall of tempera- 
ture occurs, the pulse 
falls correspondingly. 
After the third or fourth 
day the pulse exhibits 
dicrotism in many cases ; 
it may be jerky, very 
Just before death, it becomes markedly 
not the mosfc extensive pneumonia that 
Heart-failure may 
The pneumonia 



Fig. 28. 

Temperature Record in a case of Acute Lobar Pneumonia passin 
into purulent infiltration and ending in Death on the 12th day, 

compressible and intermittent, 
slow in many instances. It is 
is accompanied by the greatest flagging of the heart, 
exist before, or just as hepatization is commencing 
with the highest temperature is not the one where heart failure is 
most marked or occurs earliest. When the heart is failing, the pulse 
shows that the artery is unequally rilled by each beat. First, the force 
varies ; then waves occur, and finally true intermission. I have been able 
to detect heart-insufficiency by these variations in the pulse within twenty- 
four hours after the onset of the pneumonia, and occasionally daring the 
initial chill. In children the pulse-rate is greatly increased : it may be 200 
per minute. It is small, unequal and irregular, but never intermittent. In 
senile pneumonia the pulse is not a reliable indication. Its average rate is 
73 to 78 ; rarely does it reach 120. In old age, both in health and disease, 
the pulse has a fictitious hardness, on account of arterial rigidity. It may 
not be irregular or intermittent when the heart is, and vice versd. Inter- 
mittence of the pulse in senile pneumonia is common, independent of any 
cardiac disturbance. In all cases of senile pneumonia, the pulse should be 
counted at the heart. 



ACUTE LOBAE PNEUMONIA. 



Ill 



The skin is often hot and dry until the crisis ; but it may be bathed in 
perspiration from the onset. A moist surface is regarded as a favorable 
sign, but when, at the acme of the disease, the parched skin becomes moist 
and the patient is not relieved, it is an unfavorable symptom. In most 
cases, the expression of the countenance is characteristic. The face is anx- 
ious, and over the malar bones is a mahogany flush, not diffused as in ty- 
phus fever, but well defined and circumscribed ; it is called the "pneu- 
monic spot." The rest of the face is pale. 1 Usually, one cheek is more 
flushed than the other ; this is due to disturbance of the vaso-motor sys- 
tem. When there is a great disturbance of the circulation, or when vaso- 
motor disturbance is excessive, the lips become cyanosed. At the time of 
the crisis the lips become pale. In about 50 per cent, of cases, pneumonia 
is attended by an herpetic eruption upon the cheeks, nose, lips or eyelids. 
It is rare before the second or third day, and it may not occur until the 
crisis is reached. Herpes occurs with varying frequency in different years, 
and is more commonly met with in pneumonia than in any other febrile 
disease. One winter, nearly every case of pneumonia in Bellevue Hospital 
was accompanied by " herpes labialis." Sudamina may accompany profuse 
sweatings. In children, while the surface of the body is hot and dry, the 
extremities are cool, and the pneumonic flush is bluish or violet-colored. 
Cyanosis of the extremities is more frequent than in adults, and herpes la- 
bialis is more constant. All the cutaneous ■ symptoms are exaggerated in 
children. In old age the pneumonic flush is often the first objective sign 
of pneumonia. The eyelids alone are cyanotic. If the face is at first 
dusky, it later assumes a sallow hue, and the surface heat is succeeded 
by a cold, clammy perspiration. 

The cerebral symptoms are not very significant in the early stages of 
pneumonia. Headache is the first to occur, and may continue throughout 
the entire course of the disease. It usually diminishes after the third day. 
When severe in the evening there will be slight delirium at night, so slight 
as often to escape notice. Delirium and convulsions rarely occur except 
in the debilitated and in those of dissipated habits. It is most frequently 
met with in drunkards, and then assumes the character of delirium tre- 
mens. Sometimes in non-alcoholic pneumonia the delirium assumes an 
active, violent character. Whenever delirium is present it is important 
to make diligent search into the former habits of the patient. Pneumonia 
of the apex is oftenest accompanied by severe cerebral symptoms. The 
delirium may pass into coma. When delirium and headache are marked 
symptoms, muscular tremors (" subsultus tendinum ") are very apt to occur 
with insomnia and frightful hallucinations. These cerebral symptoms 
occur so early and are so marked in alcohol drinkers that they mask the 
pneumonia ; a physical exploration alone reveals the disease. When de- 
lirium is present in the weak and feeble it is of the low, muttering, 
" typhoid " type, and soon passes into a state of stupor. Photophobia, 



1 Bouillard regards the flush as best marked in pneumonia of the apex. Some regard the flush as best 
marked, or existing solely, on the cheek corresponding to the affected side ; others as on the opposite 
side.— Jaccoud. 



112 



DISEASES OF THE RESPIRATORY ORGANS. 



disturbances of vision, and deafness are rare. In children the cerebral 
symptoms are more prominent than in adults. Stupor and restlessness on 
the one hand, or headache, delirium and convulsions on the other, may 
usher in pneumonia in children, and they may rapidly pass into a semi- 
comatose condition. Convulsions are as common in children as they are 
rare in adults. They may be general, resembling those of epilepsy 
("Eclamptic Pneumonia"), or they may attack single muscles or groups. 
Tetanus and opisthotonos are uncommon. Delirium and coma occurring 
late are usually followed by fatal coma. The cerebral disturbances often 
strikingly resemble those of acute meningitis. In senile pneumonia head- 
ache may persist throughout the disease. It is usually accompanied by 
mild delirium, especially when the pneumonia is at the apex. It is a busy, 
active delirium, and the patient has a constant desire to get out of bed. 

The symptoms referable to the digestive tract are not important. 
Nausea and vomiting are among the initial symptoms, and occur in 
about 75 per cent, of cases. At first the tongue is covered with a white 
fur ; later it becomes dry. Anorexia is marked, and thirst is intense. 
The lips and tongue may become brown, dry and cracked, and sordes 
collect on the teeth. Diarrhoea may be an initial symptom ; it usually 
accompanies nausea and vomiting. The bowels are usually constipated. 
In children nausea and vomiting are not only common, but in 25 per 
cent, usher in the pneumonia.' They usually cease by the second day. 
Persistent diarrhoea often precedes death. In senile pneumonia the tongue 
early becomes dry, brown and shrivelled, and is protruded with difficulty. 
Although these patients may not complain of thirst, they drink with 
avidity when fluid is placed to their lips. Dysphagia is frequent. At the 
crisis critical diarrhoea is more frequent than critical sweats. Loss of 
strength occurs early, and is more marked in pneumonia than in any other 
acute disease except typhus fever. Eecovery is rapid when convalescence 
begins. 

The urine in pneumonia is scanty, high colored and of high specific grav- 
ity. The amount of urea and uric acid excreted is two or three times 
more than normal ; it increases until the crisis, and then suddenly dimin- 
ishes, falling below normal. Inorganic salts, chloride of sodium especially, 
are constantly diminished and may be wholly absent. Reappearance of the 
chlorides marks the approach of convalescence. At the crisis they are 
present in excess. Urea and uric acid are also sometimes retained in the 
system ; and at the crisis there will then be a critical diarrhoea followed 
by prolonged convalescence. Bile pigment and sometimes the bile acids 
t appear in the urine. Slight albuminuria is present in 35 per cent, of the 
cases. The severer the pneumonia the more marked the albuminuria. 

Epistaxis may occur at any time, but is most frequent at the onset and 
at the crisis. Swelling of the veins of the hands in children is an unfavor- 
able symptom . When pneumonia is to terminate fatally dyspnoea greatly 
increases, the patient suddenly " sinks," the pulse becomes small, rapid, 
intermittent and dicrotic ; moist rales are heard in the larger bronchi or 
trachea, and there are physical evidences of pulmonary oedema. The sputa 



ACUTE LOBAR PNEUMONIA. 



113 



become frothy, liquid, and blood-stained ; they may be entirely suppressed. 
The respirations are more and more hurried, and the radial pulse becomes 
imperceptible. The face is sunken and livid ; the extremities become 
cold, and the capillary circulation more and more imperfect. The body is 
bathed in a profuse cold sweat. Death is usually preceded by a semi-coma- 
tose state. The temperature may steadily rise up to the time of death, or 
there may be " defervescence." Death may occur at any period of the dis- 
ease. In alcoholic pneumonia death is preceded by active brain symptoms. 
In children death is often preceded by convulsions or coma; sometimes 
exhaustion or collapse is most marked. Cyanosis and extreme rapidity of 
pulse are common in children before death. 

Senile pneumonia may end fatally within a few hours after the onset 
in a most unexpected and quiet manner. In other cases sallowness of the 
skin, cold, clammy sweat, working of the auxiliary muscles of respiration, 
a feeble, rapid, irregular and intermittent pulse, and a sudden rise or fall of 
the temperature may precede the fatal issue. 

Abscess. — Acute pneumonia terminates in abscess in to 2 per cent, of all 
cases. It is met with oftenest in debilitated weak subjects. The sputa are 
copious and fetid, yellowish in color, consisting almost wholly of pus. The 
fever is of the hectic type, and is accompanied by rigors and sweats. The 
patient grows weak and emaciated, death resulting from exhaustion, from 
asphyxia, or from discharge of the abscess into some neighboring cavity or 
organ. 1 The physical signs of the cavity are the most reliable evidences 
of an abscess. Abscess is rare in children. In old age there are no well- 
marked signs. 

Gangrene as a termination of pneumonia has been found in about 14 
per cent, of cases. This, however, is an exceptionally high percentage. 
Its occurrence is marked by signs of sudden collapse. The pulse is rapid, 
feeble and intermittent ; the face is pale and " death-like ; " there is pro- 
fuse expectoration of blackish-green masses containing shreds of decom- 
posed lung substance having a gangrenous odor. The breath is offen- 
sive and the body has a cadaverous smell. The sickening odor of pul- 
monary gangrene is most perceptible after coughing. Gangrene has its seat 
in the lower lobes of the lung, and it is here we must search for its ill-defined 
physical signs. In old age when pneumonia is to terminate in gangrene 
typhoid symptoms are present early and death occurs in collapse, usually 
within five days from the onset. 

Purulent infiltration has symptoms that differ but slightly from those 
f)i the third stage of pneumonia. When resolution does not take place at 
the period of crisis and the temperature remains high, accompanied by 
symptoms of prostration and profuse purulent expectoration, purulent 
infiltration may be suspected. Somnolence and mild delirium are quite 
frequent during " purulent infiltration." The sputum contains a large 
number of cells in various stages of fatty degeneration. The fever has 
regular evening exacerbations, and it may range higher than at any other 

1 Fox and Green state that abscess is located preferably at the apex ; Da Costa says at the base.— Guy's 
Hospital Reports. Ser. VII. 1848. 
8 



114 



DISEASES OP THE RESPIRATORY ORGANS. 



period in the disease. The tongue becomes brown and dry, and sordes 
collect on the teeth and mouth. Recovery is slow and convalescence 
tedious. Death results from exhaustion. 

Typhoid pneumonia is a term that has been applied to a pneumonia 
attended -by typhoid symptoms. It has also been called "asthenic," 
" low, " or " nervous " pneumonia. It is marked by extreme prostration that 
may exist from the onset. In the majority of cases, well-marked pneumonic 
symptoms, after having been present for a short time, soon give place to 
intense nervous prostration and adynamic symptoms. There is no sputa, 
no dyspnoea, no pain, no cough. Scrdes collect on the teeth and gums. 
The tongue is thickly coated, and later, covered with black crusts. There 
is incontinence or retention of urine. The pulse is small and rapid. There 
is stupor, somnolence, and continual low, muttering delirium. This form 
is common in the aged. In some cases there is marked disturbance of the 
special senses — the speech being most affected. Tremor and subsultus 
tendinum are frequent. Typhoid pneumonia may be accompanied by 
glandular swellings, sharp and darting muscular pains, arthritic symptoms 
or vomiting. It is not infrequent in epidemics, and it may follow 
Bright's disease, erysipelas, alcoholismus, or phlebitis. Recovery is always 
possible, but is slow and tedious, and may not begin until the twelfth or 
fourteenth day. A modification of typhoid pneumonia sometimes accom- 
panies dysentery, intestinal catarrh or phlegmonous gastritis. There is 
great sweating, profuse colliquative diarrhoea and high fever. 

Bilious, or gastric pneumonia, is lobar pneumonia occurring in mala- 
rial districts, and accompanied by gastro-enteritis with hepatic symptoms. 
It is sometimes called "malarial pneumonia." It has the characteristics 
of a severe pneumonia, but the fever is paroxysmal. The tongue is heavily 
coated ; nausea and vomiting are common and may be persistent. The 
epigastrium is distended and tender, the skin more or less jaundiced ; the 
liver is enlarged, and there is constipation or exhausting diarrhoea ; the 
latter is accompanied by greenish-black, viscid and inodorous discharges. 
"Bilious" pneumonia may be sthenic or asthenic ; but prostration is apt 
to be nearly as marked as in the typhoid variety. The symptoms of bilious 
pneumonia have frequently led to the diagnosis of " typhoid gastric 
fever." It runs a much more protracted course and has a much longer 
period of convalescence than the typhoid variety ; vomiting is "bilious," 
and somnolence and stupor may indicate a fatal issue. 

Latent pneumonia seldom occurs in adults unless it complicates some 
disease whose symptoms are so severe that the pneumonia is obscured. 
Inter-current senile pneumonia is always latent ; and Grisolle states that 
a physical exploration gives negative results in the majority of instances. 
Senile pneumonia may run its course without expectoration, dyspnoea, 
flushed face or physical signs. Its diagnosis is then difficult. It is to be 
remembered that of all phlegmasiae of advanced life, pneumonia is the 
most frequent ; and of all the acute diseases of advanced life it causes the 
highest temperature range and the greatest prostration. When an old 
person has a slight rigor, followed by a febrile movement attended by great 



ACUTE LOBAR PNEUMONIA. 



115 



prostration for which there is no explanation, pneumonia may be suspected 
even though all its usual signs are absent. 

Intermittent pneumonia, which is by some described as a distinct type, 
is a form of acute pneumonia in which a malarial element is so pronounced 
that all the subjective and even the physical signs undergo distinct inter- 
missions, returning each day with increased severity. It may assume the 
quotidian or the tertian type. During the intermission the temperature 
may fall to the normal. Recurring chills and sweats are often present ; 
and the pneumonia is not infrequently double. By some it is regarded as 
peculiar to old age ; it is very rare at any other period. Those malarial 
influences that give rise to this type of pneumonia are more frequently met 
with in our Southern and Western States than in any other part of the 
world. 

Physical Signs. — First Stage, or Stage of Congestion.— -The physical signs 
indicative of the first stage of lobar pneumonia are usually present within 
twenty-four hours after its invasion. If the pneumonia commences in the 
central portion of the lung their appearance may be delayed till the third 
day. By studying these signs in connection with the anatomical stages of 
the disease their importance in diagnosis and prognosis can best be appre- 
ciated. 

Inspection. — The movements of the affected side are more or less re- 
stricted. The unaffected side moves as in health. In double }3neumonia 
the respiratory movements will assume the costal type, attended by increase 
in the abdominal breathing. 

Palpation. — There is more or less marked increase m the vocal fremitus 
over the affected lung ; the degree of increase corresponding to the extent 
of the congestion. 

Percussion. — There is slight dulness over that portion of the chest 
which corresponds to the affected portion of the lung. It is not well marked 
until the end of this stage, although the pulmonary capillaries are engorged 
with blood from the very first. Even at the end of this stage there some- 
times remains a slight tympanitic note. Very extensive central pneumonia 
may fail to give any signs until the second stage is reached. Absolute 
dulness in this stage is very rare. 

Auscultation. — During the "dry" stage — which, according to some, 
precedes the exudation — there will be noticed a feebleness and unnatural 
dryness of the respiratory murmur. This murmur is sometimes harsh, 
sometimes weaker than normal, losing the " breezy," rustling quality of 
normal breathing. Elsewhere it is exaggerated. As soon as the conges- 
tion is well marked, fine crackling sounds are neard at the end of inspira- 
tion — " crepitant rales " — which have been regarded as characteristic of 
this first stage, but which are usually pleuritic crepitation. These sounds 
resemble those produced by throwing salt on hot coals or rubbing the hair 
between the fingers. They are as numerous as they are minute, are un- 
affected by coughing, and remain audible for from twelve to twenty-four 
hours. This rale is of an unvarying character, and continues, i. e., is not 
inter- or remittent. If the pneumonic stages succeed each other in rapid 



116 



DISEASES OF THE RESPIRATORY ORGANS. 



succession, the crepitant rale may not be heard. They are rare in pneumonia 
developed with acute articular rheumatism. The respiratory murmur is 
feeble or assumes a broncho-vesicular character. Bronchial breathing may 
be heard in this stage (Traube). The voice sounds are slightly increased 
in intensity over the engorged spot. In children the ff pneumonic crepita- 
tion " is usually absent ; and though it may be heard at the end of a full 
inspiration after crying, it is never as fine or as distinct as in adults. There 
will be no marked increase in vocal fremitus. In old age the physical 
signs are modified by a more complete bony union of the chest walls, by 
curvature of the spine, rigidity of the bronchial tubes, by the rounded 
form of the chest, and by senile rarefaction of the lungs. 

Second, or Stage of Red Hepatization. — The physical signs of this stage are 
more diagnostic than those of either of the other stages. 

Inspection shows the expansive movements of the affected side more 
markedly diminished than in the first stage ; while those of the other side 
are increased. There may be absolute loss of motion over the affected lung. 

Palpation.— There is usually marked increase in the vocal fremitus over 
the consolidation. In some instances this is so slight that no difference can 
be detected. Very rarely it is less than on the normal sid«. The heart 
may be slightly displaced. Barely can pulsation be felt over th^ inflamed 
lung. The majority of authorities regard this pulsation as due to increased 
pulsation in the arteries of the inflamed spot, but there is no reason to 
doubt that the cardiac impulse itself can be transmitted through th^ solid- 
ified lung as well as the arterial impulse or the vibrations from the ^liordce 
vocales. In central pneumonia, vocal fremitus may be normal. Pleuritic 
effusions mask the signs. 

Percussion. — There is marked dulness over that portion of the lung 
which is the seat of the pneumonia. Over the unaffected lung there is ex- 
aggerated resonance. The nearer the hepatization to the surface the more 
marked the dulness. There is a sense of resistance accompanying the per- 
cussion. A pneumonic lung is more resistant than any other form of con- 
solidated lung. When an entire lobe is consolidated its exact outlines can 
be defined. The percussion may have a tympanitic quality anteriorly, 
but there will always be dulness posteriorly. There may be slight tympa- 
nitis just around the pneumonic spot. When an entire upper lobe is con- 
solidated a tympanitic percussion sound may be caused by vibration of the 
air in a large bronchus. The 66 cracked-pot sound " is occasionally met 
with in pneumonia over the relaxed and permeable parts of the lung in the 
immediate vicinity of the consolidation. When heard over the condensed 
portion it is caused by the sudden expulsion of air from the large bron- 
chus. This occurs most frequently in the young with thin chest walls. In 
basic pneumonia the percussion note under the clavicle of the affected side 
may be amphoric. 

Auscultation. — As soon as the air-cells are completely filled with the 
pneumonic exudation the crepitant rales cease, and bronchial respiration 
is heard over the affected lung. It often has a metallic character ; or it may 
sound like tearing a piece of linen. Bronchial respiration is more intense 



ACUTE LOBAE PNEUMONIA. 



117 



in pneumonia than in any other disease. 1 At the commencement of the 
second stage tubular breathing attends expiration only. Later, it accom- 
panies both acts. Pleuritic exudation may mask the auscultatory signs. 
Plugging of a large bronchus will prevent tubular breathing ; a violent fit 
of coughing may allow it to occur when the mucus is dislodged. The 
voice sounds are increased in intensity, and bronchophony is heard over 
the whole of the consolidated lung. Bronchophony has the same diagnos- 
tic significance as bronchial respiration because it is produced by the same 
physical condition of the lung. When the pleural cavity is partly filled 
with fluid, bronchophony is indistinct or absent below the level of the fluid; 
while at the level the voice sounds may be asgophonic. Pectoriloquy may 



First stage. 



Diminished respiratory movements 

Slight dulness on percussion 

Broncho-vesicular breathing , 

Crepitant rales 

Slight increase of vocal resonance 



Second stage. 



Lost movement 

Increased vocal fremitus 

Complete dulness on percussion 

Bronchial respiration 

Bronchophony 



Third stage. 



C Returning respiraioi'y movemen 

Diminishing dulness 

1 Bronchial, giving place to 
Broncho-vesicular breathing . 

[ Rale redux 




Fig. 29 



Diagram Illustrating the Physical Signs in the Three Stages of Lobar Pneumonia. 

be heard independent of fluid in the pleural cavity. The heart sounds are 
abnormally intense. In children dulness is especially marked in the infra- 
clavicular region. Some speak of a feeling of greater solidity below than 
above the scapula which can be perceived before the ear can detect dulness 
on percussion. Vocal fremitus may be increased, but this is not always 
to be expected. In old age, inspection and palpation give negative results. 
What is dull on percussion in old age might be regarded as resonant in 

l Laennec taught that bronchial respiration was due to the superior conducting power of condensed 
lung. Skoda combats this view, and says that bronchial respiration is generated or magnified in caverns 
and in the bronchi of condensed lung substance by the air in these cavities and bronchi vibrating in con- 
sonance with that of the trachea ; the condition necessary for this consonance is provided in the circum> 
stance that the air is pent up in confined spaces whose solid walls reflect the sonorous undulations. 



118 



DISEASES OF THE RESPIRATORY ORGANS. 



adults. Hence clulness on percussion is a relative term in senile pneumo- 
nia. When the pneumonia is superficial there is actual clulness. Tubu- 
lar or bronchial breathing marks the second stage, and is even more intense 
than in adult life. Small gurgles or mucous rales are heard in this stage. 
Bronchophony is not very common, and never distinct. iEgophony is fre- 
quent. By causing the aged patient to cough and expire violently tubular 
breathing may be heard. 

Third, or Stage of Gray Hepatization. — There is no abrupt transition 
from the second to the third stage ; the physical signs of early gray hepati- 
zation are the same as in the second stage. 

Inspection. — As resolution progresses, expansive motion on the affected 
side becomes more and more apparent. 

Palpation. — Vocal fremitus gradually diminishes. 

Percussion. — Dulness becomes less and less marked. Of all the signs 
this is the last to disappear. As the percussion sound becomes more and 
more resonant the tympanitic note is again heard in spots. It is a long 
while before normal pulmonary resonance is re-established. The dulness 
may disappear in patches. As the dulness diminishes the pitch of the 
percussion note rises. 

Auscultation. — The bronchial respiration that was present in the second 
stage gives place to broncho-vesicular breathing, which soon becomes 
"blowing," then indeterminate, and finally normal. Bronchophony gives 
way to exaggerated vocal resonance. In connection with these changes in 
the respiratory and vocal sounds the crepitant rale returns, but is soon 
obscured by larger and moister crepitating sounds — the "resolving sub- 
crepitant rale " of pneumonia — the "rdle redux." Large and small mucous, 
sibilant, and sonorous rales accompany the sub-crepitant sounds, to disap- 
pear only when resolution is complete. Not infrequently the bronchial 
rales that are developed during the stage of resolution are " consonant " or 
ringing. 1 

The physical signs of this stage are all retrogressive, and they disappear in 
the opposite order to that in which they appeared. In rare cases resolution 
is so rapid that the sub-crepitant rale is not developed. In this class of 
cases bronchial breathing and dulness on percussion continue for some 
time after the crisis. 

If the consolidated lung becomes the seat of purulent infiltration, the 
temperature remains high and symptoms of great prostration are developed. 
Bronchial breathing continues, and becomes more intense, dulness persists, 
and when rales occur they are high-pitched, sharp, and resemble fine 
gurgles. The occurrence of abscess and gangrene is indicated by the 
physical signs which attend the formation of a cavity in consolidated lung 
substance. No one of the physical signs present during a pneumonia is 
sufficient for a diagnosis ; but the manner and order of their occurrence 
and their relation to the subjective symptoms enable one to reach a positive 
diagnosis in all typical cases. The only diagnostic symptom is the sputum. 

In children bronchial breathing rarely disappears before the seventh day ; 

1 Skoda and Traube. 



ACUTE LOBAR PNEUMONIA. 



119 



it is often accompanied by the sub-crepitant rale. When resolution takes 
place, bronchial breathing and the sub-crepitant rale will disappear simul- 
taneously. If purulent infiltration occurs, large gurgling crepitation will 
be heard. Vesicular breathing is rarely heard before the eighth or ninth 
day. 

In old age, inspection, palpation and percussion give similar results to 
those in adult life. Auscultation shows the crepitating sounds to be louder, 
and gurgles large and loud are often heard at a distance from the chest. 
The rale redux is not distinctive of, or peculiar to the third stage of senile 
pneumonia. The sound heard at this stage is a muco-crepitating sound, 
i. e., a sound produced in bronchi of medium size. The physical signs of 
pulmonary abscess in the aged are very generally wanting. Distinctly local- 
ized gurgling and cavernous respiration may, with the rational signs of 
abscess, suffice for a diagnosis. The sputa will also aid, but the diagnosis 
is only approximate. In old age the physical signs are subject to greater 
variations than in adult life. 

Differential Diagnosis. — Lobar pneumonia may be confounded with pul- 
monary congestion and oedema, capillary bronchitis, pleurisy, hypostatic con- 
gestion, catarrhal pneumonia (in children), pulmonary infarction, acute 
phthisis (especially in children), meningitis and typhoid fever. 

Pneumonia begins with a chill, followed by a rapid rise in temperature 
and pain in the side ; in pulmonary congestion and oedema, there is no chill 
or rise in temperature, and no pain. The sputum of pneumonia is viscid, 
rusty and (microscopically) diagnostic ; in pulmonary congestion and oedema 
there is profuse watery, blood-stained expectoration. Pneumonia is com- 
monly unilateral, and may occur in any portion of the lung ; pulmonary 
oedema is bilateral, and usually occurs in the most dependent portions of 
the lungs. In pneumonia there is complete dulness on percussion, crep- 
itant rales and bronchial respiration ; in pulmonary oedema the dulness is 
not complete, there is no bronchial breathing, and there occur numerous 
large, liquid, sub-crepitant rales. 

The resolving stage of pneumonia may be mistaken for acute capillary 
"bronchitis ; but in the latter the sub-crepitant rale is heard all over the 
chest ; while in pneumonia it is usually limited to a small area. The ex- 
pectoration is muco-purulent in bronchitis, and the temperature range is 
lower than in pneumonia. There is no dulness on percussion, no bronchial 
breathing in capillary bronchitis; the vesicular murmur is feeble, and 
cyanosis is more marked. The breathing is labored in bronchitis, and pant- 
ing in pneumonia. 

Pneumonia is ushered in by a distinct chill followed by fever ; acute pleu- 
risy begins with chilliness or several rigors, and the temperature rarely 
rises above 100° F. The dry, hacking cough of pleurisy is accompanied by 
slight mucous expectoration, and the characteristic pneumonic sputum is 
absent. In pleurisy the face is pale and anxious, and the pulse is firm, 
small, tense and wiry ; in pneumonia the face has a mahogany flush, and 
the pulse is full and compressible. The breathing in pleurisy is "catch- 
ing in pneumonia it is " panting." There are no critical days in pleu- 



120 



DISEASES OF THE RESPIRATORY ORGANS. 



risy. Vocal fremitus is diminished or absent in pleurisy with effusion, 
there is flatness on percussion, and the sound of the percussion changes 
with a change in position of the patient. In pneumonia yocal fremitus is in- 
creased, and there is dulness — not flatness — on percussion. In pleurisy the 
respiratory sounds are feeble, and a grazing, rubbing or sticky friction- 
sound is heard ; in pneumonia there are crepitant rales and bronchial 
breathing. Bronchophony and bronchial breathing may exist in pleurisy, 
but they are always diffuse — never sharp and tubular as in pneumonia. 

Hypostatic congestion is accompanied by copious, watery, blood-stained 
expectoration ; it occurs in the most dependent portions of the lungs, dis- 
appears when the patient sits up, and is accompanied by no rational symp- 
toms except dyspnoea and expectoration. 

Lobular 'pneumonia in children is always secondary ; it is not ushered in 
by a chill, usually follows a bronchitis, and is developed in both lungs. 
There are no days of crisis, and the physical signs of pneumonia are lim- 
ited to circumscribed spots. The range of temperature in the two forms 
of pneumonia differ ; the two curves represented by Figs. 20 and 25 show 
the differences. 

Pulmonary infarction is rarely met with independent of cardiac disease 
or pysemia. It is a non-febrile disease, and intense dyspnoea, coming on 
abruptly, is its prominent symptom. In pneumonia dyspnoea comes on 
slowly. The expectoration in infarction consists of small black coagala ; in 
pneumonia it is viscid and contains few blood-globules. The dulness of 
an infarction is circumscribed, and around it moist rales are heard ; in 
pneumonia the area of dulness is extensive, and there are no moist rales. 
There is a peculiar garlic-like odor to the breath, in pulmonary infarction, 
never present in pneumonia. 

When lobar pneumonia has its seat at the apex, it may be confounded 
with acute phthisis. But the history of a well-marked chill, followed 
by the characteristic pneumonic symptoms, will enable one to exclude 
phthisis, Moreover, the fever in phthisis is subject to irregular exa- 
cerbations and remissions. If the signs of consolidation persist with lit- 
tle or no change, if the temperature at no time falls to normal, if there are 
night sweats, if emaciation is progressive — then the case is to be regarded 
as one of phthisis, even though pneumonia may have complicated it. 

In children pneumonia is so often accompanied by cerebral symptoms that 
it may be mistaken for meningitis. Meningitis comes on insidiously, the 
temperature rarely rises above 103° F., the pulse is often lower than nor- 
mal, there are no thoracic symptoms, no dyspnoea, the face is pale and anx- 
ious, and the physical signs of pneumonia are absent. 

Sometimes latent pneumonia may be mistaken for typhus fever, especially 
when typhus is prevailing. While in charge of the typhus fever patients 
on BlackwelPs Island, I frequently saw cases where such a mistake had been 
made during a typhus epidemic. In these cases there will be dry tongue, 
delirium, and high temperature. The countenance resembles that of pneu- 
monia, but the presence of the typhus eruption and the absence of the 
physical signs of pneumonia will establish the diagnosis. 



ACUTE LOBAR PKEUMO^IA. 



121 



Pneumonia with typhoid symptoms is sometimes mistaken for typhoid 
fever. The differential diagnosis is not difficult, if one remembers that the 
pneumonia which complicates typhoid fever does not come on until late in 
the fever, and the regular history of typhoid fever precedes its development. 
On the other hand, when the typhoid symptoms are present from the be- 
ginning, or come on at the end of the second stage of pneumonia, the phys- 
ical signs of pneumonia will precede the typhoid symptoms. If a patient 
over sixty years of age, with this type of pneumonia, is not seen until the 
second or third week of^his sickness, although evidences of lung consolida- 
tion may be found, it will be very difficult to decide whether the pneumonia 
is or is not complicating a typhoid fever, and under these circumstances 
the diagnosis will be difficult if not impossible. 

Prognosis. — The phenomena of the crisis of pneumonia are a sudden fall 
of temperature followed by profuse sweats and a diminution in frequency 
of respirations and pulse. The cough becomes loose, the dyspnoea abates, 
the flush disappears from the face, the sputum is more copious, loses its 
rusty hue, diminishes in viscidity and becomes "creamy," thin and watery. 
Thirst decreases, the appetite returns, pain ceases and the patient 
falls into a quiet sleep, waking extremely exhausted. Epistaxis, hae- 
maturia and hemorrhage from the bowels may occur at the cri- 
sis. After the crisis the amount of urea in the urine, which was aug- 
mented before, becomes normal and the chloride of sodium reappears. The 
crisis in children is marked by a greater fall in temperature and by a more 
profuse sweat. When children have been restless or delirious the crisis is 
marked by a state of stupor. In old age the crisis is marked by a critical 
diarrhoea rather than by a sweat. 

The fatality of pneumonia is shown by the following statistics : of 
12,421 cases treated in the hospitals at Stockholm, 11 per cent. died. In 
the Vienna hospitals 24 per cent. died. The Basle Hospital Eeports for 
thirty-two years give 23 per cent, of deaths. Grisolle reports 59 per cent, of 
deaths in those ovsr sixty. In the "U.S. Medical Eeports," May 1st, 
1861, to July, 1866, of 61,202 cases which occurred among the white troops, 
14,738 died — more than 24 per cent. ; and of 16,133 among colored troops, 
nearly 33 per cent. died. The deaths from all other inflammatory diseases 
of the respiratory system for the same time were only one-seventh as many 
as from pneumonia. 1 Of 255 cases treated in Bellevue Hospital during a 
period of four years the rate of mortality was 34 per cent. The statistics of 
private practice are very different : of Lebert's 205 cases, only 7 T 3 o-per cent, 
died. Ziemssen lost only 3J- per cent, of his cases. Bennet lost none of 
his 105 cases. (He says, however, that no complications existed.) Brundes, 
of Copenhagen, lost over 21 per cent, of his 142 cases. Fox gives to pneu- 
monia the fifth, and Walshe the third place among fatal diseases. The 
average mortality-rate from all the published reports to which I have had 
access gives 20^ per cent, of deaths. But the rate varies in different 
years. 



3 The Confederate Hospitals' Eeports give over ?0 per cent, of deaths from pneumonia for the same 
period. 



122 



DISEASES OF THE KESPIRATORY ORGANS. 



The prognosis depends more on the age than on any other single ele- 
ment. In infancy the mortality is greater than in early childhood. Be- 
tween the ages of forty and sixty the death-rate is from 10 to 25 per 
cent., while from ten to thirty years almost all of the uncomplicated cases 
recover. After sixty the prognosis is always unfavorable. Pneumonia is 
the most fatal of all acute diseases at this period of life ; most " sud- 
den deaths" in the old are from acute lobar pneumonia. Some of the most 
reliable modern authorities state that nine-tenths of deaths after the seventy- 
fifth year are from acute pneumonia. It is more fatal in females than in 
males. In some years the proportion of deaths is far greater in summer 
than either in the spring or winter ; and certain — as yet unknown — atmos- 
pheric influences are of the utmost importance in determining the death- 
rate. The extent of lung involved influences the prognosis ; double pneu- 
monia is rarely recovered from. When an entire lung is involved, the 
prognosis is not as good as when only a single lobe is involved. Apical 
pneumonia — especially in the old and very young — is more often fatal than 
basic. The feebler the patient the more unfavorable the prognosis. 

Complications render the prognosis unfavorable : of 225 of my own cases, 
87 were fatal and 168 recovered. Of these, 124 were complicated and 131 
uncomplicated. Of the complicated cases, 75 died; of the uncomplicated, 
12 died. 1 The most dangerous complications are those which exert a 
direct influence on the heart, diminishing its power and obstructing the 
flow of blood from the right ventricle. Acute infectious diseases are 
dangerous complications because they hasten heart failure. 

Pneumonia may be regarded as mild when the temperature is below 104°. 
When the fever ranges above 106° for two days, the case is unfavorable. 
A gradual rise in temperature after the fourth day is always an unfavor- 
able sign. A low temperature is dangerous only when the respirations 
are greatly accelerated. When the pulse is 120 to 130 for two or three 
days, the prognosis is bad. If the pulse reach 150 per minute, or if it 
becomes irregular, intermitting, or dicrotic, the patient rarely recovers. In 
children a rapid pulse is of less significance, and in old age the pulse is 
never a reliable guide. Prune-juice expectoration is an unfavorable sign, 
indicating extensive blood changes. When expectoration is absent in 
the second or third stage, or if it become scanty and difficult, the prog- 
nosis is unfavorable. Sudden suppression of the sputa, with coincident 
tracheal rales, indicates impending death. Delirium coming on after the 
sixth day, convulsions in children, with jactitation and subsultus, or, in 
the aged, a tendency to coma, are unfavorable signs. Exhaustion and 
prostration, accompanied by a sunken pallid face and cold, clammy sweat, 
are always dangerous. In children, bronchial breathing, after the 
seventh day, numerous subcrepitant rales, copious and persistent diar- 

1 Lebert states that he lost only 5% per cent, of his uncomplicated, and all of his complicated cases. Huss 
lost 6 per cent, of uncomplicated and 20 per cent, of complicated cases. Fox states that pneumonia com- 
plicated by endocarditis is fatal in 75 percent, of cases ; by pericarditis, in 54 per cent.; by Bright's disease, 
in 50 per cent.; and by alcoholismus, in 25 per cent. Brundes (of Copenhagen), in 120 uncomplicated cases, 
lost Q% per cent.; of 22 complicated, he lost all. The danger of complications is markedly shown by 
these statistics. 



ACUTE LOBAR PXEUMOXIA. 



123 



rhcea, and swelling of the veins of the hands are bad symptoms. In 
old age a sudden rise or fall in temperature, apathy, somnolence, and a 
sallow, anxious countenance are dangerous symptoms. Pulmonary con- 
gestion and oedema in the unaffected part of the lung often precede a fatal 
issue. The occurrence of purulent infiltration, abscess, or gangrene ren- 
ders the prognosis unfavorable. 

In pneumonia the fibrin-factors of the blood are increased (often 400 
per cent, more than normal), the heart-power is diminished, so that 
the ventricles cannot empty themselves, the columns and cords whip 
up the residual blood (already prepared for clotting), and "heart 
clots" always form when the death struggle is prolonged and cardiac 
contractions feeble. The " heart failure " is the beginning of death. 
Post-mortem results can never give all, or the true causes of death, 
but only the modes of death. If, on account of heart failure, pulmonary 
oedema and congestion occur and heart clots form, these clots cannot be 
called causes of death. Jiirgensen states that in fatal cases of pneumonia 
oedema of the lungs is probably always present, and heart clots are fre- 
quent. Death may occur, then, from heart-insufficiency, from complica- 
tions (cardiac especially), or from asphyxia. Fatal collapse may follow an 
apparently regular and well-marked crisis. 

Treatment. — If we regard pneumonia as a general disease with a charac- 
teristic local lesion, the treatment must be modified by the constitutional 
condition of each patient and by the type of the pneumonia. If it is un- 
complicated and occurs at certain periods of life, it will terminate spon- 
taneously in recovery by crisis ; but when certain complications exist, when 
certain conditions are present, and at certain ages, it is almost necessarily 
fatal. 

Any plan of treatment in such a disease, if resorted to indiscriminately, 
will prove unsatisfactory. Although a large proportion of cases will re- 
cover without treatment, yet well-directed therapeusis will save lives and 
render convalescence less tedious. The pneumonic lung no more requires 
treatment than the intestinal ulcers of typhoid fever. It is the general con- 
dition of the patient, not the local changes, which is to govern us in the 
management of each case. Agents for the arrest of local inflammation 
have no place here ; hence venesection, once generally practised, has been 
almost entirely abandoned. A careful study of the pathology of pneumo- 
nia not only leads to the conclusion that bleeding does harm, but it 
strongly contra-indicates the use of all those agents which have been em- 
ployed for the arrest of simple pnl nonary inflammation. Hence veratrum 
viride, aconite, antimony, calomel, the tartrate of potash and antimony, 
iodide of potassium, and all so-called "cardiac sedatives" have been dis- 
carded, for it is evident that they add a new load to an already overburdened 
heart. They may, for a time, lower temperature and pulse-rate, but this 
will be accomplished at the expense of heart-power. Cardiac insufficiency 
will therefore appear earlier and be more profound. 

Counter-irritation by blisters, or other irritants, to the chest (in the 
early stages) is apt to do harm ; but blisters may be applied during the third 



124 



DISEASES OF THE RESPIRATORY ORGAN'S. 



stage, to hasten resolution. The application of leeches, followed by a lin- 
seed-meal poultice or other soothing fomentation, will relieve the pain in 
the side, which is often so urgent at the onset, and, if the condition of the 
patient will allow, may be of service. If extensive pulmonary oedema oc- 
curs, dry cups applied to the chest will relieve the dyspncea, and for a 
time dispel the oedema. It has come to be a rule to incase the chest in 
a cotton-batting or flannel jacket, covered with oiled silk. This has no 
influence over the course of the pneumonia, but it promotes diaphoresis, 
protects the surface from sudden changes of temperature, and it is always 
grateful to the patient. The "jacket " is especially beneficial in children. 

Absolute rest is important ; the patient should be moved as little as 
possible, and should not be kept in a constrained posture. If signs of 
heart failure occur, he should not be allowed to sit up or talk. The sick 
room should be large, cheerful and well ventilated, and its temperature 
should range between 65° and 70° Fahr. A most important adjuvant is 
a carefully-regulated diet. The food should be. fluid or semi-fluid, and 
highly nutritious, e. g., milk, eggs, beef -tea, and concentrated broths. 
Milk is preferable to all other nourishment. 

The nervous shock which attends the onset of acute lobar pneumonia is 
greater than in any other acute disease, except, perhaps, acute peritonitis, 
and the important question presents itself : what measures shall be em- 
ployed to counteract, or mitigate, the impression made on the nerve centres 
by the morbific agent which is operating to produce the pneumonia ? The 
experience of the last five years leads me to the conclusion that during the 
developing period of the disease, when the pneumonic blow is first struck, 
and until the infiltration is complete (usually for the first four days), the 
patient is to be brought under the full influence of opium and held in a 
state of comparative comfort, by hypodermic injections of morphia, re- 
peated at regular intervals ; and that by this course a pneumonic patient 
is placed in the best condition^ not only for sustaining the primary shock, 
but for resisting the pneumonia. Thus given, opium does not interfere 
with the employment of any stimulating or anti-pyretic measures which 
may be demanded. And not only does it diminish the chances of the 
occurrence of heart failure, but the great relief and comfort which it gives 
to the sufferer in the first four days of his struggles are sufficient to com- 
mend its use. After the pneumonic infiltration is completed, opium should 
be discontinued, for paralysis of, and a consequent accumulation of secretion 
in the bronchi may greatly increase the already deficient respirations. 

In all severe types of pneumonia there are two prominent sources of 
danger — heart-insufficiency and high temperature. The two prominent 
indications for treatment are, therefore, to sustain the heart and to reduce 
the temperature. A large proportion of deaths in pneumonia directly result 
from heart failure ; alcohol, judiciously used, is the most efficient means 
for preventing or overcoming it, but its indiscriminate use is more dangerous 
than indiscriminate bleeding. Only a few ounces of brandy may be re. 
quired to carry a pneumonic patient through a critical period ; or its free 
administration may be demanded to save life. In the old and feeble, and 



ACUTE LOBAR PNEUMONIA. 



125 



in those who have been accustomed to the use of alcohol, stimulation may 
be necessary from the very onset. The indications in each case demand 
careful study; in no disease is so much discretion required in the admin- 
istration of stimulants. The pulse is the indicator of the heart's con- 
dition. A frequent, feeble, irregular or intermitting pulse calls for 
stimulants. The quantity required in any case is to be determined by its 
effect on the pulse. It is best to begin with small quantities, and care- 
fully note the effect of the first few doses. If it acts beneficially, a favor- 
able effect will bcseen in a few hours ; and then the quantity administered 
must be varied to suit each case. ' It is seldom necessary to use more than 
six or eight ounces of brandy in twenty-four hours ; but, when demanded, 
it is to be unsparingly given. A dicrotic pulse is always an indication for 
its use. The period immediately following the crisis is the time when 
stimulants are usually most required. Delirium, muscular tremor and sub- 
sultus are indications for. their use. Critical collapse in the aged must be 
combated by a very free use of stimulants. Carbonate of ammonia is 
extensively employed as a stimulant in pneumonia ; — it is claimed that 
its use diminishes the danger of heart clot, but there is no evidence in 
support of this statement;— and if given in sufficiently large doses to act 
as a stimulant it irritates the stomach. It is unquestionably inferior to 
alcohol as a cardiac stimulant. Camphor and musk are also inferior to 
alcohol, and digitalis is only of service when there are evidences of extensive 
renal congestion. 

There are two plans of treatment advocated for reducing temperature 
in pneumonia : (1) the application of cold in various ways to the surface 
of the body ; and (2) the internal administration of some one of the anti- 
pyretics. It is claimed that the temperature can be reduced by applying 
cold compresses to the chest ; a cloth of some thickness is to be wrung 
from cold water and applied every ten or fifteen minutes to the affected 
side. This not only relieves the local symptoms, but it lowers the body 
temperature and hastens the day of - crisis. Some prefer the " Esmarch. 
ice-bag " to the cold compress. When cold is used at all, I prefer the coil. 
There is no doubt but that the pain in the side and fever will be relieved 
by this means, but the relief is only temporary ; and my own experience 
leads to the belief that pneumonia treated in this way is more likely to 
extend, and that there is great danger of chilling the patient. The other 
methods of applying cold to the surface for the reduction of temperature 
in pneumonia are the cold bath, the cold pack, and cold sponging. 

The experience of American practitioners is against the cold bath and 
the cold pack. The shock of cold causes depression, which the feeble or 
old cannot rally from. And though fever is lessened, heart-failure more 
rapidly follows, and is more difficult to overcome. My own experience 
is decidedly against the use of cold on the surface for the reduction of 
temperature in pneumonia. Cold "sponging" may be practised when it 
is grateful to the patient. 

Of the internal antipyretics, antipyrin and antifebrin are largely 
employed. Of these, antifebrin is to be preferred. In many instances it 



126 



DISEASES OF THE RESPIRATORY ORGANS. 



will effect a reduction of temperature not obtainable by other antipyretics. 
In the majority of cases of pneumonia, however, sulphate of quinine is 
more efficacious than either of the newer drugs. To act antipyretically it 
must be given in doses of from gr. x. to gr. xx. within a period of not 
more than two hours. 1 The very large antipyretic doses of quinine which 
have been recommended seem to me to be attended with danger, for in 
such large doses it appears to act as a cardiac depressant, and I believe 
that with gr. x.-xv. given in one dose we obtain as certain an antipyretic 
result as with much larger doses. ~No one of the antipyretics should be 
long continued or given in large doses. 

If there is great restlessness or wakefulness during the third stage, hy- 
drate of chloral, or, better, small hypodermatics of morphia can be given. 
If there is even slight evidence of cyanosis, these remedies should be used 
with great care. When the pupils are small, belladonna or hyoscyamus may be 
given. For the relief of the distressing cough which is sometimes present, 
five grains of hydrate of chloral combined with one-twentieth of a grain of 
morphia, or twenty-five drops of chlorodyne every two hours, may be given. 
If expectoration is difficult from loss of muscular power, stimulating 
" expectorants," such as senega and turpentine, are useful. But if this 
difficulty arises from great viscidity of the sputum, alkalies will be found 
of service, and, as alkalies and neutral salines also have a diuretic and 
diaphoretic action, they are especially indicated just before the crisis. For 
the relief of the delirium of chronic alcoholism, tartar emetic and digitalis 
are highly recommended by English authorities. 

In the first stage of senile pneumonia an emetic, when not specially con- 
tra-indicated, is given in the " Salpetriere Hospital." Ipecacuanha is re- 
garded as especially indicated. The nitrate of potash and the hydro- 
chlorate of ammonia are also highly recommended in senile pneumonia. 

In children the chest should be thoroughly protected, the diet carefully 
regulated. Leeching and blistering are both harmful, and should never 
be employed. Stimulating expectorants are often indicated, and the mod- 
erate use of stimulants in feeble children is always required. During con- 
valescence, iron, quinine, mineral acids, cod-liver oil, and blood-making 
wines, should be given. 

Very recently there has been advocated an antiseptic treatment of pneu- 
monia, based upon the recognition of the specific character of the disease. 
Such treatment cannot be supposed to affect the local etiological element 
in the lung, but may have the effect of neutralizing poison elements in 
the blood and thus reducing the constitutional manifestations. It can- 
not be denied that a septic element exists in some if not in all cases ; 



1 Liebermeister gives quinine until the temperature has been reduced by it to within 4-° of the normal. 
Few American practitioners carry the antipyretic effects of quinine so far. In Ringer and Gill's experi- 
ments upon " The Influence of Quinine on Temperature'''' in health, it took at least gr. xx. to produce a fall 
of 1°. From fifty to eighty minntes elapsed before the fall occurred, and the effects lasted from forty -five 
minutes to three hours. Ringer states that in pneumonia (and some other diseases) quinine does not 
readily pass out with the urine, but is delayed in the system for considerable time, and its antipyretic 
effects are continued longer than in other diseases. Prof. Flint states that he has seen pneumonia rendered 
abortive in a certain proportion of cases by xx. to xl. grains of quinine daily, and even when this result haa 
not followed, the disease has often been favorably modified in a greater degree than by smaller doses. 



LOBULAE PKEUMONIA. 



127 



hence the sulphites and hyposulphites (20 grain doses every three hours) 
are recommended. Carbolic acid, from 1 to 5 grains, sulpho-carbolate of 
soda (5 to 20 grains every two hours), have both been used quite extensively 
as antiseptics in the treatment of pneumonia. Thymol and salicylic acid 
have risen into favor because they are powerfully antiseptic and are almost 
physiologically inert. Quinine has also been advocated for its antiseptic 
power. The antiseptic treatment of pneumonia has not yet assumed a 
definite aspect or been sufficiently tried for any definite statements to be 
made concerning it. 

LOBULAE PNEUMONIA. 

Lobular, catarrhal, or broncho-pneumonia, is always secondary, being 
preceded by, or associated with, inflammation and obstruction of the smaller 
bronchi, which lead to the consolidated lobules. It may run an acute, sub- 
acute or chronic course, and differs very decidedly both in its clinical and 
pathological history from acute lobar pneumonia. 

Morbid Anatomy. — The anatomical changes in lobular pneumonia are 
confined to scattered groups of air-vesicles, hence the gross appearance of 
the portion of lung involved will vary with the duration and extent of the 
pneumonic process. In well-marked cases there will be found scattered 
throughout one or both lungs, small, circumscribed nodules of a light, 
deep-red, or bluish color, which do not inflate when the lung is inflated. 
If they are situated near the surface of the lung, they cause small, rounded 
elevations. When they are of considerable size, a reddish fluid oozes from 
their cut surfaces on section, and a small quantity of dark blood can be 
pressed from them. They are less tough than healthy lung substance, 
and break down easily on pressure. These nodules shade off into the 
surrounding zones of lung-tissue, which may be the seat of oedema, con- 
gestion, or emphysema. The nodules vary in size from that of a pea to 
that of a hazel nut, and are very rarely granular. 1 When the lung is 
inflated these spots of consolidation are rendered more prominent, so that 
they stand out sharply defined from the adjacent lung-tissue. In some in- 
stances these isolated spots of consolidation become confluent and involve 
a large portion of lung — perhaps a whole lobe — and become pale, firm, and 
dry, resembling in color the gray hepatization of lobar pneumonia. The 
smaller bronchi are congested ; their walls are often thickened, and they 
may contain a thick, tenacious, puriform secretion which, later, may 
become dry and inspissated. W^hen a section of the lung is made they 
often stand out prominently or even rise a little above the level of 
the cut surface. A peri-bronchitis is very often associated with these 
changes. Cylindrical and fusiform dilatations of the tubes are not infre- 
quent. Often, when a small patch of consolidation is cut across, there 
will be found at its centre a dilated bronchiole filled with pus. Discolora- 
tion begins at this point and extends toward the periphery. The con- 
nective-tissue of the portion of lung involved is increased, and this, in 



1 Jurgensen says : " Granulation is never observed. 1 ' 



128 



DISEASES OF THE RESPIRATORY ORGANS. 



long-standing cases, is often pigmented. Bronchiectasis may occur at 
various points. 

A microscopical examination of an affected lobule may distinguish three 
stages in the inflammatory process. First, the air vesicles maybe more or 
less completely filled with pus and serum, containing swollen and granular 

epithelium. The capillaries in 
the walls of the air vesicles are 
usually elongated, and red glob- 
ules may escape into the air-sacs. 
In the unaffected portions of lung- 
tissue the epithelial cells appear 
large and more distinct than in 
healthy lungs. In the second 
stage the affected lobules become 
solid and airless. Their color 
changes to a pinkish gray. The 
other changes are similar to those 
that take place in the stage of red 
hepatization in lobar pneumonia, 
except that less fibrillated fibrin 
is found in the exudation, the 
pus and epithelial cells are more 
abundant, and there are fewer red 
blood globules. 1 The anatomical 
differences between the second 
pneumonia are as follows : acute 
acute lobular only portions of a 




Fig. £0. 

Alveolus from a Lung in Lobular Pneumonia. 

The capillaries (a) are distended with blood, and within 
the alveolus are seen siuollen ejnthelia (b) and pus cells 
(c). x 250. 



stages of acute 



lobar and acute lobular 
lobar pneumonia involves a whole lobe : 
lobe. Lobar pneumonia advances steadily and uninterruptedly from one 
point, usually from the base upwards, until the whole lobe is involved ; while 
lobular begins simultaneously in several lobules remote from one another. 
Moreover, these lobules are in different stages of the inflammatory process, 
e. g., one is dark, red and moist ; another is grayish and quite firm. In lob- 
ular pneumonia the small bronchi are more or less rilled with catarrhal pro- 
ducts ; while in lobar pneumonia the exudation is fibrinous and does not 
extend beyond the infundibula and minute bronchioles. 

The third stage is the stage in which occurs either resolution, cheesy 
degeneration, or purulent infiltration. Abscess and gangrene may both 
occur, but they are very rare. When resolution occurs the contents of the 
alveoli become fatty and granular and are absorbed, and the pulmonary 
epithelium is restored. Large confluent spots of catarrhal pneumonia may 
undergo cheesy degeneration. And even solitary lobules may remain 
pale and yellow, looking like so-called cheesy tubercles ; when cut into, 
a fluid escapes from their centres. Some lobules that look like cheesy 



1 Many pathologists claim that the pulmonary alveolar epithelium takes no active part in the processes 
that result in the above-described consolidation. Rindfleisch asserts an active proliferation. 



LOBULAR P1TEUMONIA. 



129 



masses are soft, never granular, and a puriform fluid flows from their 
cut surfaces. While the contents of the alveoli are undergoing cheesy 
changes, hyperplasia of the interstitial connective-tissue is taking place, 
which leads to more or less fibroid induration or " sclerosis'' of the lung. 
On the pleura covering the superficial nodules an exudation of plastic 
lymph occurs ; the bronchial glands are swollen and hypersemic. Ca- 
tarrhal pneumonia in adults occurs independently of lobular collapse or 
atelectasis. 

Etiology. — Lobular pneumonia is always secondary to obstruction in the 
air passages, especially those of capillary size. It may be excited either by 
the gradual extension of inflammatory processes from the tubes to the air- 
cells, or by the entrance of inflammatory products from the tubes into the 
air-cells. It is most frequently met with between the ages of one and three. 
The senile period also seems to predispose to it. The more imperfectly 
nourished the child, the more anti-hygienic the air, surroundings and food, 
the more liable is it to develop lobular pneumonia. Debility and a long- 
continued recumbent posture predispose to it. Indirectly, any cause of 
bronchial irritation is a predisposing cause. The bronchitis of measles, 
whooping-cough, influenza, and that which accompanies the acute in- 
fectious diseases, often leads to lobular pneumonia. It occurs in lung- 
tissue adjacent to spots of hemorrhage, or pyaemic infarctions : trauma- 
tism may induce it. It is intimately associated with all varieties of acute 
and chronic phthisis. It is claimed by some authorities that caseous 
changes — whether primary, constituting caseous pneumonia, or secondary 
to a catarrhal process — are always dependent upon the presence of tuber- 
cle bacilli. 

Symptoms. — The phenomena which attend this form of pneumonia are 
always more or less obscured by those of the disease by which it has been 
preceded. It has no early distinctive symptoms. From an anatomical 
standpoint it is evident that its symptoms should resemble those of capillary 
bronchitis. It rarely runs a regular course, — terminating after a definite 
period in either death or resolution, — but may be protracted for weeks or 
months. A large number of cases occur in the course of whooping-cough 
and measles or other diseases complicated by bronchitis. The acute form 
is met with almost exclusively in children. In adults the disease usually 
runs a sub-acute or chronic course. 

After a diffuse capillary bronchitis has existed for a variable period, 
attended by its ordinary symptoms, such as a cough with muco-purulent 
expectoration, slight rise in temperature and labored breathing, if lobular 
pneumonia is developed the labored breathing becomes panting and ac- 
celerated ; the respiration may be 100 per minute. Dyspnoea is greatly 
increased. It is rarely ushered in by a rigor or a distinct chill. The tem- 
perature will gradually rise to 104°-105°, unlike the sudden rise of lobar 
pneumonia. It runs no typical course : though exacerbations and remis- 
sions are marked, they hare no regularity : sometimes the morning, some- 
times the evening temperature is the higher. It varies with the extent 
of lung involved, and also with the rapiditv with which consolidation is 
9 



130 



DISEASES OF THE RESPIRATORY ORGANS. 



developed. This steady rise in temperature, occurring in any disease in 
which lobular pneumonia is liable to be developed, is one of its most valu- 
able diagnostic suggestive symptoms. 
When death occurs early the tempera- 
ture may rise to 108°. The pulse rate 
often reaches 140 to 150. 1 In twenty- 
four to forty-eight hours the pulse be- 
comes small, compressible, and feeble, 
though at first it is full and hard. The 
cough, which during the bronchitis was 
loose, "bronchial," and paroxysmal, 
now becomes dry, hacking, and non- 
paroxysmal. It is usually very pain- 
ful. The expectoration is seldom 
seen in children ; but Ave may find 
in the matters vomited clumps of 
tenacious, often blood-streaked muco- 

Tempcrature Record in a case of Acute Lobular 

Pneumonia in a child. (Recovery.) pUS. 

After a time the dyspnoea becomes constant. The breathing is shallow, 
inspiration is short, the chest expanding but very slightly. The auxiliary 
muscles are called into play, and there is marked expansion of the nares 
during inspiration. The pale and anxious face becomes cyanotic, and the 
restlessness and jactitation give place to a lethargic semi-comatose state, 
interrupted by occasional but ineffectual attempts to cough. Towards the 
end the cough almost entirely ceases. Diarrhoea frequently increases the 
exhaustion ; and vomiting which may accompany or follow the cough, 
while rare at the onset of the disease, is frequent in its advanced stages. 
Anorexia is an early symptom, though young children will take the breast, 
while older children cannot be made to swallow even the blandest liquids. 
The tongue may become dry ; sordes collect on the lips and teeth ; aphthous 
stomatitis is common. Emaciation is rapid. The sub-acute form often 
occurs in the bronchitis of strumous children, and in that which accom- 
panies measles and whooping-cough. Its occurrence is marked by an 
elevation of temperature, but the rise is not so great nor so sudden as in 
acute cases ; it rises gradually until it reaches 103° F. or 104° F. The 
cough becomes more severe and metallic in character, and the respira- 
tion changes from the labored respiration of bronchitis, to the rapid 
panting respiration of pneumonia. The patient begins to lose flesh, 
becomes pale, has profuse sweatings and fits of exhaustion ; the 
appetite becomes capricious or is entirely lost ; loss of strength and 
emaciation are progressive ; the face appears bloated, small indolent ab- 
scesses appear on the nates and back, the patient assumes the appearance 
of extreme anasmia, and finally death slowly comes from wasting and 
exhaustion. 





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! Jiirgensen states that he has found the pulse often over 200 a minute. 



LOBULAR PXEUMOXIA. 



131 



Perhaps, when hope of recovery has been abandoned after a prolonged 
illness, resolution of the consolidated lung takes place, and a slow though 
complete recovery is reached. When the disease is to end fatally the tem- 
perature rises rapidly, cyanosis increases, the respiration becomes irregular 
in rhythm, and the comatose state is interrupted by convulsions in which 
death occurs. Death may occur suddenly in the midst of a violent fit of 
coughing. The disease may terminate with symptoms which resemble those 
of well-marked tubercular meningitis. When recovery occurs, it is very slow, 
pulse-rate, temperature, cough, and dyspnoea all imperceptibly diminish- 
ing. There is no rapid fall in temperature, such as occurs in croupous 
pneumonia. In a few cases, especially in older children, slight delirium 
will occur at night. The urine contains chlorides and slight traces of 
albumen. 

Chronic lobular pneumonia differs from acute in the severity rather 
than the character of its symptoms. When it supervenes upon some ca- 
tarrhal affection of the bronchi of moderate severity — a whooping-cough or 
an attack of measles — the temperature gradually rises until it reaches 102° 
or 103° Fahr. Exacerbations and remissions then occur which are more 
irregular than in the acute or sub-acute variety. The respirations increase 
in frequency. The increase in the pulse-rate, the dyspnoea, the anorexia, 
the loss of flesh and strength — all are more marked than in the acute form 
and much more persistent. The interference with respiration is greater 
than in lobar pneumonia. As muscular weakness increases the auxiliary 
and normal respiratory muscles become more and more enfeebled, and the 
supply of oxygen becomes, in some cases, so much diminished as to cause 
complete muscular paralysis. From all of these causes, and perhaps from 
the prolonged fever, the heart becomes feeble. Should recovery occur, the 
fall of temperature and the decline of the other symptoms are gradual, and 
there is great liability to a second attack during the protracted convalescence. 
A spot of consolidation often remains after recovery is apparently complete. 
Bronchiectasis, fibroid induration of the lung and emphysema are frequent 
sequelae ; and in children as well as in adults, phthisis is a not infrequent 
sequela. The pneumonic symptoms are much less pronounced in adults 
than in children, except when, in the latter, the disease supervenes uj^on 
diphtheria. In the old and feeeble, especially when they have lain in one 
position for a long time, lobular pneumonia occurs as the result of hypo- 
stasis, independent of bronchial catarrh. In senile bronchial catarrhs 
gravitation determines the lobular pneumonia, and it is not infrequently 
unilateral. If epidemic influenza is complicated by lobular pneumonia 
the sputa, in adults, may be quite free and blood-streaked, but never 
rusty. 

Physical Signs. — Inspection. In well-marked cases the expansive move- 
ment of the chest is diminished ; the diaphragmatic depression is deepened 
and the lower ribs may appear retracted. Should there be extensive pul- 
monary collapse the chest walls will be retracted. 

Palpation. — Slight increase in vocal fremitus may exist over isolated 
spots, if the pneumonic nodules are large and near the surface. 



132 



DISEASES OF THE KESPIRATORY ORGANS. 



Percussion. — There is slight dulness over the consolidated spots. The 
diminished pulmonary resonance in lobular pneumonia is not easily distin- 
guished from lobular collapse, and since collapse is symmetrical, usually 
involving both posterior bases, the difficulty is increased. One should 
therefore percuss, in succession, over similar areas on either side of the 
chest, for if a spot of dulness on one side has no counterpart on the other, 
one may be sure that it corresponds to a spot of pneumonic consolidation, 
and not to collapse. The upper part of the chest may be extra resonant 
and even tympanitic if there is much emphysema. 

Auscultation. — On auscultation, small mucous rales resembling sub-crep- 
itant rales, having a fine, crackling and metallic character, are heard over 
the spots where there is dulness. These rales are audible both with inspi- 
ration and expiration. They are not as fine as, and are more superficial 
than ordinary pneumonic crepitation. In children, during and after a fit 
of crying, fine crepitating sounds may be heard which were not audible 
during quiet respiration. The breathing is less vesicular and may even be 
broncho-vesicular. There is increased vocal resonance and perhaps bron- 
chophony. The respiration in unaffected portions of the lung is more or 
less exaggerated. When there is an extensive bronchitis with the pneumo- 
nia, moist, dry and bubbling rales, varying from the finest to the coarsest, 
may be heard all over the chest. 

Differential Diagnosis. — Lobular pneumonia may be confounded with 
croupous pneumonia, capiUary bronchitis, acute tuberculosis and pulmo- 
nary collapse. 

The differentiation between lobar and lobular pneumonia has been 
given. 

CapiUary bronchitis may be primary ; lobular pneumonia is always 
secondary. The range of temperature in capillary bronchitis is lower than 
in lobular pneumonia. The breathing is labored in capillary bronchitis and 
panting in pneumonia. Capillary bronchitis is marked by exaggerated 
resonance on percussion ; lobular pneumonia by dulness. In capillary 
bronchitis rales are heard all over the chest and there is no bronchial 
character to the breathing ; while in pneumonia fine rales are heard over 
the dull spots accompanied by broncho-vesicular respiration. 

Acute tuberculosis is accompanied by a higher temperature than lob- 
ular pneumonia and the pyrexia precedes the physical signs of bronchitis ; 
whereas in lobular pneumonia the signs of a bronchitis precede the physical 
evidences of consolidation. Lobular pneumonia occurs oftenest in the 
child (1 to 4 years) ; tuberculosis occurs in early adult life. Acute tuber- 
culosis is attended by more rapid exhaustion and emaciation, and haemop- 
tysis is not infrequent. The presence of brain symptoms is in favor of 
tuberculosis. The history of an inherited tendency to tubercular disease is 
rarely absent in tuberculosis. 

In collapse of the lung there is a tympanitic quality to the percussion 
note over the unaffected portions. The affected side is more retracted, 
and sinking of the ribs and elevation of the diaphragm are more marked 
than in pneumonia. In collapse the respiratory murmur is feeble or absent 



LOBULAR PlvEUMOXIA. 



133 



and has no bronchial character. Rales are rare in a collapsed portion of 
lung. Vocal resonance and fremitus are diminished. 1 

Prognosis. — The prognosis in lobular pneumonia is determined almost 
entirely by the conditions which precede and attend its development. In 
children under five the average mortality is one in five. The younger and 
feebler the subject, the more unfavorable the prognosis. The prognosis 
is better when it follows measles than when it occurs after whooping- 
cough and scarlatina or when it complicates renal or heart disease. When 
the initial bronchitis is severe and extensive, when the temperature rises 
rapidly to 105° to 106° Fahr., when there is cyanosis, muscular paralysis, 
and the pulse is feeble and frequent, the prognosis is very unfavorable. 
Lobular pneumonia occurring in a rachitic subject is always grave. The 
greater the extent of lung involved the more unfavorable the prognosis. 
The more abrupt the onset the defter the prognosis. The average duration 
of acute lobular pneumonia is from ten to fourteen days : death may occur 
within the first week. Chronic lobular pneumonia may be complicated by 
capillary bronchitis, fibroid induration of the lung, tuberculosis, pleurisy, 
emphysema and pneumothorax. A very frequent complication is acute 
intestinal catarrh. It may be complicated by pyaemia and pulmonary 
infarcts rton-pycemic in origin. Death may result from asthenia, asphyxia, 
or from complications. 

Treatment. — It must be borne in mind in the treatment of this affection, 
that it is a secondary disease and that its occurrence indicates that the pa- 
tient is in an enfeebled condition. All depressing remedies must be avoided; 
even when the disease assumes a very active form depletion is not allow- 
able. When the bronchitis is extensive, vapor inhalations and the internal 
use of muriate of ammonia are to be employed in accordance with the plan 
proposed in the treatment of capillary bronchitis in children. The patient 
should be kept in a warm room, the temperature of which should never 
fall below 60 c F. The ventilation should be as thorough as possible, but all 
draughts and sudden changes of temperature should be avoided. The air 
should be kept moist and the body should be covered with flannel. Some 
recommend cold compresses to the chest ; the cold pack is likewise advocated. 
Cold baths or baths from 77° to 86°, which are subsequently lowered to 60° 
Fahr., are also advocated even for young children. Jiirgensen recommends 
that a small stream of cold water be thrown just over the upper part of the 
back of the neck, the irrigation of which produces the most violent respira- 
tory efforts. My experience has been altogether against cold applications ; 
and I regard the application of counter-irritants, blisters, etc., especially to 
young children, as productive of more harm than good. I prefer that the 
chest should be enveloped in linseed or mild mustard poultices. Or, in 
very young children, it may be rubbed two or three times a day with a 
stimulating: liniment and wrapped in cotton-batting covered with oiled 
silk. 

1 Jurgensen states that the differential diagnosis between collapse and catarrhal pnenmonia can be 
determined only in two ways : the diminution in volume of a certain portion of the lung, if distinctly 
demonstrated, is evidk.- ce of simple collapse, an increase in volume is evidence of infiltration. In pulmo- 
nary collapse there is not the rise of temperature which always attends broncho-pneumonia 



134 



DISEASES OF THE RESPIRATORY ORGANS. 



During the whole course of the disease the food should be fluid, 
nutritious, and administered in small quantities and at short intervals. 
Brandy or gin in milk, ten to twenty drops every three or four hours, 
may be given to a very young infant, and the quantity may be increased 
until the pulse is increased in force, the respirations .become less frequent, 
and the distress and cyanosis diminish. As a rule stimulants must be 
commenced at the very onset of the disease and continued throughout 
its entire course ; the quantity to be administered is to be determined 
by the necessities of each case. The drug which has most power in 
reducing temperature and combating asthenia is the sulphate of qui- 
nine, which may be given in full doses during the period of fever ; and 
as an aid to resolution it is most serviceable in small doses during the 
active period of the disease. If the attendant bronchitis is extensive, 
and the accumulation in the tubes obstructs the entrance of air into 
the lungs, emetic doses of ipecacuanha will often afford great relief. 
Apomorphia is advocated by some, but the danger of its producing 
collapse is very great in young children. Under no consideration is 
opium to be given. Oil of turpentine, five drops every four hours, is 
often beneficial in chronic cases. While a patient with acute lobular 
pneumonia should always be kept in bed, it cannot be too constantly 
borne in mind that he should not constantly lie upon his back, for collapse 
and hypostasis are apt to occur in a lung whose power of resistance is 
diminished. Convalescence should be managed with the greatest care, for 
fatigue and exposure may induce bronchitis, a second attack of lobular 
pneumonia, and quite probably the advent of phthisis will be hastened, if 
a tendency to that disease exists. If the disease is prolonged and emacia- 
tion is marked, cod -liver oil, iron by hydrogen, or the syrup of the iodide 
of iron should be given, with a change of air. 



INTERSTITIAL PNEUMONIA. 

Interstitial pneumonia is a fibroid induration of the lung due to chronic 
inflammation involving its fibrous framework. Multiplication of the con- 
nective-tissue elements in the pulmonary septa takes place, which leads to 
progressive obliteration of the alveolar cavities and conversion of portions 
of the lung into callous fibrous masses. It has been called chronic fibroid, 
and chronic interstitial pneumonia ; also scirrhus and cirrhosis of the 
lung. 1 

Morbid Anatomy. — The new tissue formation in this variety of pneumo- 
nia may involve the walls of the air-vesicles, the bronchi, the blood-vessels, 
and the pleura. It may be arranged in the form of nodules, bands, or ir- 
regular patches, and it may involve an entire lobe. The lung is sometimes 
shrunken from one-third to one-quarter its normal size. The first change is 



1 Chomel and Grisolle state that it is very rare. Fox (Reynolds' Practice, p. 245) says it is rare except 
m connection with tubercles ; but Niemeyer (Practice Medicine, vol. i. p. 195) states that it is one of the 
most frequent pulmonary diseases. 



INTERSTITIAL PNEUMONIA. 



135 




hyperemia of the intercellular and interlobular tissue, followed by the de- 
velopment of fibro-nucleated tissue from the alveolar and bronchial walls, 
and from the interlobular connective-tissue. At the same time the alveo- 
lar epithelium undergoes more or less pro- 
liferation. As the new tissue contracts, it 
slowly replaces and obliterates the alveolar 
structure. As a consequence, the calibre of 
the air-cells is diminished. The new tissue 
development may reach such an extent that all 
of the air-cells of that portion of the lung 
which is the seat of the process may be oblit- 
erated, and no trace of lung- tissue remain. 
This is not infrequently observed in the sub- 
pleural tissue, and at the apex of the lung 
in chronic pleuritis. The alveolar cavities, 
when not obliterated, are empty or contain ex- 
udation products. Frequently, dense fibrous 
bands pass in from a thickened pleura, 
and the changes are more localized. The 
nuclei of the capillaries participate in these 
fibroid changes. 1 In a few instances the proc- 
ess begins, and is chiefly located, in the 
tissue about the bronchi and the blood- 
vessels. 

On section of a lung or portion of a lung that is the seat of interstitial 
pneumonia, there is a creaking sound with the movement of the knife, ac- 
companied by a sense of resistance that normal lung never offers. The 
lung substance tears with difficulty. The cut portion is firm, dry, hard, 
solid and shining, its color varying : at times it is of a dull, glistening, 
Blaty blue ; at others whitish, resembling an amyloid organ ; or it may be 
yellowish red. 2 The bluish -colored lung is called by some " gray black- 
fibroid induration." 3 Sometimes the cut surface presents a marbled appear- 
ance, due to the irregular pigmentation of the interstitial tissue. The bron- 
chi are usually dilated in those portions where the fibroid changes are well 
marked. The dilated tubes may form cavities of considerable size, and 
their mucous surfaces are often ulcerated, or the seat of intense passive 
hyperemia. Bronchial dilatations rarely occur unless there has been a pre- 
ceding peri-bronchitis, which has diminished the elasticity of the bronchial 
tubes. As the new connective-tissue develops at different points, the weak- 
ened bronchi become constricted, and as a result of this constriction bron- 
chiectases form, the dilatation being increased by the violent inspiratory 
efforts that attend the fits of coughing which are so common in interstitial 
pneumonia. It has been maintained that with the diminution in size of 
the lung, there is compensatory retraction of the chest-walls ; but that this 



Fig. 32. 
Interstitial Pneumonia. 

Section of Lung through one of the 
interlobular septa with the contiguous 
'vesicular structure. 

A A. Band of new connective-tissue 
from an interlobular septum — much 
thickened and containing many lym- 
phoid and large nucleated cells. 

B B B. Pulmonary alveoli on one side 
of the lobular septum with walls 
thickened and infiltrated. Changed 
epilhelia are seen crowding the air' 
vesicles, x 200. 



1 Fox in ''Reynolds' System.'" 

2 " Red induration of chronic pneumonia."— Fox. 

3 Reynolds' System. Art. Pneumonia. 



136 



DISEASES OF THE RESPIRATORY ORGAKS. 



compensation being inadequate to the loss in size, dilatation of the bronchi 
occurs, to restore the equilibrium. 1 

Microscopically, the new tissue is seen as a dense homogeneous, or ob- 
scurely fibrillated mass, containing comparatively few cells. Pigmentation 
is especially marked about the vessels, and shades off gradually into the 
new tissue. The arteries are not obliterated, but when cut across stand 
gaping in the section. 2 The pleura of the affected lung is thickened and 
adherent. The bronchial lymphatic glands may be hypertrophied, indu- 
rated, or cheesy. The heart is somewhat hypertrophied, and nearly always 
displaced when there is considerable retraction. Granular kidney and 
granular or cirrhotic liver are frequent accompaniments ; and all these 
changes are ascribed to the existence of a "fibroid diathesis." 3 

Etiology. — Interstitial pneumonia is always secondary — a conservative 
process in many instances. All protracted inflammatory processes in the 
lungs are attended by more or less interstitial pneumonia. All pulmonary 
phthisis, unless it run a very acute course, is attended by it. It is the 
limit of progression in many cases of peri-bronchitis, and occurs in all lung 
tissue which is the seat of neoplasms, infarctions, encapsulated abscesses, 
etc. Chronic bronchitis inducing a dry pleurisy, with the gradual devel- 
opment of thickenings and adhesions, is a frequent determining cause of 
interstitial pneumonia ; it progresses more rapidly when starting from the 
pleura, than from any other centre. Interstitial pneumonia is more apt to 
develop in the gouty and rheumatic, after pleurisy or bronchitis, than in 
any other class. Niemeyer states that it may result from simple "col- 
lapse." 

Symptoms.— The subjective symptoms of interstitial pneumonia are at 
no time well defined ; and it is impossible to determine the exact period of 
its commencement, for in the majority of cases its symptoms are continu- 
ous with those of the pre-existing disease. If, after a lobular or pleuro- 
pneumonia, the dulness on percussion, bronchial breathing, absence of the 
vesicular respiration, slight elevation of temperature, cough and dysp- 
noea continue beyond the period at which resolution should occur, the de- 

1 Sir D. Corrigan. Ziemssen records a case where dilatation of the bronchi occurred in both lungs, 
while induration was found only in one. Secondary inflammation of the indurated parts is regarded by 
Traube as one of the most common causes of gangrene of the lung. In 100 cases of bronchiectasis gangrene 
occurred in eight. 

2 Cornil and Ranvier describe a senile (? physiological) condition of lung called slaty induration of 
the apex. The tissue is hard, elastic, non-crepitant and black ; upon the surface it sometimes presents de- 
pressed cicatrices of the pleura and dense fibrous adhesions. Upon section there is seen a dense tissue 
formed of thickened septa, limiting retracted alveoli ; or there are emphysematous dilatations surrounded 
by a dense fibrous-tissue which is infiltrated with black pigment. Caseous or calcareous nodules lodged in 
minute cystic cavities are also formed in the midst of this fibrous-tissue. The nodules are altered pus. 
Here we also find spicule of bone at the apex in some cases. 

3 Rokitansky, in his Pathological Anatomy, thus describes a bronchiectatic cavity : "We find a bron- 
chial tube widened into a fusiform or rounded pouch : in the latter case the dilatation often being greater 
on one side than another, so that a greater part of the bronchial sac lies out of the axis of the bronchial 
tube. In rare cases the size of such a pouch may equal that of a hen's egg. They will often contain a bean, 
a hazel-nut, or a walnut. We further find, either that any one of the bronchial tubes may become ex- 
panded into a pouch of this kind, the tube retaining its normal calibre on either side of the dilatation ; or 
else quite a large tract of the bronchial ramifications may undergo enlargement. Then many such sacs of 
different size are so grouped together that they form, as it were, a vast sinuous case with many branches, 
whose individual pouches are bounded and separated from one another by ledges or valvular folds of the 
bronchial wall." 



INTERSTITIAL PNEUMONIA. 



137 



velopment of interstitial pneumonia may be suspected. Dyspnoea is a con- 
stant symptom, and is increased by active exercise, and by lying on the 
unaffected side. Cough is rarely absent, and, as the disease progresses, it 
becomes paroxysmal. It may be accompanied by a copious muco-purulent 
or gray-black fetid expectoration. Sometimes it will separate, on standing, 
into three layers: — the lowest contains the solid matter, and is yellow in color; 
the middle is a greenish fluid ; and the surface is frothy, containing mucus 
and fat-granules. If there are deep-seated bronchiectases, the cough is har- 
assing and painful ; when ulceration of the bronchial mucous membrane 
exists, haemoptysis is not infrequent. The pyrexia has no regular or typ- 
ical course ; the temperature is often highest in the evening, rarely rising 
above 102° F. The morning temperature may be normal. The respira- 
tions and pulse are but slightly accelerated, there will be gradual loss of 
flesh and strength, night-sweats, dyspeptic symptoms, and not infrequently 
diarrhoea. The fever assumes a hectic type, and the consequent anaemia 
and interference with the pulmonary circulation lead to general dropsy. In 
some instances a large portion of lung may remain indurated for a long 
time, without giving rise to any symptoms except dyspnoea. The patient 
always lies on the affected side ; any other position increases dyspnoea and 
cough. 

Physical Signs. — Inspection. After retraction of the lung has occurred, 
inspection will show retraction of the chest-walls over the indurated por- 
tion of lung, with marked loss of expansion on the affected side. With - 
out these signs the diagnosis of interstitial pneumonia cannot be made. 
The younger the patient,, the more the chest-walls are retracted. There 
will be bulging of the healthy side, and increased respiratory movement. 
The apex-beat will be displaced to the right or left, according as the right 
or left lung is the seat of induration. In some rare instances it is so dis- 
placed as to be seen under the right nipple or under the left clavicle. 1 

Palpation. — Vocal fremitus is usually increased over the affected portion 
of the lung, but it may be diminished. 

Percussion elicits a dull note, "toneless" or "wooden "in character. 
The note is high pitched, and somewhat tubular. A sense of resistance is 
imparted to the hand in percussing. The normal lung may overlap its 
shrunken, indurated fellow ; hence, dulness will not be as well marked an- 
teriorly as posteriorly. It may even be normal in front and dull and wooden 
behind. The percussion note over the opposite lung is extra-resonant. 

Auscultation. — There is a loss of vesicular quality in the respiration over 
the affected portions of lung, and the breathing is more or less bron- 
chial in character. The bronchial sounds are loud and sometimes am- 
phoric. Bronchophony and pectoriloquy are not infrequently present. 
Rales are heard, varying from the large, moist, metallic, to the high-pitched 
bubbling. The rales may only be audible after coughing. The respiration 
in the unaffected side will be exaggerated. 

Differential Diagnosis. — Interstitial pneumonia may be confounded with 



1 Niemeycr states that the " depression of the infra- and supra-clavicular regions which accompanies 
pulmonary consumption is due to interstitial pneumonic induration." 



138 



DISEASES OF THE RESPIRATORY ORGANS. 



vleurisy with retraction, cancer of the lung, collapse of one lung, and pul- 
monary phthisis. It is often difficult to distinguish fibroid pneumonia 
from pleurisy with retraction, and without the aid of an intelligent history 
it is impossible. There will be retraction of the chest-walls in both. The 
retraction from pleurisy is uneven, the ribs are twisted, and the spine more 
or less curved. In interstitial pneumonia the retraction is uniform, and 
there is a general diminution in size of the affected side. Haemoptysis, fetid 
expectoration, and pyrexia may be present in induration of the lung, but 
not in pleurisy with retraction. Bronchial respiration is usually present in 
pneumonia, while the respiratory sounds are feeble or entirely absent over 
the affected side in pleurisy. 

In distinguishing fibroid induration of the lung from cancer of the lung, 
although the physical signs of the two conditions are similar, the history of 
the two diseases is so different that by it alone a differential diagnosis can 
be made. Then the existence or non-existence of cancer in other parts 
of the body is important, for primary cancer of the lung or pleura is rarely 
met with. After the cancer has become sufficiently extensive to simulate 
the physical signs of pneumonia, there can be but little difficulty in the 
diagnosis. For, at that late period, the constitutional disturbances attend- 
ing the development of a cancer, as manifested by the cachectic look and 
the glandular enlargements, will make the way to a correct diagnosis quite 
plain. If the disease has lasted two years or over, cancer is excluded. 

Collapse of an entire lung is exceedingly rare, and can only be caused by 
a tumor pressing on a main bronchus. In collapse the respiratory sounds 
would be feeble or absent, and there would be no cough, expectoration, or 
constitutional symptoms. If pressure on the trachea or a main bronchus 
is long continued, the lung supplied by the compressed bronchus will be 
studded with hepatized lobules, collapsed lobules, and interstitial pneumo- 
nia ; the diagnosis will be determined, not by the physical signs, but by the 
presence of the tumor. 

Prognosis. — Interstitial pneumonia is never a direct cause of death. 
Such patients live for years, and suffer only from dyspnoea. As it is a sec- 
ondary disease, the prognosis will be determined by the primary disease. 
Extensive induration of the lung, following a slowly resolving croupous 
pneumonia and accompanying a chronic bronchitis, may continue for years 
after bronchial dilatations have occurred. The dangers and causes of 
death are intercurrent pulmonary affections, marasmus, haemoptysis, and 
secondary right heart dilatation, accompanied by tricuspid regurgitation. 
If gangrene occurs in indurated tissue, it rapidly extends, and causes death 
by exhaustion or septicaemia. Some cases of sudden and unexpected death 
occur from thrombosis of the pulmonary artery. 

Treatment. — Advanced interstitial pneumonia is incurable. Cicatricial 
tissue, once formed in the lungs, remains during the life of the patient. 
Something may be done to prevent its further development ; if it is devel- 
oped from a bronchitis or a pleurisy, it is important to guard against the 
recurrence of the bronchitis or pleurisy. Under these circumstances, the 
hygienic and climatic conditions are all important, and the individual 



PNEUMO^OKOSTIOSIS. 



139 



should live in the climate best suited to his condition. High altitudes are 
always indicated. 

Besides residence in a proper climate, the patient should be warmly clad, 
and efforts should be made to improve the general health. Cod-liver oil 
and iron are serviceable in most cases. 



PXEU.MOXOKOXIOSTS . 

Pneumonokoniosis is a general term implying deposit of dust in the 
lungs. The specific term anthracosis is usually employed in the general 
sense, and the secondary inflammatory changes are included in the disease. 
The more frequent forms are, anthracosis, from coal and carbons ; sidero- 
sis, including all metal dusts ; chalicosis, covering mineral dusts ; tabacosis, 
from tobacco ; and byssinosis, induced by any vegetable fibre ; commonly 
these diseases are known as stonecutter's phthisis, miller's lung, potter's 
asthma, and " scooper's " pneumonia. 

Morbid Anatomy. — Under conditions of gradual inhalation, all the mineral 
and insoluble forms of dust slowly infiltrate the lung until the bronchial 
walls, interlobular septa, lymph channels, and lymphatic glands are more 
or less completely filled. Inflammatory changes are induced which are 
largely fibroid in character, and which can be differentiated anatomically 
from fibroid pneumonia or fibroid tuberculosis only by the presence of the 
exciting dust elements and the absence of tubercular tissue. Tubercular 
changes may supervene, but are not frequent. 

The morbid appearances of the lungs are the same as in fibroid pneumonia, 
with the addition of grades of pigmentation ranging from a light brown 
or bluish black mottling, and striation, to a uniform black, with the pig- 
ment so abundant as to stain the fingers and fill the secretions with pig- 
ment particles. The bronchial glands are always more or less affected, and 
may cut like lumps of coal dust. Acute inflammatory processes may be 
induced by long exposure to peculiarly irritating particles. The changes 
are those of an acute pleuro-pneumonia. The pleura is red, thickened, and 
covered with plastic exudation ; the consolidated lung is soft, pulpy, and 
deeply congested ; the alveoli are filled with exudation products which 
extend to the smaller bronchi ; and elements of the exciting irritant may 
be found with the microscope. 

Etiology. — All forms of dust not soluble in the bronchial secretion may 
induce pneumonokoniosis. Mineral and metal dusts are usually inhaled 
slowly and intermittingly, and induce fibroid conditions. Vegetable ele- 
ments cause bronchitis primarily ; tobacco induces constitutional rather 
than local symptoms ; and the dust from grain, more particularly oats, is 
the most common cause of acute pneumonic conditions, owing to its pecul- 
iar properties and the unexampL 1 duration of single exposures. Grain 
" scoopers " work in confined places, as the holds of vessels, often for 
thirty-six hours, and at times for three or four days, with intermissions 
of only a few minutes for food and rest. 



140 



DISEASES OF THE RESPIRATORY ORGANS. 



Symptoms. — The symptoms all depend upon the form of secondary 
inflammation. In the acute cases an acute muco-purulent bronchitis is 
followed in one or two days by the local evidences of pulmonary consolida- 
tion in both lungs, attended by asthenic fever of 103°-105° F. Delirium 
is a prominent symptom. The pneumonic sputa are at first "rusty " or 
hemorrhagic, then purulent and exceedingly offensive. 

The disease lasts from ten days to two weeks, and recovery is prolonged 
over one or two months. 

Cough and dyspnoea are the only symptoms of simple dust deposits. 
Later, both the physical and rational signs of fibroid pneumonia, compen- 
satory emphysema, and bronchiectasis will develop. Tubercular compli- 
cations are rare, but may be present. 

Diagnosis. — This can be made only from the history, as the physical 
signs of the pneumonic and fibroid conditions are not modified by the 
etiology. 

Prognosis. — The prognosis depends upon removal of the cause and the 
extent of changes already present. 

Recovery from the acute condition is the rule, while death is unfortu- 
nately long delayed, even in the most distressing forms of fibroid pneu- 
monia. 

Treatment. — Prophylaxis is of paramount importance. Free ventila- 
tion must be secured so far as possible, and further inhalation of dust 
prevented by respirators. A large, fine, flat sponge forms one of the best, 
as it can be frequently removed and cleansed. Treatment of the acute 
pneumonia is tonic and symptomatic ; for the chronic condition it is the 
same as for bronchitis, emphysema, and fibroid pneumonia, when united 
from other causes. 



HYPEBiEMIA OF THE LUNGS. 141 



HYPEREMIA OF THE LUNGS. 

Hyperemia of the lungs is a condition in which there is an excess of blood 
in the lungs ; it may be local or general, active or passive. Active hyper- 
semia, or fluxion, is not of so frequent occurrence as passive hyperemia or con- 
gestion. The former is due to increased afflux of blood ; the latter to ob- 
structive causes which slow the current and favor accumulation of the blood 
in the pulmonary capillaries. Active pulmonary hyperemia may be associ- 
ated with violent and accelerated action of the heart. It may be developed 
in young persons with contracted chest by violent exercise, like running or 
jumping. It may follow sudden checking of an habitual flow, mental ex- 
citement, or the drinking of large quantities of alcohol. Sudden diminution 
of the atmospheric pressure (as during a violent inspiration), e. g., in croup, 
laryngitis, or whooping-cough, may cause active hyperemia. It may be 
developed by the inhalation of stimulating gases or a highly rarefied atmos- 
phere such as is met with at high elevations. 

Passive hypersemia, or pulmonary congestion, depends upon an obstruc- 
tion to the return circulation. It occurs with varying appearances and 
anatomical characteristics that have led to its subdivision into splenization, 
brown induration, and hypostatic congestion. A form of active hypersemia 
has, because of its physiological cause and situation, been called compensa- 
tory hypercemia. Other divisions are sometimes made, but all the varieties 
can properly be classified under these heads. 

Morbid Anatomy. — In active hypersemia the lungs contain more blood 
than normal. On section a bright red frothy fluid flows, and if the active 
hyperemia be local and compensatory, extensive oedema may result. The 
mucous membrane of the bronchial tubes may be minutely injected. The 
alveolar epithelium undergoes nutritive changes, and becomes swollen and 
granular. The pulmonary capillaries stand out turgid and distinct in the 
alveolar wall. 

In passive hyperaemia the lungs, wholly or in part, are distended, of a 
dark blue or dark red color, crepitating little, and are heavier and less elas- 
tic than normal. The process begins in the lower lobes and then becomes 
general. On section, dark blood, often in considerable quantity, flows freely 
from the cut surface, but the lung-tissue retains its dark color because much 
blood still remains in the capillary vessels. The interstitial tissue is often 
oedematous and studded with points of extravasation. The bronchial tubes 
and pleurae show post-mortem staining. Epithelial changes are very com- 
mon, and the alveoli may contain many swollen and granular cells that have 
become detached. Even fibrin and leucocytes are found in the air-cells in 
simple congestion. 1 



1 Cornil and Ranvier. 



142 



DISEASES OF THE RESPIRATORY ORGANS. 



Splenization is a form of congestion which has received its name from 
the close resemblance which the affected portion of lung-tissue bears to the 
spleen. The portion of lung which is the seat of this form of congestion 
is of a darker color than normal, and scattered throughout its substance 
will be seen little red or yellowish-white points ; these little points are sim- 
ply blood extravasations. Lung-tissue, in a condition of splenization, is of 
a dark reddish-blue, brown, or black color, airless, firmer than normal, 
crepitates less freely, has a more uniform homogeneous appearance upon its 
cut surface, and is less moist than normal lung-tissue ; a dark fluid will 
sometimes ooze from its cut surface, but not so freely as in the other forms 
of hyperemia, and the fluid is more watery in appearance. In splenization 
there is swelling of the alveolar walls, dilatation and tortuosity of the 
vessels, and a more or less collapsed state of the lung ; and when a con- 
gested lung is also deprived of air it looks like muscle, and the condition is 
then called " carnification of the lung." In the development of this con- 
dition hyperemia occurs and is followed by interstitial oedema ; it is 
this interstitial oedema that distinguishes splenization from hyperemia. It 
occurs in connection with typhoid and typhus fever, measles or any disease 
in which there are certain blood changes, and it is always developed 
slowly. 

Hypostatic congestion is a term applied to that form of hyperemia which 
occurs in the most dependent parts of- the lungs ; it is usually bilateral in 
those dying of diseases which have confined them in bed for a long time. 
It very closely resembles splenization, but the lung-tissue is very friable in- 
stead of doughy, and the little whitish or reddish points which are seen in 
splenization are absent in hypostatic congestion. The lung texture itself is 
but little altered. Low forms of pneumonia are liable to occur in hypostatic 
congested parts of the lung, and hence some call it " hypostatic pneumo- 
nia," and others again call it splenification (differing from the above de- 
scribed splenization). 

Compensatory, or collateral, congestion, is that form of congestion which 
occurs in one portion of the lungs, because of obstructed circulation in some 
other portion. The pulmonary congestion in unaffected portions of the lung 
in pneumonia and pleurisy is an example of this form. The same kind 
occurs in collapsed lung-tissue, and about points of venous obstruction, 
tumors, emphysema, etc., etc. 

Brown, or 'pigment, induration 1 , by some called the 'pneumonia of heart 
disease, is a form of congestion especially connected with obstruction or re- 
gurgitation at the mitral orifice. The lung is distended, firm, heavy, seldom 
very moist, of a dark brown or red color, and usually contains only a moder- 
ate amount of air. It is dotted with yellowish or brownish spots, usually 
of small size, while its own color is generally red. The capillaries of the 
lung are exceedingly enlarged, both in width and length ; sometimes they 
are three times as long as normal, and encroach on the lumen of the al- 
veoli. The brown or yellow spots are due to old blood extravasations which 
have undergone granular and pigment degenerations ; red spots from recent 



1 First described by Virchow, in 1847. 



BROWN INDURATION OF THE LUNGS. 



143 



extravasations are often found beside the old ones. Some parts of the lung 
may present these changes very markedly, while others are but little 
affected. Within the air-cells are usually found large cells which have un- 
dergone more or less pigmentation. In and around the connective-tissue cells 
are seen these pigment granules in great number. All of these changes 
result from prolonged interference 
with the return circulation. Inter- 
stitial connective-tissue thicken- 
ings occur in this form. The 
pigmentation which is present is 
the result of the long-continued 
retention of blood in the parts, 
and the consequent changes in the 
blood itself. Minute blood extra- 
vasations, or even diffuse pulmo- 
nary hemorrhage, may occur with 
brown induration. The pulmo- 
nary arteries and veins are enlarged 
and congested, and the smooth 
muscular fibres of the parenchyma 
of the lung may undergo hypertro- 
phy. A brownish fluid sometimes 
flows from the cut surface (Vir- 
chow's " brown oedema "). 

Etiology.— The causes of the dif- 
ferent varieties of pulmonary hy- 
persemia I have sutficiently considered in connection with their morbid 
anatomy, so that they do not require separate consideration. 

Symptoms. — It is difficult to distinguish the symptoms of pulmonary con- 
gestion from those of pulmonary oedema, and also from those of diseases 
in which it is liable to occur as a complication. If the congestion is con- 
siderable, there is more or less dyspnoea, cough, and expectoration. Blood- 
stained, watery expectoration is the prominent objective symptom of pul- 
monary congestion. The advent of active hyper cerata is usually very 
sudden. Dyspnoea, more or less marked, is present in both active and 
passive hyperemia ; it arises from decreased alveolar capacity and conse- 
quent diminished supply of oxygenated blood to the system. The dyspnoea 
is often urgent if the congestion is extensive, but in many cases of passive 
hyperemia there will be little change in the respiration ; the patient be- 
comes accustomed to habitual dyspnoea and suffers no special inconven- 
ience except moderate shortness of breath on physical exertion; especially is 
this the case in brown induration of the lungs; — a feeling of tightness or 
oppression is often experienced in the chest, but pain is rarely present. In 
extreme cases of passive hypersemia there is usually lividity of the lips and 
extremities, and a sense of prostration ; all the symptoms which attend 
imperfect aeration of the blood are developed, and the patient dies as in 
pulmonary oedema. The temperature may be elevated ; in pigment indu- 




Section of Lung showing a single Alveolus in Brown 
Induration. 

W. Wall of alveolus thickened and containing masses 

of pigment. Pg. 
VV. Capillaries, swollen, tortuous; at B, the vessel 

rupturing, blood escapes into the alveolus. 
P. Infiltration of pus. 

E. Epithelium, swollen, distorted and pigmented. 

x 250. 



144 



DISEASES OF THE RESPIRATORY ORGANS. 



ration it may be 100° to 102°, according to Fox, and even in other simpla 
forms slight pyrexia is not uncommon. 

The Physical Signs of pulmonary hyperemia are not well marked ; the 
movements of the chest are increased and the respiration more or less la- 
bored in character. The percussion sound is at first abnormally resonant, 
perhaps tympanitic, but as oedema is developed in the congested portion and 
in brown induration of the lung, it becomes somewhat dull. On ausculta- 
tion, the respiratory murmur is feeble or harsh ; in brown induration of 
the lung there is a feebleness of the normal vesicular murmur, the inspira- 
tory sound becomes harsh, and the expiratory becomes prolonged. Abundant 
small, bubbling rales are heard when oedema accompanies the hyperemia, 
as is almost always the case when it is active. 1 The physical signs in hy- 
postatic congestion depend on the position of the patient, but are best 
marked, as a rule, behind and in the infrascapular spaces. 

Differential Diagnosis. — The diagnosis of pulmonary congestion is not 
difficult if one considers the circumstances under which it occurs, and the 
two prominent symptoms, viz.: the dyspnoea, and the copious, watery, 
blood-stained expectoration* If, in the progress of acute pneumonia, watery, 
blood-stained expectoration is present, and the dyspnoea is severe, pulmo- 
nary congestion and oedema may be recognized as having occurred in that 
portion of lung not involved by the pneumonia. There is a blood-stained 
expectoration present in pneumonia, but it is of a tenacious character, and 
entirely unlike the copious, watery, blood-stained sputum of pulmonary 
congestion and cedema. The existence of pulmonary oedema being estab- 
lished, it is impossible to determine, either by the rational or physical signs, 
whether the attendant hyperemia is active or passive in character ; but in 
the majority of cases the circumstances under which it occurs will decide 
the question. Pulmonary congestion is readily distinguished from spas- 
modic asthma by the absence of the characteristic rales of asthma. 

Prognosis. — Active pulmonary hyperemia is usually rapid in its course, 
and either terminates in complete recovery, in pneumonia and pulmonary 
hemorrhage, or destroys life in a few hours. Recovery from acute hyper- 
emia is attended by sero-frothy sputa. Patients suffering from the disease 
can generally be relieved at its onset from the dangers which attend it. 
The prognosis in passive hyperemia depends altogether upon the condition 
with which it occurs. When it occurs with heart disease the prognosis 
will vary according to the exact condition of the heart, it may then last for 
years, or if the patient is in the advanced stages of heart disease, and an 
intense pulmonary congestion comes on suddenly, the prognosis is unfavor- 
able ; in brown induration, the prognosis is uncertain. Extensive pulmo- 
nary congestion in the form of splenization leads to unfavorable results. 
As a rule, pulmonary congestion and oedema are very serious affections, 
because they complicate already existing dangerous conditions. 

Treatment. — In cases of active hyperemia coming on abruptly, and rap- 
idly assuming a threatening aspect, an effort must be made to lessen the 



1 Powell says a fine fnspiratory crepitant rale is heard in heart-disease congestion, and that there are 
repeated bronchial catarrhs. 



PULMONARY (EDEMA. 



145 



quantity of blood in the pulmonary vessels. This is best accomplished by 
the application of wet or dry cups oyer the entire chest, or over the seat of 
the congestion, or, perhaps, in extreme cases, by opening a vein in the 
arm ; these remedies to be followed by steam inhalations, poultices, and 
warmth to the extremities ; — saline purges are beneficial. Digitalis may be 
given in active hyperemia from alcohol. In congestion the attention must 
be turned to the condition in connection with which it occurs, and the 
pulmonary circulation must be regulated by overcoming or controlling the 
cause of the congestion. If it depends on feeble action of the heart, adminis- 
ter stimulants ; as stimulants, ammonia, quinine and ether are especially 
valuable in addition to alcohol. Stimulants are especially demanded in 
hypostatic congestion, and the position of the patient must be constantly 
varied. Deep, full inspirations are of service. If the hyperemia is caused 
by forcible heart's action (the organ being diseased), give aconite in full 
doses. Hydragogue cathartics are indicated when pulmonary oedema is also 
present. When dependent on valvular lesions, the treatment indicated for 
these lesions must be employed. 

PULMONARY (EDEMA. 

Pulmonary oedema is a secondary affection which may be complicated 
by pulmonary congestion or may occur independently of it. 

Morbid Anatomy. — The anatomical lesion of pulmonary oedema consists 
in the presence of serum in the cavity of the alveoli and in the interstitial 
tissue of the lungs ; if it is associated with pulmonary congestion the serum 
will be blood-stained ; if there is no pulmonary congestion present, the 
serum in the cavity of the alveoli and interstitial tissue will be light colored. 
Lungs which are the seat of pulmonary oedema do not collapse when the 
thoracic cavity is opened. Unless congestion is present, that portion of the 
lung which is the seat of the oedema is paler than normal lung-tissue. 
"When the cedematous portion is pressed upon with the finger the indenta- 
tion remains. The weight of the lung is increased. 

On section, serum exudes or can be easily expressed from the cut surface. 
The serum is usually frothy unless the air cel'ls are filled with serum. By 
this means we are able to determine the amount of oedema present. 
(Edema may occur in any portion of the lung, but it is most frequently 
met with in the most dependent portion. The pleural surfaces are moist, 
and the pleural cavities may contain some serum. When oedema of the 
lungs is found at a post-mortem examination, it is impossible to decide, by 
simple inspection, whether it occurred before or after death. In order to 
determine its exact import it is necessary to know the physical signs and 
symptoms present previous to death. 

Etiology. — Pulmonary oedema, as has already been stated, is a secondary 
affection. It may be caused by hydrsemia resulting from general dropsy 
depending upon Bright's disease, scorbutus, purpura, anaemia, etc. It 
occurs in portions of lung which are the seat of pulmonary hyperaemia 
(active or passive), but especially when the hyperaemia is due to heart-fail- 
10 



146 



DISEASES OF THE RESPIRATORY ORGANS. 



ure. It may be found in lung-tissue which is adjacent to parts that are 
the seat of inflammatory or irritative processes, as pneumonia, capillary 
bronchitis, miliary tuberculosis, etc. When the circulation has been 
obstructed in one portion of the lung, oedema 1 may arise in another portion 
of the same lung ; its occurrence in connection with pneumonia is not 
infrequent under such circumstances, and is often an early indication of 
the necessity of prompt and careful attention in order to avert its fatal ten- 
dencies. Want of " tone " in the vessels, from pressure on the vagus or the 
pulmonary plexus, may cause it. It occurs in the course of acute general 
diseases, such as typhoid, typhus, and scarlet fevers, with feeble heart 
action, especially in the aged and feeble. Under such circumstances the 
posterior portion of the lungs is usually the seat of the oedema, and its pro- 
duction is aided by gravitation. 

Symptoms. — The prominent rational symptoms of oedema of the lungs 
are increased frequency in the respiration and dyspnoea. Frequently the 
dyspnoea is sudden in its advent and extreme, amounting to orthopncea. 
The temperature remains normal. The pulse, if increased in frequency, 
is feeble. There is more or less cough attended by a frothy, watery expec- 
toration, which is colorless unless pulmonary congestion is present ; then 
it is more or less blood-stained. The cough often has a peculiar "retch- 
ing " character. If the oedema is extensive, or if it complicates some pul- 
monary disease, the lips become blue, the extremities livid and cold, and 
the patient presents a more or less cyanosed appearance. 

Physical Signs. — The signs furnished by inspection and palpation are 
negative. There is more or less dulness on percussion (never complete), 
over the seat of the oedema; usually the dulness is equally diffused over 
the posterior surface of the chest on both sides, and is best marked at the 
most dependent portion of the lungs. It is usually more extensive at one 
base than at the other. On auscultation the respiratory murmur is feeble, 
sometimes entirely absent, or harsh in character. With inspiration and 
the commencement of expiration, small-sized bubbling rales are heard over 
the seat of the oedema. Sometimes these rales greatly resemble pneumonic 
crepitation, but they may generally be distinguished from it by their 
liquid character. The absence of any bronchial character to the respira- 
tory sound excludes the presence of pneumonic consolidation. Vocal 
fremitus and resonance may be increased or diminished; both are quite 
unreliable as a means of diagnosis. 

Differential Diagnosis. — (Edema of the lungs may be confounded with the 
first stage of pneumonia, with hydrothorax, and with capillary bronchitis. 
It is distinguished from pneumonia by the absence of a chill followed by 
febrile symptoms, by the liquid character of the rales, and by its occurrence 
on both sides at the most dependent portion of the lungs. A patient in 
the last stage of Bright's disease may suddenly develop high temperature 
and a cough, but in such a case the absence of a chill, as well as the bub- 
bling character of the rales, will enable one to recognize the condition as 



1 Cohnheim states that it is the inflammatory state of the vessels, rather than increase in blood pres& 
ure (compensatory), that causes oedema in this (third) class. 



PULMONARY (EDEMA. 



1-47 



pulmonary oedema, not pneumonia. The expectoration in the two diseases 
is ver} r dissimilar. 

The physical signs of pulmonary oedema and hydrothorax are quite 
distinctive. (Edema may be distinguished from hydrothorax by the 
presence of rales, and by the fact that the level of duhiess is not- changed 
by a change in the position of the patient, while in hydrothorax the 
upper border of the area of dulness, recognized by percussion while the 
patient is sitting or standing, will immediately shift its position when the 
patient stoops forward. 

The onset of the capillary bronchitis, from which pulmonary oedema 
is to be distinguished, is almost always accompanied by fever. The 
expectoration differs in character from that of pulmonary oedema. In 
capillary bronchitis it is at first scanty and tenacious, and even when 
the disease is fully established, although it may be abundant, it is still 
tenacious. In pulmonary oedema the expectoration is always frothy 
and watery in character and abundant. In oedema there is always some 
dulness on percussion, often it is well marked ; in capillary bronchitis 
there is no percussion dulness, but, on the contrary, exaggerated resonance. 
In both affections the rales closely resemble each other ; they are usually 
more abundant in capillary bronchitis than in oedema. The two diseases 
are liable to occur together ; but the presence or absence of fever, and the 
character of the expectoration, are generally sufficient to enable one to 
make a correct diagnosis. 

Prognosis. — This mainly depends upon the condition of the patient at the 
time of the occurrence of the oedema. A large number of persons die 
(often suddenly) from pulmonary oedema in connection with general 
dropsy ; especially is there danger when it occurs with the general dropsy 
depending upon renal or cardiac disease. When one lung is the seat of 
pneumonic inflammation, not infrequently oedema is suddenly developed 
in the other lung and destroys life. In continued fevers, phthisis, and 
other exhausting diseases, pulmonary oedema clue to cardiac insufficiency 
often occurs as the immediate cause of the fatal issue. Extensive pulmo- 
nary oedema, sufficient to give rise to extreme dyspnoea and a cyanosed con- 
dition of the face and extremities, is of serious import and should not be 
lightly regarded ; it necessitates a very guarded prognosis. 

Treatment. — The treatment of this affection will depend almost exclus- 
ively upon the condition with which it is associated. If it occurs in con- 
nection with Bri ght's disease, the excretory function of the kidneys must 
be increased, and the vicarious excretory power of the bowels and skin 
brought into active operation with hydragogue cathartics, diuretics and 
diaphoretics ; all of these eliminating forces must be crowded to their ut- 
most. Dry cups must he applied over the thoracic and lumbar regions as 
often as the patient will bear them, in numbers varying from twenty to fifty 
at each application. If it occurs in connection with typhus or typhoid fever, 
stimulants are indicated, for it does not generally make its appearance in con- 
nection with these diseases until symptoms of heart exhaustion are present. 
If the heart's action is feeble, its power must be increased ; under such cir- 



148 



DISEASES OF THE RESPIRATORY ORGANS. 



cum stances, the administration of digitalis will be of service. When the 
oedema occurs in connection with pulmonary congestion, counter-irritation, 
regulation of the heart's action, or any means which will have a tendency 
to relieve or arrest the congestion, should be employed. In those diseases in 
which there are feebleness of the circulation and depression of the vital 
powers, it is important that the patient should not remain constantly in one 
position. He should frequently be moved, in order to prevent gravitation 
of the blood to the most dependent portion of the lungs. Care must 
also be taken that the lungs are filled and emptied as frequently and fully 
as possible. 

PULMONARY INFARCTION. 

{Embolic Pneumonia.) 

There are two well-defined varieties of hemorrhage or extravasation of 
blood into the lungs; the circumscribed and the diffused. The latter con- 
dition is more properly denominated pneumorrhagia. Circumscribed pul- 
monary hemorrhage is called hemorrhagic nodular in farction, nodular pul- 
monary apoplexy, and, recently, Jiirgensen has given it the name of embolic 
pneumonitis, names that are certainly misleading. The lung-tissue is not 
torn or rent in circumscribed pulmonary hemorrhage. In describing this 
condition, I shall adopt the term "pulmonary infarction " 

Morbid Anatomy. — Lung-tissue, which is the seat of infarctions, is heav- 
ier than normal and has a tough feel ; if the infarctions are near the sur- 
face of the lung, they can readily be felt. Their more frequent seat is at 
the centre of the inferior lobe, near the root of the lung and at its periph- 
ery, for at the surface the anastomoses are fewer and the circulation feebler 
than elsewhere in the lung. They often occupy the sharp border of the 
lung. The pleura over these spots is congested or covered by a fibrinous 
exudation. In extensive infarctions, a sero- fibrinous or a sero-hemorrhagic 
etfusion takes place in the pleural cavity sufficient to somewhat compress 
the lung. The lung-tissue immediately surrounding the infarction may be 
normal, congested, oedematous or blood-stained. 

On section of a fresh nodule it is seen to be wedge-shaped, the apex of 
the wedge looking toward the root, and the base toward the periphery of 
the lung. The nodules vary in size from that of a pin's head to an inch 
or more in diameter. There are usually several in each lung. The cut 
surface of a fresh infarction is firm, maroon-colored, moist, and airless ; 
and from it flows a considerable quantity of bright blood. Older nodules 
cut with a cheese-like section and resemble in color a dark blood clot, they 
are distinctly granular and quite dry, firm pressure causing only a small 
quantity of blood to flow from their cut surfaces. They are readily broken 
down into small masses. The brownish colored triangular spots have a 
snarp line of demarcation which distinguishes them from the normal lung- 
tissue. An embolus will nearly always be found obstructing the artery 
ieading to the infarcted portion of the lung. 1 These nodules may undergo 



1 Virchow and Cohnheim both state that a plug does not necessarily exist in all cases : that enfeebled 
capillaries may alone be the cause. 



PULMONARY IKFARCTIOK. 



U9 




a variety of changes. Resolution is the most frequent, and takes place as 
follows : — the alveoli and terminal bronchioles fill with blood and become 
completely airless : the blood rapidly coagulates, and its color changes 
from the maroon of a recent clot to a chocolate, yellow, red, or gray color. 
The fibrin, if present, becomes granular and 
fatty. The blood globules undergo disorgan- 
ization, showing well-marked fatty changes, 
and all that remains of them are haematoidin 
and hsematin crystals, the amount of which 
left after partial absorption, determines the 
color of the infarction. The infarction is 
now in a condition to be gradually and com- 
pletely absorbed or expectorated. The re- 
stored lung may be but little damaged, a 
pigmented stain alone remaining to mark the 
site of the infarction. After a varying length 
of time air again enters the air-cells that 
were formerly filled with blood. 1 

Microscopically the portion of the lung 
which is the seat of nodular infarction shows 
the capillaries distended with blood ; and the 
arteries and veins adjoining are obstructed by 
coagula 2 which are red and soft in recent, and 
whitish and hard in old infarctions. Red, 
yellow, or brownish -black pigment granules 
are mingled with the granular and vesicular elements that fill the air 
cells, and the alveolar septa are thinned from pressure, and contain a vary- 
ing number of red blood corpuscles " Coagulation-necrosis " is said to 
diminish the number of nuclei in the alveolar walls. 3 

When resolution does not occur, a cyst may form whose walls finally conv 
tract and form a dark pigmented cicatricial spot, in whose indurated tis- 
sue are found cheesy masses or calcareous plates. Again, infarctions may 
excite adjacent pneumonic inflammation, which in some instances may be 
so intense as to cause gangrene. G-angrene under such circumstances is rather 
ft result of compression of the nutrient vessel (the bronchial artery). Usually 
gangrene only occurs when the embolus arrives from a gangrenous region. 

When an embolism occurs in jjycemia or some allied state, and is stamped 
with pyaemic infection, the infarction will suppurate and an abscess will 
be formed whose anatomical characteristics do not differ from those of ordi- 
nary abscesses.* 

1 Rokitansky claims that "the matters extravasated may become fluid again, and become partly ab- 
sorbed and partly expelled through the bronchi. The parenchyma of the lung then gradually returns to its 
normal condition." 

2 Kiittner states that " emboli do not alicays cause infarcts: for, although the pulmonary vessels are of 
the ' terminal 1 class, yet blood may reach the plugged vessels from bronchial vessels that enter the lung 
and from surrounding; capillaries." 

3 Cohnheim and Weigert. 

4 Cohnheim states that "when we find in the lungs infarcts and abscesses an embolus has lodged on 
the hither side of the point of obstruction and has caused the abscess : while infarction depends purely 



Fig. 34. 

Diagram showing hemorrhagic infarct. 

A. Embolus obliterating the artery. 

B. Centre of infarct, disintegrating. 
CC. Area of extravasation. 

D. Vein filed with secondary throm- 
bus. (After Weber.) 



150 



DISEASES OF THE RESPIRATORY ORGAKS. 



Etiology. — Pulmonary infarctions are either the result of rupture of the 
capillaries or small veins from augmented pressure following intense (me- 
chanical) passive hyperemia (as in mitral disease) ; or of the plugging of 
a branch of the pulmonary artery by an embolus. In the first variety the 
mechanism is simple : from too great pressure the capillaries are distended, 
stasis results, and an infarction is formed. In the second variety the plug 
causes arrest of the current, and the corresponding vascular area becomes 
filled with stagnant blood that is forced back into it from the adjoining 
veins and capillaries — "venous regurgitation." The arteries do not anas- 
tomose. The arrangement of the vascular distribution determines the pyra- 
midal or ' i wedge-like " shape of the infarct. Specific infectious emboli 
induce pulmonary (so-called pyaemic) abscesses; — non-specific emboli produce 
hemorrhagic infarction. Cohnheim states that a specific plug can never 
produce both infarcts and abscesses. This view is not taken by other ob- 
servers. Disease of the valves of the right heart and feeble heart power are 
the two chief causes of the formation of coagulum within the heart, which, 
breaking off, plugs a branch of the pulmonary artery. Any foreign body 
sufficiently small in size, or a clot from any part of the systemic venous 
system, may find its way to the right heart and thus cause an infarction. 3 
It is supposed that thrombi may form in the pulmonary artery in cases of 
heart disease, i. e., be of "independent" origin. Blood from the nasal or 
buccal cavities, or blood from the bronchial tubes, may make its way into 
the bronchioles and alveoli, and induce an appearance difficult to distin- 
guish from embolic infarction. It is admitted as possible that thrombi 
formed in the left heart may break off, go the round of the circulation and 
finally lodge in some branch of the pulmonary artery. 

Phthisis, scurvy, purpura hemorrhagica, gangrene of the lung, cholera, 
acute yellow atrophy, typhoid and yellow fever are not infrequently accom- 
panied by pneumorrhagia of the circumscribed variety. Sometimes no 
cause can be found to account for a pulmonary infarction. Recent experi- 
ments have shown that infarction does not take place unless arterial blood 
from some source is still sent into the part after its main supply is cut off. 3 



on the mechanical action of the simple embolus in the terminal artery." Harvard (in Quain's Diet.) thus 
describes the pysemic— the metastatic abscess in the lungs: "Embolic passive hyperemia is complicated by 
suppuration ; but this suppuration is incomplete and consists rather in a rapid breaking down of the tis- 
sues, than in the formation of a large number of pus cells ; while the cnaracteristic deep purple congested 
zone around the affected spot is much intensified. Some describe this as a true sphacelus of the part ; but 
there is no necrosis, and no foul decomposition of the patch affected in the suppurated form of embolic 
inflammation." When abscesses form, disintegration begins at the centre of the pyfemic infarction, and 
yellow croupous deposits form on the pleura over it, causing adhesions, and (Rokitansky) " a rounded 
nodular prominence like a boil projects." 

1 Rokitansky believes that an embolus always exists where there is a hemorrhagic pulmonary infarct. 
It may be difficult to find it, but it exists. But Cohnheim and Virchow state that emboli are not always 
present. Simple rupture of enfeebled capillaries may be the sole event. Stagnant venous blood is inca- 
pable of nourishing the walls of the tubes that hold it, and the effused corpuscles speedily fill the adjacent 
alveoli. 

2 Bed-sores, ulcerations, thrombosis of the femoral vein, phlegmasia alba dolens, wounds and maras- 
mic thrombosis are common peripheral sources of emboli. 

3 Fat Embolism in the Lungs.— The discovery that the smaller vessels in the lungs were often plugged 
with fat granules, giving rise to fat embolism, was made by Wagner and Zenker. Fat emboli have been 
connected with the origin of metastatic abscesses by some who were inclined to regard fatal pulmonary 
oedema and congestion as direct results thereof. Of this, more proof is wanted. When the long bones 
are broken, some medullary fat gets into the circulation ; but enough may enter that, when passing 



PULMO^AKY INFARCTION. 



151 



Symptoms. — The subjective symptoms of pulmonary infarction are few and 
indefinite. A small infarction will only be attended by the expectoration 
of small blood clots. When one large or several small infarctions occur in 
the lungs of one who has had chronic heart disease, the " cardiac " dyspnoea 
will be increased ; there will be a sense of constriction about the chest, 
attended by an ill-defined sense of the occurrence of some severe pulmo- 
nary lesion ; irregular, intermittent and disturbed heart action nearly alwavs 
precedes this occurrence. These symptoms are more apt to occur during 
or after some severe physical exertion or intense mental excitement, and 
are accompanied by the expectoration of small airless blood-coagula mixed 
with tenacious mucus. During the first three days the temperature some- 
times rises to 101° and 102° F. Cerebral symptoms are frequently present. 
Syncope may occur in patients with weak hearts. If the infarction is 
large, or if a number occur at the same time, collapse, intense dyspnoea and 
convulsions may immediately follow its occurrence. If the infarction 
involves the surface of the lung and gives rise to local pleurisy, pain will 
be a prominent symptom. Dark, scanty hemoptysis is the pathognomonic 
sign of pulmonary infarction. The rational symptoms of " pyemic " infarc- 
tions are less marked than those of hemorrhagic. The cough and expec- 
toration, the increase in the frequency of the respiration out of proportion 
to any rise in the pre-existing temperature, the constriction across the 
chest, and the dyspnoea taken in connection with the physical signs and the 
history will generally lead to the diagnosis of what some now call embolic 
pneumonia. 1 

Physical Signs. — Inspection and palpation give negative results, but there 
may be increased vocal fremitus over a large superficial infarction. 

Percussion may — in the case of superficial and large infarctions — give 
localized dulness corresponding to the site of the infarction. 

Auscultation may give bronchial breathing or bronchial expiration, espe- 
cially in the mammary and mid-axillary regions ; and sub-crepitant and 
crepitant rales may be heard in the immediate neighborhood of the infarc- 
tions. Co-existent peripheral oedema and pre-existing emphysema may, 
and frequently do, prevent any morbid physical phenomena from being ap- 
preciated. 

Differential Diagnosis. — The etiology, the sputa, and the spots of localized 
dulness are the diagnostic points ; of these the etiology is the most impor- 
tant. The sputa of cancer and of echinococci of the lung maybe similar to 
that of infarction ; but the long duration and the attendant signs of cancer, 
and the microscopical examination for hooklets, in the case of hydatids, 
will soon decide the question. 

Prognosis. — In the slight circumscribed pulmonary infarction dependent 

through the lungs, it is deposited in the small arteries of this organ, and perhaps, subsequently, of other 
organs. This is all the more liable to occur when the heart action is feeble. The fat. not only comes from 
fracture of bones, but puriform softening of right cardiac thrombi may cause it. Inflammation of bones, 
with or without operation, may induce it, and, also, osteo-myelitis, or softening of the marrow. The 
acetonemia that has long been regarded as causing death in diabetes, is by many supposed to be inert, 
compared with fat embolism of the lungs, in hastening death in diabetes. Fat embolism may be the direct 
result of general lipjemia. 
1 Jiirgensen, Ziem. Encyc, Vol. i. 



152 



DISEASES OF THE KESPIRATORY ORGANS. 



upon or accompanying heart disease, or occurring with a condition 
that is not pyaemia, the prognosis is good. Non-embolic infarctions, 
and even small non-specific embolic infarcts may be absorbed. The 
larger and more numerous the infarctions the worse the prognosis. A 
large infarction may quickly terminate fatally by collapse. 1 In all pyaemic 
infarctions and in those occurring with cardiac thrombosis, the prognosis is 
bad. 

Treatment. — The treatment of pulmonary infarction is, for the most part, 
expectant. When valvular lesions of the heart exist, the main thing is to 
regulate the heart's action and increase its power. Absolute rest in bed, 
and the administration of stimulants combined with small doses of digitalis, 3 
are indicated, but they must be given with great care and their effects care- 
fully watched. Stimulation may be made to the extremities, such as hot 
water or mustard sinapisms, and dry cups are to be freely applied over the 
chest. Venesection is contraindicated. But collateral hyperemia and 
oedema, attended by great dyspnoea and lividity, may demand wet cups and 
even bleeding from the arm. Both give temporary relief and they avert 
danger. The constitutional condition of the patient is always to be con- 
sidered. In pyaemic pulmonary infarction the treatment consists in sup- 
porting the patient by free administration of stimulants, quinine and iron. 
Dry cups may be frequently applied over the chest. If pleurisy and pneu- 
monia occur they are to be treated as complications. 

DIFFUSE PULMO^AEY APOPLEXY. 3 

In diffuse pulmonary hemorrhage or apoplexy the lung- tissue becomes 
torn and infiltrated with blood, which may be either fluid or coagulated. 
If situated near the surface of the lung the pleura may be lacerated. Gen- 
erally the cavity made in the lung-tissue by the extravasation is of consid- 
erable size, and the coagulated or semi-coagulated blood in this cavity has 
all the characteristics of a blood clot. These apoplectic extravasations are 
never circumscribed, are usually of much larger size than infarctions, 
and greatly resemble apoplectic extravasations in the brain, being a mass 
of blood in shreddy cedematous and infiltrated parenchyma. They may 
prove immediately fatal, especially when the pleura is perforated. If the 
patient survives the shock of the accident, recovery usually takes place 
either by adhesion of the torn surfaces of the lung after absorption of the 
extravasated blood, or by the formation of a connective-tissue capsule 
around the clot, after which the latter undergoes a cheesy, cretaceous, or 
pigment degeneration, and remains permanently imbedded in the lung- 
tissue. It is rarely transformed into a serous cyst. This form of pul- 

1 Jiirgensen states that "embolic abscesses are not necessarily fatal to life ; " and that "the prognosis 
always" depends more upon the primary disease than upon the accident which we call pneumonia by em- 
bolism. 

2 Gerhardt states that digitalis is not the drug for cardiac stimulation, but recommends large doses of 
morphia, hypodermatically, for the dyspnoea, and musk and alcohol to excite the heart. 

3 This use of the word apoplexy is unfortunate both for etymological reasons and because of its asso- 
ciations, but it has become genera]. 



GANGRENE OF THE LUNGS. 



153 



monary apoplexy is much less frequently met with than the circumscribed 
form. 

Diffused pulmonary apoplexy may occur from a very large infarction, but 
this is comparatively rare, It generally occurs as a result of changes in 
the walls of the arteries. A branch of the pulmonary artery may be the 
seat of an aneurism, usually of small size ; or the hemorrhage may occur in 
connection with an aneurism of some other vessel, as the aorta, which has 
ruptured into the lung substance. It may occur as the result of a fall or 
shock ; it may also be of traumatic origin, resulting from fracture of the 
ribs, gunshot wounds, etc. Its most frequent cause is the rupture of tho- 
racic aneurisms. Disease of the pulmonary artery other than aneurismal, 
has caused it. Erosions from cancer, gangrene or abscesses, may induce it. 
(Hertz. ) It occurs oftenest in males (three to one), and after the twenty- 
first year. 

Symptoms. — Profuse haemoptysis, dyspnoea, lividity, or a sense of oppres- 
sion, and often a condition bordering on collapse, are the chief symptoms 
of "diffuse pneumorrhagia." Convulsions occur, and the patient may suf- 
focate from the bronchi becoming filled with blood. 

Physical Signs. — The symptoms which mark the occurrence of diffuse 
pulmonary apoplexy are usually not well defined, and it may be difficult 
to positively determine its existence. There may be a profuse hemorrhage 
with the development of extensive pneumonic consolidation, but this 
will not distinguish it from other diffuse pulmonary hemorrhages. This 
form of apoplexy often goes unrecognized until the post-mortem exami- 
nation. 

Prognosis. — This is always grave. Recovery is only possible when the 
extravasation is of small size and the rent in the lung substance slight. 

Treatment. — The diffuse variety of pulmonary apoplexy is not amenable 
to treatment ; in most cases the patient dies before he rallies from thy 
shock of the hemorrhage. Cold internally and externally, ergot hypoder- 
matically, and a solution of chloride of iron — all may be given if he rallies 
from the shock. During the collapse which follows the shock, alcohol an^ 
diffusible stimulants must be freely administered. 



GANGRENE OF THE LUNGS. 

There are two varieties of pulmonary gangrene : the circumscribed and 
the diffused. Circumscribed gangrene of the lungs is of much more fre- 
quent occurrence than the diffused variety. It usually involves the periph- 
ery of the lower lobes. If a bronchus opens into a gangrenous patch, in- 
flammation of the bronchus results. 

Morbid Anatomy. — In circumscribed gangrene, small isolated portions of 
lung-tissue, usually of a single lobe, become converted into bluish-green 
fetid sloughs, which at first are firm and surrounded by oedematous lung- 
tissue, but soon decompose into an ichorous fluid containing pus, pigment, 
crystals of ammonio-magnesian phosphate, tyrosin, margarin, leucin, 



154 



DISEASES OF THE RESPIRATORY ORGANS. 



vibriones, and bacteria, which may be discharged through a bronchus and 
leave a ragged, sloughy cavity surrounded by inflamed lung-tissue. Com- 
monly, one gangrenous patch is solid, while another is becoming diffluent 
at its centre. A zone of catarrhal pneumonia nearly always surrounds a 
ciroumscribed patch. Vessels may traverse this cavity, but, as coagula 
rapidly form in them, hemorrhage rarely occurs. Sometimes, by the gan- 
grenous process, an opening is formed into the pleural cavity and causes 
acute pleurisy or pyo-pneumothorax. Sometimes a spot of circumscribed 
gangrene becomes the centre of diffuse gangrene. In exceptional cases, 
the disorganized portion is expelled, a fibrous capsule forms, and healthy 
pus is produced. In such cases, the cavity may ultimately close up and 
cicatrize. Sometimes the pulmonary, but oftener the bronchial, arteries 
are plugged. 

In diffused gangrene of the lung, an entire lobe is not infrequently involved, 
and sometimes an entire lung ; unlike the preceding form, there is no line 
of demarcation ; the gangrenous processes are not abruptly limited, but 
gradually merge into ©edematous or hepatized lung-tissue. The affected 
pulmonary tissue is more or less decomposed, and converted into a putrid 
mass within an anfractuous cavity, containing, also, swarms of bacteria, 
floating in a grayish-black fluid; as the gangrenous process reaches the 
pleura this membrane becomes destroyed. Kecovery under these circum- 
stances rarely, if ever, takes place, the patient dying of septicaemia or pyae- 
mia. Secondary gangrenous patches may be found in the same or opposite 
lung. 

Etiology. — The conditions under which gangrene of lung-tissue may oc- 
cur are numerous. Pulmonary gangrene has resulted from inhalation of 
noxious gases. In children it has followed cancrum oris. It may occur as 
the result of certain local pulmonary diseases, such as acute or chronic 
pneumonia, cancer, hydatids, bronchial dilatation, hemorrhagic infarc- 
tions, obstruction of the nutrient vessels leading to the gangrenous por- 
tions, or from the entrance of foreign particles, e.g., bits of food swallowed 
by those with bulbar paralysis. It may result from erosive processes, e. g., 
abscesses, ulcers or cancer. Putrefaction in bronchiectatic or phthisical 
cavities may lead to it. Traumatism not infrequently causes it. Pulmo- 
nary gangrene may occur in connection with blood-poisoning, such as is 
met with in low fevers, pyaemia, septicaemia, glanders, etc. Gangrene 
of the lungs sometimes occurs in certain nervous diseases, as dementia, soft- 
ening of the brain, epilepsy and chronic alcoholismus. It is difficult to 
explain the occurrence of diffuse pulmonary gangrene in lunatics and 
drunkards. 

Symptoms. — The symptoms of pulmonary gangrene, at its commence- 
ment, are often very obscure. When it develops from hemorrhagic infarc- 
tion, its presence cannot generally be diagnosticated until the gangrenous 
process reaches a bronchial tube of considerable size. There may be dysp- 



1 Cornil and Ranvier thus explain the loss of substance in circumscribed gangrene : " putrefaction and 
molecular destruction commence at the point where the gangrened inflammation comes in contact with the 
external air." 



GAXGEEXE OF THE LTOGS. 



155 



ncea, cough, and pain. The two symptoms which most positively indicate 
the existence of pulmonary gangrene, are an extremely fetid breath, and 
the expectoration of gangrenous material ; sometimes the fetid breath pre- 
cedes the characteristic expectoration. The expectoration has usually a 
dirty black or brown color, and contains small black masses, and in rare 
instances wavy elastic fibres of lung-tissue are to be found in it; more 
or less blood is often present, and death may occur from hemorrhage. The 
sputa are yellow, or brown : L e., purulent or bloody ; alkaline at first, but 
acid on standing ; and in a test tube they form three layers : an upper oi 
gray froth ; a middle, clear and watery; and a lower containing shreds oi 
lung-tissue. In some cases there is but slight constitutional disturb- 
ance, and the gangrenous process goes on for weeks before there are any 
general symptoms to indicate its presence. In other cases the greatest 
prostration is experienced from the beginning, the pulse becomes small and 
frequent, and the vital powers rapidly give way before the septic fever. 
Dyspnoea is in proportion to the prostration. Occasionally, death takes 
place from the exhaustion resulting from slow hectic fever. When diffuse 
gangrene of the lung occurs in connection with pneumonia, its occurrence 
is marked by a sudden prostration, accompanied by a small irregular pulse, 
a disturbed, anxious countenance, a fetid breath, and a black liquid expec- 
toration having a gangrenous odor. If the gangrenous material is swal- 
lowed, as sometimes happens, severe diarrhoea and tympanitic distention of 
the abdomen occur. Gastritis sometimes results from swallowing putrid 
masses of sputa. In some cases of gangrene the temperature runs very 
high. 

Physical Signs. — The physical signs of pulmonary gangrene are often ob- 
scure, and never distinctive. They are those of local consolidation followed 
by the evidences of breaking down of lung-tissue, and the formation of cavi- 
ties in the lung substance. Percussion elicits a dull or tympanitic note ; 
and after loose crepitation, gurgles and amphoric breathing are heard. 
There are no special signs indicating the nature of the disorganizing proc- 
ess ; sometimes it is preceded by the signs of pneumonia, generally it is 
accompanied by signs of bronchitis, and in the later stages of the disease 
there are physical evidences of the formation of cavities in the lung-sub- 
stance. 

Differential Diagnosis, — The diagnosis of gangrene of the lungs rests 
almost entirely on the characteristic odor and appearance of the expectora- 
tion ; prior to their occurrence the existence of gangrene cannot be deter- 
mined. Gangrenous expectoration, accompanied by the physical evidences 
of softening and excavation of pulmonary substance, is sufficient for its 
diagnosis. Certain conditions may arise in which it will be difficult 
to make a differential diagnosis ; for example, in some cases of fetid bron- 
chitis there may be a profuse, greenish, sero-purulent expectoration, at- 
tended by an extremely fetid odor, not distinguishable from that of gam 
grene, and yet no true gangrene of the lung exists. But as bronchiectasis 
is nearly always present with fetid bronchitis, the physical signs of the lat- 
ter would be very different from those of a gangrenous focus. ( Vide p. 77.) 



156 



DISEASES OP THE RESPIRATORY ORGANS. 



Again, gangrene of the lung may exist without any perceptible fetor to th« 
breath or expectoration, or any of the other attendant symptoms of gan- 
grene. Under such circumstances the gangrenous portion of the lung does 
not communicate with a patent bronchial tube. Again, local gangrene 
may occur in a phthisical cavity ; when it does it is yery difficult to distin- 
guish it from true gangrene of the lung, especially if the patient is seen for 
the first time just as the gangrenous process is established. In this case 
the previous history would alone enable one to make a diagnosis. A fetid 
abscess is generally distinguished from true pulmonary gangrene not by the 
character of the fetor, but by the fact that the signs of excavation precede 
the occurrence of the fetor, while in true gangrene of the lung the signs of 
excavation follow the gangrenous expectoration. The sputa in abscess are 
decidedly purulent, and fetor does not usually occur until some time after 
they are expectorated. In all cases, in order to make a correct diagnosis, it 
is necessary to have found, in addition to the fetid breath and expectora- 
tion, decomposed pulmonary tissue in the expectorated matter. 

Prognosis. — The prognosis is always unfavorable, although the circum- 
scribed form is not regarded as absolutely fatal. Recovery can only take 
place in those cases where the gangrene is circumscribed and limited to a 
small portion of the lung- tissue. Under such circumstances it is possible 
for the slough to separate and be discharged, and induration and final cica- 
trization of lung-tissue to take place. Circumscribed gangrene may be 
latent, and it often progresses slowly, simulating anaemia. Diffuse pulmo- 
nary gangrene is always fatal. Sometimes death is the result of profuse 
hemorrhage ; at other times it is due to perforation of the pleura ; but 
more frequently the patient dies from the exhaustion which attends the 
septic infection. Gangrene may terminate by an external opening. It 
may be complicated by emphysema of the cellular-tissue, hemorrhage, 
pneumothorax, or peritonitis. Death often occurs within three days after 
the first gangrenous expectoration. 

Treatment. — Under no circumstances are depressing remedies to be given. 
On the contrary, the vital powers of the patient must be sustained in every 
possible way by the administration of stimulants, tonics, and a most nutri- 
tious diet. Opium may be given in moderate doses to alleviate pain, allay 
the cough, and overcome constitutional irritation. Quinine is to be given 
for any fever that may exist. I have never found antiseptic inhalations to 
produce the beneficial effects claimed for them by some authorities, nor have 
I been able, by the internal administration of ^ chloride of potash, to obtain 
satisfactory results. If antiseptic sprays are used, thymol and salicylic acid 
are the best. Traube gives acetate of lead and tannin preparations with 
opium. Charcoal, carbolic acid, creosote and chloride of sodium are recom- 
mended as deodorizers and internal disinfectants. Bromine, chlorine, oxy- 
gen, and permanganate of potash are similarly given. My own experience 
leads me to believe that all remedies of this class are powerless either to 
arrest the gangrenous processor even mitigate its unpleasant effects. It has 
been suggested that the lung-cavities should be tapped and washed out. 



ATELECTASIS. 



157 



PULMONARY ANAEMIA. 

Anaemia of the lungs may be due to local or general causes. In general 
anaemia from any cause, the lungs are paler and lighter than normal. In- 
dependent of senile atrophy, it is never met with except in conditions of 
extreme general anaemia. Local pulmonary anaemia may be caused by 
the compression of local emphysema ; and by obstruction of the pulmonary 
artery or its branches. 

Symptoms. — Dyspnoea and palpitation are its only signs. 



ATELECTASIS. 

{Pulmonary Collapse.) 

Pulmonary atelectasis is a condition of the lungs where there is partial 
or total absence of air in the alveoli. When acquired, it is denominated 
pulmonary collapse or compression of the lung. Atelectasis is physiolog- 
ical in foetal life, and may be described as absolute absence of air from the 
alveoli. 

Morbid Anatomy. — In the new-born, atelectasis is usually lobular; rarely 
is more than one-half of a lobe involved. The lower lobes are oftenest the 
seat of atelectasis, then the tongue-like prolongations of the upper left lobe 
and the middle lobe of the right lung. The affected portions appear as 
sunken masses of violet or blue-red color ; they do not crepitate, have a soft 
feel, but are tough, and resistant, and sink in water. In the atelectatic 
spots little yellow tubercle-like masses are found,— so-called " bronchial 
abscesses" vesicular bronchitis, and granulations purulentes. 

On section, the atelectatic part is brownish-red, smooth {not granular), 
airless, and in the earlier stages dilatable ; later on, not. The walls of the 
alveoli are approximated, touch, and, according to some, grow together. 
Fatty degeneration and cell proliferation occur in the collapsed spots. A 
whole lung may be involved, but usually only a lobe or a portion of a lobe. 
The collapsed portions contrast strongly with the surrounding parts. Its seat 
is most often in the periphery and the lower lobes of the lung. The affected 
portion has the same tough, "liver-like" characteristics as in congenital 
atelectasis, the difference being that in acquired collapse the lobular points 
are disseminated. The collapsed portion maybe engorged and oedematous, 
a condition sometimes called " splenization." The bronchi leading to 
the collapsed lobules are usually congested and plugged. When collapse 
occurs from pressure — compression of the lung — the part involved and 
its extent depend on the site and extent of the pressure. The air cells in 
the collapsed portion may or may not be wholly voi4 of air. It is flesh- 
like ; and for a time can be inflated and caused to return to its normal size 
and condition. If the inspiration is insufficient and the expiratory efforts 
normal in force, after a time all air will be expelled, and the dry 5 tough 



158 



DISEASES OE THE RESPIRATORY ORGANS. 



gray-red mass assumes a condition known as " carnification " ; and in timo 
only a fibrous or connective-tissue cicatrix remains. Small blood-clots may 
be found in the affected lobes, that are frequently decolorized and perhaps 
adherent to the walls of the vessels, whose calibres are impervious or oblit- 
erated. 1 

Etiology. — Congenital atelectasis occurs in feeble infants, in those born 
prematurely, and in those whose bronchi, nares or other parts accessory to 
respiration are plugged with mucus. Pulmonary collapse is rarer in adults 
than in young children. Any disease or condition that weakens or ob- 
structs the power of inspiration may induce it. Brain diseases are some- 
times accompanied by it. Too tight clothing about the chest of feeble 
children may lead to it. Paralysis of the vagus is said to cause it, and 
muscular paralysis from disease of the cord may lead to it. The most 
frequent cause is some catarrhal condition of the respiratory tract that 
induces the formation of a plug in a small bronchus; e.g., capil- 
lary bronchitis, catarrhal pneumonia and bronchitis with tenacious secre- 
tion. Twenty-five per cent, of the total mortality of very young in- 
fants may be safely set down to pulmonary collapse, following bronchitis. 
Co'lapse from compression of the lung results from fluid, pus, air or blood 
in the pleural cavity ; from mediastinal tumors, from rachitic and spinal 
deformities, and, rarely, from abdominal tumors. 

Symptoms. — In the new-born, atelectasis is shown by feeble breathing, 
slight motion of the chest, a low, almost inaudible, " whining" cry, lividity 
and coldness of extremities, constant sleepiness, and often muscular twitch- 
ings and convulsions. The child cannot nurse. Since the foramen ovale 
and ductus arteriosus so often remain open in congenital atelectasis, 
anomalies of the circulation may cause asphyxia, convulsions, suffoca- 
tion and death. Blood clots may form in the cerebral sinuses. 2 In 
collapse there is labored breathing, dyspnoea, frequent respirations (70 
to 100 per minute), and a cough with muco-purulent expectoration. Chil- 
dren utter the low, whining cry. Passive hyperemia and oedema of the ex- 
tremities and central organs are common results of pulmonary collapse. 
The pulse is small and feeble, the skin cool, the urine scanty. There is 
an interval between inspiration and expiration, instead of after expiration. 
The whole act is "shallow." 

Physical Signs. — Inspection shows compensatory retraction of the most 
yielding portions of the thorax during the act of inspiration, and the inter- 
costal spaces retract. On percussion precordial clulness is increased ; there 
may be dulness when there is much condensation, but if emphysematous 
patches develop about the collapsed lobules the dulness may have a tym- 
panitic quality. On auscultation respiratory sounds may be feeble or ab- 
sent. Later there may be bronchial breathing and bronchophony. Bales 
may be due to associated bronchitis ; they are coarse and sonorous. The 



J LichtheinVs recent experiments go to prove Virchow's assertion that air, shut in by closure of a bron 
chus, is absorbed by the blond-vessels, and also that elasticity of the lung acts until the air is completelj 
absorbed.— Arch.f. exper. Palhologie u. Pharm., vol. x., p. 54. 

8 Virchow's Archiv., Bd. xi., p. 240. 



PULMONARY EMPHYSEMA. 



153 



physical signs of compression are merely those of the causative condition, 
e. g., hydrothorax, pleurisy with effusion, etc., etc. 

Differential Diagnosis. — Pneumonia is distinguished by the fever, flushed 
face, fine rales, lobar instead of lobular outline of dulness, pain, and ab- 
sence of "inspiratory retraction." Miliary tuberculosis is distinguished 
by the fever, cough, and wasting, all of which will precede the physical 
signs. The history of the parents will here aid us. In pleurisy with 
effusion the flatness and change in line of flatness with a change in the 
patient's position will establish the diagnosis. 

Prognosis. — Extreme atelectasis is rarely recovered from. Occurring 
with whooping-cough it is especially fatal. Emphysema, bronchitis, lobu- 
lar pneumonia, tuberculosis and pleurisy may complicate it. Asphyxia or 
complications cause death. When compression occurs from tumors, 
hydro- or jmeumo-thorax the prognosis is more unfavorable than with 
other causes. Cheesy pneumonia or phthisis may follow atelectasis or 
collapse. 

Treatment. — In the new-born the treatment should be that described in 
works on diseases of children and obstetrics. Efforts at full inspira- 
tion should be encouraged. Cold water may be poured over the neck and 
chest. A stream of water thrown on the nuchal region is said to excite 
violent and strong inspiratory impulses. Counter-irritation and stimulating 
embrocations are recommended. The catarrh that induces collapse must 
be treated with stimulating expectorants, or, in children, with emetics. 
Arsenic, belladonna, and salts of potash and ammonia are recommended. 
In compression remove the cause when possible, e.g., the emphysema and 
hydrothorax. In all cases tonics and stimulants with good nourishment 
are demanded ; the " depletory " plan is never indicated. Inhalation of 
compressed air may do good. Never let the diaphragm's action be im- 
peded by clothing or a distended abdomen. 



PULMO?s T ABY EMPHYSEMA. 

Pulmonary emphysema is seldom met with unless associated with more 
or less bronchitis ; and emphysematous persons are especially liable to at- 
tacks of spasmodic asthma. Emphysema is essentially a chronic affection ; 
it comes on slowly, and when once developed is permanent. 

By the term is understood either an abnormal accumulation of air 
within the air-cells or an infiltration of air into the sub-pleural and inter- 
stitial connective-tissue. There are two recognized varieties, termed, 
first, vesicular emphysema ; second, interlobular emphysema. The first 
is by far the more frequent and more important affection. There are 
no definite rules for the diagnosis of interlobular emphysema, and it rarely 
occurs except in connection with advanced vesicular emphysema. "When 
the unqualified term emphysema is used, reference is always had to the 
Vesicular variety. 

Morbid Anatomy. — In emphysema, there may be simple dilatation of the 



160 



DISEASES OF THE RESPIRATORY ORGANS. 



air-cells without rupture of their walls ; or there may be dilatation of the 
air-cells with rupture of their walls. The rupture of the air-cells leads to 
the formation of what may be called air-sacs, which vary in size from that 
of a pin's head to that of a pigeon's egg, and even larger. Both forms of 
the affection, the vesicular arid the interlobular, are generally present in 
cases in which these larger air-sacs have formed. The changes which take 
place in the anatomical structure of the lung in this affection are as fol- 
lows : in slight cases there is dilatation of the infundibula, and a dimin- 
ished prominence of the alveolar walls, followed, later, by their rupture and 
partial disappearance ; as a result, a small air-sac is formed, in which lit- 
tle ledges and filaments of tissue alone mark the site of the alveolar septa. 
At this time there is no well-marked line of demarcation between the 
infundibulum and the alveoli. As the disease advances rupture of the 
walls of these little air-sacs occurs and establishes a communication between 
their cavities. The openings thus made between the air-sacs are at the 
very central portion of the sac, where the wall is thinnest. By this grad- 
ual enlargement and the union of many small sacs, a large air cavity is 
formed, across and along the walls of which exist remains of the original 
tissue. These larger air-sacs communicate with the bronchi, which are 

sometimes enlarged. The result of 
this destruction of the alveolar septa 
is the abolition of the capillary 
plexus which is normally spread over 
the walls of the air-cells. At times 
ovoid collections of fat granules are 
seen in the thinned septa. Whether 
these fat cells are in the nuclei of 
the capillaries, or in the inter-capil- 
lary cells is undetermined ; — prob- 
ably they are in both. This fatty 
metamorphosis as a rule precedes the 
dilatation, and is not constant. Fatty 
granules are found in the protoplasm 
about the nuclei of the epithelial 
cells taken from an emphysematous 
vesicle. The small branches of the 
pulmonary artery are the longest retained ; they become dilated and looped, 
and communicate by anastomosis with the pulmonary vein, and thus the 
circuit of the pulmonary circulation is kept up, but it is not nearly so free 
or abundant as that which exists normally. The pulmonary circulation 
is therefore materially interfered with by this structural change. 

Well-marked emphysema generally affects both lungs ; it is most 
marked in the upper lobes, especially along their anterior borders. 
Emphysematous degeneration throughout both lungs is rare. If the 
emphysema is compensatory its site will vary with that of the produc- 
ing cause. When it is the result of strong pleuritic adhesions, it most fre- 
quently affects the anterior border of the lung. In partial collapse of the 




Fig. 35. 

Pulmonary Emphysema, first stage. 

Ectasy of the central cavity of the infundibula, a, a, a 
1-100. After Rindfleixch. 



PULMONARY EMPHYSEMA. 



161 



lung following obstruction of the bronchi, or in inexpansibility from 
disease of its structure, emphysema will usually be limited to the vicinity of 
the bronchial obstructions or the structural disease. When emphysema is 
the result of forced inspiration with closure of the glottis, as occurs in vio- 
lent spasmodic croup, etc., the apex and anterior borders of the lungs are 
mainly involved. 

Emphysematous lungs do not collapse when the thoracic cavity is 
opened. In well-marked cases, the lungs meet and overlap each other 
in the median line. The left overlaps the superficial cardiac region, 
both extend lower than normal, and the heart is pushed downwards and 
nearer to the median line than normal. The diaphragm may also be 
pushed below its normal position, and all of the abdominal viscera crowded 
out of their normal situations in consequence. In some cases the liver has 
been so displaced as to lie entirely below the free border of the ribs. The 
lungs removed from the thoracic cavity bear the impress of the ribs as 
furrows on their surface. Indentations made by pressure of the fingers on 
the surface of the lung are permanent, showing a loss of elasticity. The 
dilated alveoli may at times be seen on the surface of the lung through the 
pleura, or on section maybe found distributed through its substance ; they 
are, however, much more apparent after the lung has been blown up and 
dried. They appear as whitish or gray prominences, or as spherical vesic- 
ular appendages filled with air. When the air-sacs are large they protrude 
beyond the surface of the lung, and generally have a globular form ; in 
some cases they seem to be separated by a neck from the rest of the lung, 
looking like appendages to it. In well-marked examples of emphysema, 
the whole anterior surface of the lungs may be covered over with air-sacs, 
sometimes resembling the lungs of reptiles. The color of an emphy- 
sematous lung is usually abnormally pale ; it is soft and cushion-like to 
the touch ; it crepitates but little when pressed between the thumb and 
finger ; it sinks in water less readily than healthy lung-tissue, for though 
its volume is increased, its weight is diminished. By pressure the air can 
be forced out of the larger and smaller sacs into the bronchi. The evi- 
dences of bronchitis are usually present in the bronchial tubes. The pa- 
renchyma of the lung may present lesions which may be either a cause or 
a complication of emphysema. Phthisis and pneumonia, although of rare 
occurrence, are not as infrequent as many writers would have us suppose. 
As a rule in advanced cases of emphysema, the right heart will be found 
hypertrophied and dilated ; as soon as the systemic circulation is inter- 
fered with, the left ventricle becomes hypertrophied, and this hypertrophy 
will for a time compensate for the obstruction to the return circulation, but 
as a result of this interference when it is long-continued, anatomical changes 
take place in the liver, kidneys and spleen, which are similar in character 
to those which occur in connection with valvular heart lesions, and give 
rise to general dropsy ; changes of this class, however, belong to the remoter 
lesions of emphysema. 

Senile emphysema differs from the variety which has just been described 
in the following respects : the lungs are not only diminished in weight but 
11 



162 



DISEASES OF THE RESPIRATORY ORGANS. 



very markedly in size ; the lobes are usually united, and their fissures di- 
rected vertically instead of horizontally ; the lower lobes having lost the 
most in bulk, their surface is irregular, and their structure is composed of 
enlarged air vesicles and sacs which are the result of the natural atrophy 
of the lung-tissue which takes place in old age. In the aged the walls of 
the emphysematous cavities are usually deeply pigmented. The lung often 
consists merely of a number of large cavities. 

In interlobular emphysema an air-vesicle or sac ruptures, so that the 
air escapes into the interlobular cellular-tissue, forming sacs of large or 
small size. These sacs, or rather these collections of air, may form be- 
neath the pleura, or, extending between the lobules of the lung and along 
its vessels, reach its root, spread into the mediastinal cellular- tissue, and be 
distributed over the neck and subcutaneous cellular- tissue of the body. The 
size of the air-sacs beneath the pleura may be only that of small vesicles, 
and these limited to the circumference of a lobule, or they may reach the 
size of the stomach. "They look like a membrane uplifted by foam." 
They may be distinguished from the vesicular dilatations by being 
freely movable beneath the pleura. Perforation of the pleura, produc- 
ing pneumothorax, is a rare result of interlobular emphysema. More 
or less interlobular emphysema is always present in advanced vesicular 
emphysema. 

Etiology. — The causes of emphysema may be divided into primary and 
secondary, or compensatory. Primary emphysema may exist independently 
of, or be associated with bronchitis. Among its causes are forced expiratory 
efforts, the glottis being closed or narrowed as in violent coughing, strain- 
ing at stool, etc. In a few rare instances the emphysematous distention is 
produced during strong inspiratory efforts. In both instances the disease is 
developed in the upper lobes of the lung. Another cause of this variety of 
emphysema is, that there exists in many persons either an hereditary or an 
acquired impairment of the elasticity of the lungs which renders them more 
readily dilatable and more easily torn. There are three prominent theories 
which have been advanced to account for this : first, that it is due to fatty 
degeneration of the alveolar walls. The constancy of this change has not 
as yet been demonstrated. It is true that molecules of fat are sometimes 
seen in the alveolar septa, but they may be the result rather than the cause 
of the emphysema. Secondly, there is a theory that the weakness of the 
alveolar walls is due to the growth of the inter-capillary nuclei. Thirdly, 
that it is due to the fibroid degeneration of the alveolar septa. No one of 
these theories has as yet received full confirmation ; a co-operation of all' of 
them, more particularly of the last two, is necessary in many cases to satis- 
factorily explain the production of the disease. Recently another cause for 
the development of this form of emphysema has been advanced, viz. : an 
abnormal increase in the capacity of the chest, due to excessive growth of 
its walls. This theory as yet lacks proof. 

The causes of secondary emphysema are conveniently considered under 
three subdivisions, in all of which the emphysema is best denominated com- 
pensatory. The first of these subdivisions comprises all cases in which the 



PULMOK"AEY EMPHYSEMA. 



163 



emphysema is developed around small portions of lung rendered inexpansible 
by disease of its tissue, as, for example, lobular collapse from obstruction of a 
small bronchus, a lobular pneumonia, a pulmonary infarction, etc. ; the lob- 
ules adjacent to those that are thus rendered inexpansible become over-dis- 
tended by a forced inspiration or a forced expiration during a violent fit of 
coughing. Some would make these obstructions, operating in different parts 
of the lung, a primary cause. A second subdivision comprises those cases 
where a large portion of lung, either from some internal cause, as pneumo- 
nia, hypostasis, atelectasis, etc., or, from some external cause, as pleurisy, 
etc., is rendered inexpansible, and emphysema is developed in healthy por- 
tions. In both of these subdivisions the. capacity and mobility of the chest 
remaining normal, the usual, and especially forced, inspiratory efforts 
require extra distention of the alveoli to compensate for those rendered 
more or less useless. A third subdivision includes those cases secondary to 
croup, lobular pneumonia, whooping-cough, pressure on the trachea or 
main bronchi. The emphysematous distention in this class of patients is pro- 
duced during inspiration. It is questionable, however, whether compensatory 
emphysema is ever developed when the walls of the air-cells have not been 
enfeebled. Interlobular emphysema is produced by forced expiration with 
narrowed glottis, as during severe cough, parturition, straining at stool, 
etc. It is usually preceded by vesicular emphysema. It may also occur 
from perforation of the lung from without, as in fracture of the ribs. 
Senile emphysema is mainly an atrophy of the alveolar septa, which become 
obliterated, so that vesicles coalesce. It is due to impaired nutrition, which 
affects the lungs as well as other organs in old age. 

Symptoms. — The prominent and most constant subjective symptom of 
emphysema is dyspnoea. It is a dyspnoea which is increased by physical 
exercise, by the occurrence of fresh attacks of bronchitis, and by spasm of 
the bronchi, such as occurs in spasmodic asthma. When the emphysema 
is well marked, very slight exertion will give rise to dyspnoea ; when the 
emphysema is slight, only violent exertion will be followed by it. It is 
mitigated by a warm atmosphere, and returns with increased severity during 
the cold of winter. There is often a "smothering" sensation in the chest, 
and when present it is constant. In congenital cases the only symptom 
during childhood and early adult life is a moderate degree of dyspnoea. In 
advanced cases of the disease the dyspnoea is liable to be paroxysmal, the 
paroxysms depending upon a tendency to spasm which emphysema in its 
development seems to impart to the bronchi. A cough is usually present, 
but it is due to bronchial irritation, and unless bronchitis exists the cough 
may be wanting. The expectoration varies w r ith the extent and character 
of the accompanying bronchitis, and it is not uncommonly a part of the his- 
tory of the emphysema ; if it occurs independently of bronchitis it will 
have nothing characteristic about it. Usually there is no pain in the chest 
dependent upon the emphysema. In advanced cases the countenance is 
peculiar and somewhat characteristic ; it is of a dusky hue and has a puffy 
appearance which contrasts remarkably with the wasted appearance of the 
rest of the body. The nostrils are distended, thickened, and vascu 1 ar, and 



164 



DISEASES OF THE RESPIRATORY ORGANS. 



expand with each inspiration ; the angles of the mouth are drawn down* 
ward, the voice is feeble, the patient stoops in the act d walking, and his 
whole body has a cachectic appearance ; the capillary circulation of the 
extremities is markedly imperfect, as shown upon the slightest exertion. 
There is a gradual, though steady loss of flesh and strength. Usually, the 
disease is not attended by febrile excitement ; the pulse is not accelerated, 
but is markedly feeble, and the temperature of the body sub-normal. 

The other symptoms observed in connection with emphysema are indirect, 
and due to interference with the circulation. Not only is there always dis- 
turbance of the capillary circulation in the extremities, but the face and 
neck present a fulness or even a turgidity of the blood-vessels altogether ab- 
normal. The distention of the jugular veins, and the lividity of the face 
and hands, are unquestionably due to the interference with the circulation 
through the right heart, but do not occur until that stage is reached 
in which there is more or less hypertrophy and dilatation of the right ven- 
tricle. Patients who have reached this stage become very purple in the 
face after and during fits of coughing, often presenting the appearance of 
impending suffocation. The paroxysms are perfectly characteristic ; an 
attack of coughing comes on, grows more and more severe, gathers more 
or less of the spasmodic element, and when it has reached its climax the 
face and hands become livid, and the patient is completely exhausted. 
Vertigo is a common symptom in advanced emphysema ; it is most apt to 
be developed during a fit of coughing, and depends upon the interference 
with the return circulation from the head. Slight haemoptysis may occur. 
Emphysema of itself does not give rise to dropsy, although in advanced 
cases the feet and ankles are almost always cedematous. The oedema is the 
result of cardiac or renal complications. Ordinarily, there is more or less 
disturbance of the digestive organs in these advanced cases ; the disturbance 
is due to catarrh of the stomach, the result of passive hyperaemiaof the mu- 
cous membrane of the stomach from failure of the right heart. For a like 
reason other functions are more or less disturbed. Emphysematous patients 
are especially liable to hemorrhoids, and very often have profuse bleeding 
from the rectum. As has been already stated, the development of emphy- 
sema is almost always slow ; in rare instances it advances rapidly, and it is 
then called acute. If, from the rational symptoms, there is any doubt as 
to the diagnosis of emphysema, the doubt will disappear after a physical 
exploration of the chest, for the physical signs in a well-marked case are 
characteristic. 

Physical Signs. — On inspection, it will be noticed that there are alterations 
in the shape and movements of the chest. There is an unnatural elevation 
and arching of the sternum (as if from congenital deformity), and an un- 
natural bulging of the infra-clavicular and mammary region, which gives 
to the chest a more rounded appearance than in health : this has been 
termed "oarrel-shaped" The scapulae are brought forward, and there may 
be antero-posterior curvature of the spine, which gives to this class of pa- 
tients a stooping posture which is habitual. The muscles of the neck are 
unnaturally prominent. The lower portion of the chest seems contracted. 



PULMONARY EMPHYSEMA. 



165 



and the intercostal spaces are depressed and wider than above. If the em- 
physema is extensive, the apex of the heart will be found beating lower 
down than normal and more toward the median line ; if the right side of 

the heart is extensively dilated there will be an epigastric impulse this 

impulse is due to an increase in the size of the heart, and to its being 
crowded to the right, and lower down in the thoracic cavity. In some in- 
stances, when the general symptoms of emphysema are well marked, the 
lungs are atrophied instead of abnormally dilated, and no bulging of the 
chest (either general or local) occurs. The movements of the chest walls 
are also altered and peculiar. At the upper portion expansion on inspira- 
tion is diminished or entirely wanting ; the whole chest moves vertically 
up and down with inspiration and expiration, as if it were passively lifted 
from the shoulders, and composed of one solid piece; while below, the chest, 
instead of being dilated with inspiration, is contracted. The respiratory 
efforts are labored, and the breathing is chiefly abdominal. The diaphragm 
seems to be more actively engaged than the chest walls in the process of 
respiration. In cases far advanced, the existence of emphysema can be 
made out by inspection alone. 

On palpation the vocal fremitus varies : it may fall below, or equal, or it 
may exceed that in health. In senile emphysema, the vocal fremitus is 
usually increased. 

The intensity of the percussion sound is increased, the pitch is lowered, 
the pulmonary quality of the sound is greatly diminished, and it becomes 
vesiculo-tympanitic — that is, there is added to the vesicular element a tym- 
panitic quality which is the characteristic percussion sound of emphysema, 
and is not met in connection with any other pulmonary disease. The per- 
cussion note is not materially affected, either by forced inspiration or by 
forced expiration. The precordial region is usually resonant, owing to the 
distended lungs coming between the heart and the wall of the chest. 

On auscultation, the inspiratory sound is either short or feeble, or act- 
ually suppressed, while the expiratory is greatly prolonged, the ratio of the 
two being as one to four instead of four to one. As a rule, the pitch of 
both the inspiratory and expiratory sound is lower than in health. In some 
extreme cases of emphysema, the respiratory sounds are of equal length, 
greatly exaggerated in intensity, and of a harsh, sibilant or sonorous quality, 
the harsh quality undoubtedly being due to diminution in the calibre of the 
minute bronchial tubes. In some cases, when interlobular and vesicular 
emphysema are combined, a crumpling sound is heard, which has been des- 
ignated as the i( crumpling sound of emphysema." This sound has been 
said to resemble the crepitant rale, but it more nearly resembles the sound 
of crumpling parchment, than the crackling sound of the crepitant rale; 
but " Laennec's rale" — a modification of the sub-crepitant rale — is very 
often heard. The vocal sounds vary greatly ; they may be diminished, or 
altogether absent, or their intensity may be greatly increased. The heart 
sounds are feeble. The sphygmograph may afford valuable information. 

Differential Diagnosis. — Slight emphysema cannot be diagnosticated with 
certainty; but those advanced emphysematous cases which give rise to sc- 



166 



DISEASES OF THE RESPIRATORY ORGANS. 



vere dyspnoea and cyanosis arc readily distinguished, by a physical exami- 
nation of the thorax, from other diseases which manifest similar symptoms. 
The disease with which emphysema is especially liable to be confounded is 
pneumothorax. If the physical signs of the two diseases are properly ap- 
preciated, it is not difficult to distinguish between them. In emphysema 
the percussion sound, although somewhat tympanitic in character, still re- 
tains a pulmonary quality, and there is a vesicular element to the respira- 
tory sound, while in pneumothorax the percussion sound has a well-marked 
purely tympanitic character, and the respiratory sound, if audible, is am- 
phoric in character with no vesicular element. Emphysema affects both 
sides, pneumothorax only one side. The symptoms of pneumothorax come 
on suddenly, while those of emphysema are slowly developed, and are never 
so urgent as those of pneumothorax. A diagnosis of compensatory em- 
physema may not be made out during life, but the fact being well estab- 
lished that it does almost invariably exist in certain conditions, the proba- 
bility of its existence should always be borne in mind in the study, exam- 
ination, and treatment of those pulmonary diseases in which it is liable to 
occur. 

Prognosis. — Emphysema rarely if ever destroys life ; but, when once de- 
veloped, is never recovered from, and incapacitates the person to a greater 
or less degree for active exercise, rendering life at least uncomfortable. It 
strongly predisposes to bronchitis and renders existing bronchitis severe. 
Acute bronchitis of the smaller tubes is an extremely grave affection when 
it occurs in an emphysematous person. Again, emphysema develops heart 
disease. The impediment to the pulmonary circulation, which exists as 
the result of emphysematous changes in the lung substance, gives rise to 
an overloaded state of the right cardiac cavities, which in time leads to 
their permanent dilatation and to hypertrophy of their walls ; insufficiency 
of the tricuspid valves follows, and the resulting regurgitation through the 
tricuspid orifice into the right ventricle causes obstruction to the systemic 
venous circulation, and as a result there is congestion and a permanent dis- 
turbance of the function of the kidneys, liver, etc. In giving a prognosis 
in any case of emphysema, the liability to this complication should be con- 
sidered. Emphysema also predisposes to fatty degeneration of the different 
organs and tissues of the body, the result of an impoverished state of the 
blood. The occurrence of these secondary affections renders emphysema a 
serious disease. It is undoubtedly a more serious affection when it occurs 
in childhood or adult life, than in old age. Pleurisy, asthma, bronchitis 
and anaemia are the most frequent complications. 

Treatment. — The treatment of this affection will be briefly considered un- 
der two heads : first, the treatment of the disease itself ; secondly, the 
treatment of secondary changes in other organs, which changes are more or 
less directly induced by the emphysema. Accepting the view that the 
lesions in this disease in the lung-tissue are the result of imperfect or dis- 
ordered nutrition, we may reasonably expect that, by improving the nutri- 
tion, the progress of the degeneration may be checked or arrested, and per- 
haps even the elasticity of the unaffected portion of the lung may be re- 



PULMONARY EMPHYSEMA. 



16? 



stored. The most rational method of treatment is that by which we aim 
to remedy faulty nutrition in other organs and tissues. With this object 
in view, the drug which is of the greatest service is iron. This remedy 
should be taken daily with meals, for a long period, by persons who have 
emphysema or in whom it is developing. In this class of cases, the prepa- 
ration which I prefer is the ethereal tincture of the acetate of iron ; sul- 
phate of quinine in small doses may be given with the iron in most cases 
with benefit. Strychnia, which has some reputation in the treatment of 
this disease, I am confident has no power in arresting its development, and 
it has seemed to me to increase the frequency and violence of the parox- 
ysms of dyspnoea, and thus hasten rather than retard the emphysematous 
development. If an emphysematous patient has dyspeptic symptoms the 
mineral acids in combination with bitter vegetable infusions will be found 
of service. When there is a tendency to great emaciation, I have found 
cod-liver oil of service. Stimulants, vinous and spirituous, when taken 
in small quantities after or during meals, often give beneficial results, and 
when their use is followed by marked improvement in the general condition 
of the patient, they should be used in the treatment of the disease. 

The regulation of the diet, and the general management of the emphy- 
sematous patient is, however, of much greater importance than the medical 
treatment. The diet should be of the most nutritious character, and com- 
posed largely of animal food ; overloading the stomach should be especially 
avoided, as well as everything which has a tendency to produce flatulence. 
The food should not be bulky or watery in character, and should be as di- 
gestible as possible ; the quantity of liquids taken into the stomach should 
always be small. Exercise in the open air should be taken systematically, 
but fatigue should be avoided. All sudden, violent exercise, or great physi- 
cal exertion must be strictly prohibited. The condition of the skin should 
be carefully considered. Emphysematous patients should not expose them- 
selves to cold. All localities where attacks of spasmodic asthma are liable 
to be developed should be carefully avoided, as also everything which may 
develop dyspnoea or predispose the patient to asthmatic attacks. The in- 
halation of compressed air is highly esteemed by the Germans. The patient 
should live in the open air as much as possible, and in such conditions as 
will make the minimum of effort sufficient for respiration. The rule for 
all emphysematous persons is to change their residence to that locality 
where they surfer the least and are not troubled with dyspnoea. The treat- 
ment of those complications which accompany, or are induced by, the em- 
physema is also of importance in arresting the progress of the disease. Of 
these accompaniments, bronchitis (generally chronic) stands first. The 
dyspnoea may be so urgent as to demand treatment of itself ; the quebracho 
bark has recently received much attention as the drug for emphysematous 
dyspnoea. In addition to all that can be accomplished by change of cli- 
mate and other hygienic measures in the management of that form of bron- 
chitis which is so constant an accompaniment of emphysema, there is one 
drug which I have found especially serviceable, viz., iodide of potassium. 
, It should be given in doses varying from five to twenty grains, three times 



168 



DISEASES OF THE KESPIKATORY OEGA>5"S. 



during the day, and its administration should be continued at intervals over 
a long period. The treatment of diseases of the heart, liver and kidneys, 
which occur as complications or accompaniments of emphysema, will be 
considered in connection with the history of cardiac, renal and hepatic 
diseases. 

CANCER OF THE LUNGS. 



There is no variety of cancer which has not been found in the lungs. Can- 
cer here is usually secondary to cancerous development in other parts of 
the body. It may extend to the lungs by direct peripheral extension of a 
cancer of the mediastinum or other adjacent parts, or by metastasis from 
distant cancer ; and in either case it begins in the connective-tissue either 
of the walls of the air-cells, the interlobular tissue, the bronchial tubes, or 
the pleural or subpleural tissues. 
Morbid Anatomy. — Medullary or encephaloid cancer is the most frequent 

variety met with in the 
lungs ; next is scirrhus, 
then epithelioma, and 
melanotic cancer. Me- 
dullary cancer of the lungs 
occurs in the form of nod- 
ules of various sizes scat- 
tered through the lung- 
substance, or a large 
portion of lung may be- 
come the seat of medul- 
lary infiltration. Discrete 
nodules of medullary 
cancer cause great de- 
struction of tissue and 
hemorrhage. Primary 
cancer usually involves 



only one lung, and is often 



infiltrated or disseminated 
in nodules the size of 
peas, while secondary can* 
cer affects both lungs and 
is generally nodular, the 
nodules varying m size. 
By the union of the nod- 
ules an entire lung some- 
times becomes involved. 
After a time the cancerous tissue may undergo fatty degeneration and 
softening, and the pulmonary vessels and bronchi are either involved in the 
cancerous development or are obliterated by its pressure. Scirrhus develops 
most frequently in the bronchi. 

The unaffected portion of lung-tissue may be normal, cedematous or pneu- 




Cancer of the Lung. 

Section rf Lung throuah a small cancerous nodule. TJie illustration 
shows only a part of the nodule with the air-vesicles bounding the 
upper and left hand sides. 

A. Fibrous stroma of the cancer. 
B B. Empty alveoli of the cancer. 

C C. Cancer alveoli filled with large nucleated cells of various forms. 
1) D. Walls of air-vesicles bordering the nodule. 
EE. Lung alveoli. filled with cells 'of same character as those filling 
the alveoli of the cancer, x 250. 



CANCER OF THE LUNGS. 



169 



monic ; extensive pleuritic thickenings and adhesions are present in most 
cases. Authorities differ as to which lung is oftener involved, and there 
*ire not sufficient statistics to decide the question. The lymphatics of the 
lungs are the channels along which the process extends. Hemorrhagic pleu- 
risy, cancer of the pleura and bronchial glands, and hydrothorax, usually 
co-exist. The infundibula are filled with cancerous elements, about which 
is extensive pigmentation. The alveolar walls may be intact, but their ves- 
sels are engorged. There is no newly formed stroma in pulmonary cancer ; 
the alveolar septa take the place of a stroma. 

Etiology. — The etiology of pulmonary cancer is the same as the etiology 
of cancer in general. Hereditary predisposition may be regarded as an ele- 
ment in its production. It is most frequently met with between the ages of 
twenty and sixty, and is more common in males than females. As has 
already been stated, it is generally secondary to cancerous developments in 
other organs of the body. In the female, cancer of the breast usually pre- 
cedes the development of cancer of the lungs. It may be secondary to car- 
cinoma of the bones, testicles, uterus, stomach, liver, or oesophagus. 

Symptoms. — Cancer of the lung usually comes on very insidiously, with 
few subjective symptoms. There is usually pain in the chest and a cough 
accompanied by a muco-hemorrhagic expectoration resembling currant-jelly, 
which occasionally contains cancerous elements. More or less dyspnoea is 
present, especially if mediastinal tumors co-exist. The cancerous cachexia 
may or may not be present. As the disease advances, emaciation, fever, 
night-sweats, with failure of strength, become more and more marked, and 
this steadily increasing weakness and emaciation is one of the most constant 
rational symptoms. The "pressure effects " producing lividity, oedema, dys- 
phagia, and laryngeal symptoms, are like those of a thoracic aneurism. The 
glands in the axilla and above the clavicle are nearly always enlarged. If 
dyspnoea, cough, haemoptysis, pain in the chest, rapid emaciation, and 
cachexia should come on in one from whom a carcinomatous breast had 
been extirpated, there would be reason to suspect the development of cancer 
of the lung. Signs of pleurisy, bronchitis, emphysema, or catarrhal pneu- 
monia, may mask the signs of pulmonary cancer. 

Physical Signs. — These will vary according to the seat and extent of the 
cancerous development. If the lung is extensively involved with nodular 
cancer, inspection will show enlargement of the affected side with widening 
of the intercostal spaces and deficiency or entire absence of respiratory 
motion. Vocal fremitus may be diminished or absent. On percussion 
there will be complete dulness attended by friction over the space corre- 
sponding to the cancer. The signs of a cavity are sometimes present. 
On auscultation the respiratory sounds may be feeble or absent, or, if a 
large open bronchus is intimately connected with the cancerous mass, 
bronchial respiration may be heard. Disseminated cancer of the lungs 
cannot be distinguished, by physical examination, from general bronchitis. 
In the infiltrated form the lung is often contracted, and, as a consequence, 
there is retraction of the ehest-walls on the affected side. 

Differential Diagnosis. — Pulmonary cancer is liable to be confounded with 



170 



DISEASES OF THE RESPIRATORY ORGANS. 



pleurisy with effusion. In cancer, the percussion dulness usually begins at 
the upper portion of the chest, while in pleurisy it begins at the lower 
portion. In cancer the dulness is most marked in front, in pleurisy it is 
most marked behind. In cancer there are isolated spots of resonance in 
the area of dulness, while in pleurisy the dulness is uniform over all the 
space occupied by the fluid. In pleurisy the line of dulness changes with 
the position of the patient ; this never varies in cancer. 

It may also be mistaken for thoracic aneurism and for phthisis. The his- 
tory, the long duration and the physical signs of the latter will soon enable 
a diagnosis to be made. It may also be mistaken for fibroid induration of 
the lung, but its secondary character, more rapid course, greater marasmus 
and emaciation, and the absence of wooden dulness over an extensive tract, 
with retraction of the chest- walls, will suffice to make a diagnosis. 

Prognosis. — The prognosis is always unfavorable, death occurs either 
from local or general causes in from six months to two years. 

Treatment. — This is altogether palliative, and is restricted to the relief of 
symptoms. 

NON- MALIGNANT GROWTHS IN THE LUNGS. 

Non-malignant growths in the lungs are of little pathological or clinical 
interest. 

Sarcomatous growths starting in the alveoli or in the inter- alveolar septa 
are always secondary ; primary sarcoma of the bones is very apt to be fol- 
lowed by secondary pulmonary sarcoma. Melanotic sarcoma occurs with 
extensive pigmentation. 

Fibromata occur as small hard masses varying in size from that of a pea 
to that of a hazel nut. They rarely occur singly. 

Lipomata are usually situated beneath the pleura in the form of slightly 
flattened spherules. 

Enchondromata — usually secondary to enchondromata of bones — are met 
with as discrete, irregularly roundish masses sometimes reaching the size of 
an egg and partly or wholly calcified — at times densely ossified. 

Osteomata occur in lungs which are the seat of fibroid pneumonia. Vir- 
chow describes one the size of a man's fist. They are usually small and 
multiple. They may be branched, following the line of new connective- 
tissue developments. 

Simple melanotic tumors in the lungs are similar in constitution, both to 
the naked eye and microscopically, to the interstitial pneumonia of miners, 
except that the black granules are small and round instead of angular. A 
melanotic tumor of the lung may invade the vertebral column in such a 
manner as to destroy the bodies of one or more of the vertebrae, thus giving 
rise to one variety of Pott's disease. 

Dermoid cysts, myxoma, and hematoma are very rarely met with in the 
lungs ; any of these tumors may displace, compress, or cause atrophy and 
absorption of lung-tissue ; they may cause an excess of air in one part of 
the lung and a deficiency in another ; they may cause congestion or anae- 
mia ; may ulcerate and form cavities ; may induce acute local catarrhal 



SYPHILITIC DISEASE OF THE LUNG. 



171 



pneumonia or fibroid induration. They may lead to bronchial irritation, 
induce pleurisy, or erode adjacent organs or bones. The general symptoms 
of non-malignant tumors within the lung are dyspnoea, which may depend 
upon pressure on the heart or trachea ; aphonia from pressure on the re- 
current laryngeal nerve ; pain from pleurisy or pressure ; cyanosis and 
dropsy of the head, neck and upper extremity, the result of pressure on the 
veins ; and changes in the pulse from pressure on the pneumogastric. There 
may be dysphagia. Cough and expectoration come from pulmonary hyper- 
emia and oedema. 

On inspection there may be local bulging or general enlarge?nent of the 
affected side with diminished respiratory movements. Vocal fremitus may 
be increased, or, if the tumor is large and presses on a large bronchus, it 
may be diminished or absent. There is an irregular outline of dulness over 
the seat of the tumor. On auscultation there may be bronchophony and 
bronchial breathing, or feeble respiration and feeble voice sounds over the 
seat of the tumor. 

Differential Diagnosis. — Pleurisy, phthisis and pneumonia are excluded 
very readily by their febrile phenomena, constitutional symptoms and phys- 
ical signs. The prognosis is always unfavorable, and the treatment is wholly 
symptomatic. 

SYPHILITIC DISEASE OE THE LUXG. 

The most common and certain changes in the lungs which can be ascribed 
to syphilis are gummata. 

Morbid Anatomy. — They vary in size from a pea to an egg, and are single 
or multiple ; they appear in the lungs as well-defined rounded tumors, often 
surrounded by a fibrous capsule, and are usually situated in the deeper pul- 
monary structures. Syphilitic fibroid infiltration originating about the 
interlobular blood-vessels, about gummata, or from an ulcerating peri- 
bronchitis does not become caseous, but may ulcerate or become gangre- 
nous. " Syphilitic pneumonia of the new-born" white hepatization, or 
" epithelioma as it is variously called, is a diffuse infiltration of one or both 
lungs. The organ is heavy, enlarged, dense, resistant and indenred by the 
ribs. White dry spots are seen on section. There is thickening of the alve- 
olar walls and minute bronchi, and thickening and obliteration of the pul- 
monary vessels. Syphilitic affection of the bronchial tubes is, in such cases, 
extensive. Gummata may be developed in the nodules of syphilitic pneu- 
monia. The bronchial glands are enlarged and often cheesy. Abscesses 
may form from suppuration in gummatous patches. The pleura may show 
fibroid thickening. Senile syphilitic gummata bear a close resemblance to 
caseous tubercle, but are much less friable — syphilitic patients often become 
phthisical, and there are good grounds for the belief that the phthisical 
developments commence in a proliferation of the pulmonary connective- 
tissue which terminates in the formation of gummata, and tha^ these gum- 
mata have a course and results similar to those of tubercle. 

Symptoms.— The symptoms are either the physical signs of a iumor, or of 
interstitial pneumonia. The diagnosis is reached by exclusion. The treat- 
ment is antisyphilitic. 



172 



DISEASES OF THE KESPIRATORY ORGANS. 



ATROPHY OF THE LUNG. 

This may be general or partial. 

Morbid Anatomy. — An atrophied lung is small, dry, anaemic, and some« 
what pigmented ; it pits readily and can be compressed into a very small 
space. In extreme old age the lungs atrophy, they crepitate less, the pleura 
over them is less moist than normal, and they cannot be inflated as normal 
lungs can. They lie close to the vertebral column, and their surface is un- 
even and " crumpled ;" the fissures change their position ; the lobes may 
be attached to one another by pedicles ; the alveoli have no definite form; 
and the cells are enlarged. The change in the lobes may bring the apex 
down to the base of the thoracic cavity. Atrophied lungs are " marbled " 
by lines and dots. The pulmonary artery and its branches are diminished 
in size, and the bronchial tubes are thinned. The first step toward atrophy 
is a general disappearance of the capillaries in the alveolar septa. Some 
fatty degeneration is always present. When it is the result of pressure by 
tumors, or liquid in the pleural cavity, the atrophy is generally limited to 
one lobe, and the atrophied part presents the lesions of interstitial pneu- 
monia. Pigmentation and atrophy, whether local or general, are usually 
associated. It is commonly best marked in the superior lobes. Sometimes 
the lobes appear to be adherent to one another. The right heart is gen- 
erally found in a condition known as " brown atrophy. " Bronchitis nearly 
always complicates it. The diaphragm is thin, flabby, and pale. 

Etiology. — Old age, pulmonary emphysema, and general marasmus are 
frequent causes of pulmonarj 7 atrophy. Pressure of a tumor or fluid ac- 
cumulation within the thoracic cavity may induce local atrophy. 1 

Symptoms. — Dyspnoea, cyanosis, and oedema and coldness of the extrem- 
ities are its only constant rational signs. 

Inspection reveals a small thorax ; the lower ribs are approximated, giv- 
ing a " pigeon-breasted " appearance. The whole thorax moves as if it 
were one piece, as in emphysema, and the chest movements are restricted. 

Percussion. — The percussion note is particularly loud, clear, and resonant ; 
but the pulmonary area is less than normal. The extent of the precordial 
dulness is increased. 

Auscultation. — The respiratory sounds lose their vesicular character and 
are feeble. 

Atrophy of the lung admits of no treatment. 

HYDATIDS OF THE LUNG. 

In this country hydatids of the lung is a rare disease. There is usually 
one tumor, and its most common seat is the lower portion of the right lung. 

Morbid Anatomy. — The cysts vary in size from that of an egg to that of a 
cocoa-nut. They are usually single, but may be multiple. They may be 
situated wholly w r ithin the lung, or be an outgrowth from the liver into the 
pleural cavity. The walls of the cysts vary in thickness and density. They 
develop in the interstitial tissue to which the parent sac is firmly adherent. 

1 Buhl (in Virchow's Archiv., Bel. XL, p 275) describes an atrophy observed by him in three cases of 
typhus fever analogous to acute yellow atrophy of the liver. He thinks it is due to a high L'rade of desqua- 
mative pneumonia, which latter disease will then come in the list of causes. 



HYDATIDS OF THE LUNG. 



J 73 




These ejsts may cause serious pulmonary complications by their pressure. 
They may suppurate and be discharged into the bronchi, and then a cavity 
may remain. In many cases a pulmonary hydatid cyst is the result of an 
hydatid of the liver which has ruptured through the diaphragm. Some 
authorities state that primary hydatids of the lung is a condition yet to be 
met with. General pleurisy is of rare occurrence ; for the slow growth of 
the tumor excites local adhesions rather than a general pleurisy. In some 
instances an hydatid cyst ruptures into the pleural cavity and causes 
empyema. Bronchitis, pneumonia, and gangrene may be excited in the 
surrounding tissue by the pressure of the hydatid tumor. 

Etiology. — Hydatids of the lung are nearly always secondary to hydatids 
of the liver. The affection is met with most in the Norse countries of 
Europe, where men and animals live together. 

Symptoms. — Hydatids of the lung, when small, give rise to no symptoms 
by which they can be detected ; but as they enlarge 
they excite bronchitis, attended by cough, with 
mnco-purulent expectoration, pain in the chest, a 
sense of suffocation, hemoptysis, night sweats, pallor 
and emaciation. When blood is expectorated goose- 
berry-like skins (the sacs of echinococci) or hook- 
lets may be found in the expectorated matter. Unless 
the daughter-cysts, or hooklets, are expectorated the 
diagnosis can never be positive. When an hydatid 
attains any considerable size it may cause bulging 3r 
of the chest wall and displace the mediastinum and Hydatids of the Lung. 

diaphragm. The circumscribed dulness on perCUS- Microscopical appearance of 
. . n , ,1 • ■, , i p t t* i i elements found in the sputum. 

sion, which may extend to the right or left of the A Hook8fr(m headofT(erda 
median line, with absence of respiratory sound and Echmococcus. 
vocal fremitus over the area of dulness, is a strong c.'SSSSk x 250. 
evidence of pulmonary hydatids. 

Differential Diagnosis. — The rupture of the cyst and the escape of its con- 
tents into a bronchial tube are its only diagnostic features and will prevent 
it from being confounded with any other condition. If an hydatid is super- 
ficial a portion of the fluid may be withdrawn by aspiration, and a micro- 
scopical examination will establish the diagnosis. It is impossible to dis- 
tinguish between hydatid tumors at the base of the right lung and those in 
the right lobe of the liver. 

Prognosis. — These tumors sometimes disappear by spontaneous retrogress 
sion, or by discharge into a bronchial tube ; or suppuration may be estab- 
lished in the cysts which afterward undergo calcification. Eecovery occurs 
in fifty per cent, of cases. Rarely do patients die from emaciation or ma- 
rasmus. They may die from suffocation, when the cysts rupture into the 
bronchi, from long-continued suppuration, or from an empyema estab- 
lished by the rupture of a cyst into the pleural cavity. Inflammation of 
any of the three adjacent serous membranes may cause death, or this may 
result from extensive hemorrhage and from gangrene. 

Treatment. — They should be treated as hydatids of the liver. It is a 
question if they should be injected with iodine. 



174 



DISEASES OF THE RESPIRATORY ORGANS. 



PLEURISY. 

Pleurisy is either a partial or general inflammation of one or both pleurae. 
It may run an acute, sub-acute, or chronic course, and have for its prod- 
ucts fibrin, serum and fibrin, serum, fibrin and pus, or new connective- 
tissue. I shall describe four varieties of pleurisy : — 

(1) Plastic or Acute Pleurisy ; (2) Serofibrinous or Sub-acute Pleurisy ; 
(3) Suppurative Pleurisy or Empyema ; (4) Interstitial Pleurisy. 

It is infrequent that the inflammatory products are confined to any one 
element. It is rather the preponderance of either the serous, fibrinous, 
or cellular element of the exudation that gives character to the disease. 
Most cases of pleurisy present at different stages, in varied proportions, 
all the inflammatory products except pus. 

PLASTIC OR ACUTE PLEURISY. 

In this variety the symptoms are well defined, the course rapid, and the 
exudation principally fibrinous. 

Morbid Anatomy. — The first stage of the inflammatory process is marked 
by a reddening of some part of the pleural membrane from hyperemia of 
the capillaries of the serous and sub-serous tissue with degeneration of the 
endothelial cells. The pleura loses its natural glistening appearance on 
account of a slight fibrinous exudation and the swelling and increase in 
number of its fixed connective-tissue cells, These changes take place dur- 
ing the first forty-eight hours. Following this, the fibrinous exudation 
increases and the free surface of the pleura assumes a rough, shaggy ap- 
pearance. If any serum exudes it gravitates to the most dependent por- 
tions of the pleural sac. In the substance of the pleura and in the fibrinous 
exudation new cells are now found which are young connective- tissue or 
pus cells. These cells are at first more numerous on the inner surface of 
the pleura. As the inflammation progresses they increase in number 
and collect on the free surface of the pleura under the fibrinous exudation. 
By the fifth day of the pleurisy new blood-vessels are formed in the fibri- 
nous exudation and become connected with the original vessels of the pleura. 

The nature of the subsequent changes will depend upon the intensity of 
the inflammatory process ; in the milder types the fibrin gradually dimin- 
ishes and disappears, some of the cells become fatty and are absorbed, and 
the remainder enter into the formation of abasement substance which grad- 
ually increases and finally a permanent new connective- tissue forms upon 
the inner surface of the pleura. If the inflammatory process subsides with- 
out much serous effusion, the opposing surfaces of the pulmonary and costal 
pleurae come into contact and adhesions are formed between them composed 
of permanent connective-tissue containing long, slender vessels. These 
adhesions follow the general law that governs all new connective-tissue : 
they may be permanent, or — their blood supply becoming insufficient — 
they may undergo fatty degeneration and be absorbed, the thickened pleura 
alone remaining to tell of the past inflammation. When an individual has 



PLASTIC OR ACUTE PLEURISY. 



175 



once had this form of pleurisy he will always have a permanent lesion. 
This pathological process may be completed in two weeks, or a serofibrin- 
ous effusion may not be absorbed for months, and then the pleuritic thick- 
ening becomes very extensive. 

Etiology.— The etiology of plastic pleurisy is sometimes very obscure. 
Exposure to wet and cold has been regarded as one of its most frequent 
causes, but it is very doubtful if it ever occurs as the result of simple expo- 
sure to wet and cold. In all cases that have come under my observation 
where it has followed such exposure, I have been able to find some previously 
existing predisposing cause. It may be the result of a penetrating wound, 
or blows upon the chest walls. Fracture of the ribs, if the broken ends of 
the ribs penetrate the pleura, may cause it. It is often a complication of 
other diseases, such as pyaemia, the exanthematous fevers, acute and chronic 
alcoholismus, acute rheumatism, Bright's disease, pneumonia, etc. Some- 
times it is the result of extension of inflammation from adjacent organs and 
tissues. While a certain proportion of cases of acute pleurisy are undoubt- 
edly of tubercular origin, the claim that all pleurisy is tubercular has not 
been sustained. It may occur at any age. Although it has been claimed 
that it never occurs in young children, my experience leads me to believe 
that it is of quite frequent occurrence in children of two or three years 
of age, and pus is usually formed in the pleurisies of children which 
occur as complications or sequelae of the exanthematous fevers. When- 
ever acute pleurisy occurs on the right side, it is important to determine 
if it is, or is not, the result of an extension of inflammation from the 
liver. 

Symptoms. — Plastic pleurisy may be mild or severe ; in either case it is 
ushered in by well-marked symptoms. The most prominent and constant 
at its onset is a sharp stitch-like pain in some portion of the chest ; it usu- 
ally is referred to the nipple of 
the affected side. Each inspira- 
tion increases its severity. The 
patient, to prevent motion of 
the affected side, assumes a pe- 
culiar position, leaning forward 
and toward that side. At first 
the countenance is pale and 
anxious ; after a few hours it 
becomes flushed. The pulse is 
accelerated, beating from 90 to 
120 per minute ; it is firm, 
small and tense in character — 
in this respect differing from 
the pulse of all other pulmonary fig. 38. 

diseases. The respiration is Temperature in a case of Acute Pleurisy. Patient set. 24. 

.Rccovcrv 

hurried and difficult ; each in- 
spiration is jerking in character; as soon as the general symptoms of 
pyrexia are present, the pain, in most esses, diminishes— in a small pro- 





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176 



DISEASES OF THE RESPIRATORY ORGANS. 



nortion of cases it maintains its intensity throughout the attack. The 
temperature follows no regular course and has no fixed relation to the pulse 
or respiration ; in ordinary cases it rarely rises aboye 100° F. ; in very severe 
cases it may reach 104° F. There is a short, dry, tearing cough, which 
is very distressing ; the patient restrains it as much as possible on account 
of the intense pain which it produces. In very severe cases of acute pleurisy, 
where the fibrinous exudation is very abundant and takes place rapidly, 
causing compression of the lung, the primary symptoms are very violent, 
resembling those of pneumonia. A distinct chill is followed by high 
fever, the temperature often reaching 105° F. The countenance assumes 
an anxious expression, the pulse beats 120 per minute and is feeble, but the 
pain in the side is not so severe as in the milder cases. Under these circum- 
stances, at the onset of the attack it is difficult to distinguish it from croup- 
ouspneumonia. Such severe cases are rare ; when they do occur they are apt 
to prove fatal. There are occasionally very mild cases of acute pleurisy which 
are attended by few of the subjective symptoms of pleurisy : the febrile move- 
ment is slight, the pain in the side is not severe, and cough and dyspnoea may 
be entirely absent. These patients continue their ordinary occupations, com- 
plaining only of an uneasy sensation in the side, and the disease would 
pass unrecognized but for the physical signs. Although the rational symp- 
toms of plastic pleurisy may vary in different cases and in some be very 
obscure ; the physical signs at once dispel all doubts. 

Physical Signs. — During the first twenty-four hours of plastic pleurisy, 
inspection will show the movements of the chest wall on the affected side 
to be more or less restricted. Palpation, percussion, and mensuration will 
give negative results. On auscultation the respiratory murmur will be 
found feeble over the affected side, and jerking in character both on in- 
spiration and expiration, and a grazing friction sound will be heard ; this 

friction sound will be most intense 
at the end of inspiration. 

As the plastic exudation takes place 
inspection will show a greater loss of 
expansive motion on the affected 
side ; and on palpation there will be a 
diminution of the vocal fremitus over 
its seat. On percussion there will 
be slight dulness over the seat of the 
pleurisy. The amount and extent of 
the dulness will correspond to the 
amount of the plastic exudation. 
Upon auscultation the respiratory 
murmur will be distant and feeble 
or entirely absent, and a crepitating 
friction sound will be heard both with 



Normal respiratory sound?. . . 



Crepitating friction 
sounds 



Respiratory mur- 
mur feeble or 
absent 

Flatness on percus- 
sion 

Absent vocal fre- 
mitus 

Absent voice 




Fig. 39. 



Diagram illustrating Physical Signs in Acute Plen- i T , Grin V {1 f ; nri nn rl Pvrnraf irm • it 
risy with a small amount of Effusion. Alter Da aspiration ana expiration , \X> 
Costa. 



IS 



usually most intense with inspiration ; 
this sound sometimes very closely resembles the so-called crepitant rale and 



PLASTIC OR ACUTE PLEURISY. 



177 



may be mistaken for it. At times this sound loses its crepitant character 
and becomes rubbing and sticky ; it is always due to the rubbing together 
of the two roughened pleural surfaces. Often it will not be heard unless 
the patient cough or take a deep inspiration. If the pleurisy is confined 
to the diaphragmatic or mediastinal pleura the friction sound will not 
be heard. 

If a considerable fluid effusion accompany the plastic exudation, the 
expansive movements on the affected side will be more restricted, and 
the vocal fremitus at the bottom of the pleural cavity will be markedly 
diminished. Upon percussion there will be flatness over the region occu- 
pied by the fluid. It is difficult, however, to recognize the presence of 
a small amount of fluid effusion, for the level of the fluid is not appre- 
ciably changed by changing the position of the patient. On auscultation 
the respiratory sounds will be absent below the level of the fluid, and 
feeble above it ; and both respiratory acts will be accompanied by the 
friction sound. 

During the period of absorption of the fluid and plastic exudation there 
will be a gradual return of the pulmonary resonance and of the normal, 
vocal, and respiratory sounds, and as the roughened pleural surfaces play 
upon each other, the friction sound will assume more of a rubbing char- 
acter. In some instances the friction sounds remain audible for a long 
time after the disappearance of all the other signs of pleurisy. Eetraction 
of the affected side does not follow acute pleurisy except in rare instances, 
when the inflammation has been very severe and a large plastic effusion 
has taken place. In those having extensive plastic exudations in acute 
pleurisy which compress the lung, the respiratory sound may assume a 
bronchial character and be mistaken for that of a pneumonic condition. 

Differential Diagnosis. — In the majority of cases the diagnosis of plastic 
pleurisy is easily made. Acute pneumonia is the only disease with which 
it is liable to be confounded. In both affections there are dyspnoea, fever, 
and cough ; but in pleurisy the temperature rarely rises above 100° F., 
while in pneumonia it usually reaches 103° F. within the first twenty-four 
hours. The cough of pleurisy is short and hacking, and is attended by 
little or no expectoration, whereas in nearly every case of pneumonia expec- 
toration is present, and the substance expectorated is characteristic of the 
pneumonia. The countenance at the onset of pleurisy is pale and anxious ; 
in pneumonia it is flushed and the cheeks have a purple hue. There is also 
a very marked difference in the physical signs of the two diseases. In pleu- 
risy the vocal fremitus over the affected portion of the pleura is somewhat 
diminished ; in pneumonia it is more or less increased. In pleurisy the 
respiration is feeble ; in pneumonia it is rude or bronchial. In pleurisy a 
grazing, rubbing, or crepitating friction sound is heard with both respira- 
tory acts. In pneumonia the crepitant rale is heard at the end of inspira- 
tion. Sometimes it is difficult to distinguish a crepitating friction sound 
from a sub-crepitant rale, but, as the sub-crepitant rale is not present until 
the last stage of pneumonia, the question will not arise if the patient is seen 
before that period has arrived. 

12 



178 



DISEASES OF THE RESPIRATORY ORGANS. 



Occasionally it is difficult to make a differential diagnosis between inter- 
costal neuralgia or pleurodynia, and acute pleurisy. Intercostal neuralgia 
or pleurodynia may be attended by many of the ushering-in symptoms of 
acute pleurisy. They may come on after exposure, be attended by violent 
pain in the side, jerking respirations, anxious countenance, and often by 
considerable fever. On physical examination the respiration may be as 
feeble as in the first stage of pleurisy. The presence or absence of a pleuritic 
friction sound, and the painful points on pressure, are the principal points 
of difference. 

Prognosis. — The prognosis m plastic pleurisy is generally good. Its natu- 
ral termination is in recovery within two or three weeks after its commence- 
ment. But it is to be remembered that patients even with the milder form 
of the disease are liable to have frequent pleuritic thickenings and adhesions 
between the pulmonary and costal pleurae. These thickenings predispose 
to other attacks of pleurisy, and each new attack interferes more and more 
with the expansion of the lungs and leads to the development of intersti- 
tial pneumonia or bronchitis, and finally to fibrous phthisis. If this form 
of pleurisy complicates any grave form of disease, as septicaemia, pyaemia, 
Bright's disease, etc., there is a liability to acute empyema. In some very 
acute cases, where there is a large plastic exudation, death may result in a 
few days. 

Treatment. — The only remedial agent which has seemed to me to have a 
controlling power over acute pleurisy is opium. The best method of admin- 
istering it is by the hypodermic injection of morphine. It has been claimed 
that free blood-letting at the commencement of an acute pleurisy will arrest 
its progress. But the facts deduced from recorded cases are strongly against 
this statement. A free general bleeding will undoubtedly relieve the pleu- 
ritic pain with great promptitude, but no more so than a hypodermic of 
morphine, and the morphine does not increase the liability to a large serous 
effusion, as does general bleeding. For the successful management of 
ordinary acute pleurisy all that I have found necessary is to place the 
patient in bed. This is important, however mild the attack may be. The 
sick room should be well ventilated and kept at an even temperature of about 
65° F. The patient should be allowed to assume that position in bed which 
he finds most comfortable. He should be forbidden to talk, and should be 
prevented from making any unnecessary movements, and a nutritious diet 
without stimulants should be given him. If he is robust, three or four 
leeches may be applied over the seat of pain, and followed by an anodyne 
poultice. Hypodermics of morphine must be given in sufficient quantities 
to relieve all pain. After the first week the morphine can usually be dis- 
continued and the patient will be able to sit up, and, at the end of three 
weeks, to resume his ordinary occupation unless it requires great physical 
exertion. If there is an abundant plastic or serous exudation the convales- 
cence will be reached more slowly and the recovery will be less complete. 
In such cases there will be some crippling of the lung, and pain and uneasi- 
ness in the affected side will continue for months. After recovery it is well 
to inform the patient that he may expect pain after active physical exer- 
cise. If the patient presents the signs of anaemia, the syrup of the iodide 



SEROFIBRINOUS OR SUB-ACUTE PLEURISY. 



179 



of iron should bo given in teaspoonful doses three or four times each day. 
Stimulants should rarely be allowed before the third week. Counter-irri- 
tation by means of cups and blisters is rarely of service in the treatment of 
this form of pleurisy. I have found in some cases, when the pain in the 
side continued after the friction sound had disappeared, that the use of the 
constant current over the affected side for twenty minutes at a time gives 
almost instantaneous relief. 

SEROFIBRINOUS OR SUB-ACUTE PLEURISY. 
{Pleurisy with Effusion.) 

This is the most common form of pleurisy, and the inflammatory process 
usually invades the whole of the pleura on the side affected. It may 
commence at any point on the pleural surface, but it most frequently com- 
mences on the costal portion. 

Morbid Anatomy. — The anatomical changes in this form are similar 
to those which take place in acute pleurisy, except that the new tissue 
formations are more extensive, the pleural membrane more uniformly 
thickened, and more frequently the seat of tubercle, and there is more 
abundant serous effusion containing flocculi of lymph. The pleural 
cavity may be partly or completely filled with fluid. The entire pleura 
becomes coated with a layer of fibrin varying in thickness, usually most 
abundant on its costal portion. New connective-tissue cells and base- 
ment substance are mingled with the exudation. Sometimes the serous 
effusion contains blood globules from the rupture of the thin-walled 
vessels in the new connective-tissue. It is the large amount of serous 
effusion, containing more or less cellular elements, that distinguishes 
sub-acute from acute pleurisy. This indicates a difference in the grade 
rather than in the nature of the inflammatory process. When the cell ele- 
ments are abundant it is characterized as a sero-purulent effusion. If the 
pleural cavity is not filled with fluid, the effusion will occupy the most 
dependent portion of the pleural cavity. It may be confined to circum- 
scribed portions of the pleural cavity by adhesions. If it occupy the most 
depending portion of the cavity the adjacent lung-tissue will be compressed 
and pushed upward. When the pleural cavity is filled with fluid the in- 
tercostal spaces will be more or less bulging, the diaphragm will be pushed 
downward, and the abdominal viscera upon either side may be displaced 
downward ; the heart will be displaced either to the right or left, accord- 
ing as the fluid occupies the left or right pleural cavity. The lung on the 
affected side is compressed either toward the vertebral column or upward 
and inward against the mediastinum. Occasionally the lung occupies 
the anterior portion of the pleural cavity and the fluid the posterior 
portion ; the direction of the compression is influenced by the location 
and extent of previous pleuritic adhesions. If no adhesions exist the 
lung may be compressed to one-eighth of its normal size, and assume a 
pale-red or greenish color, have a tough, leathery feel, and be entirely 
void of air. With the compression of the lung there may be compression 
of the bronchi, but the larger bronchial tubes usually remain pervious. 

If recovery takes place the fluid disappears by absorption, the fibrin 



180 



DISEASES OF THE RESPIRATORY ORGANS. 



undergoes fatty metamorphosis, liquefies, and slowly disappears. As the 
fluid disappears the thickened pleural surfaces come in contact, and more 
or less extensive adhesions form between the two surfaces. On account of 
the changes which take place in the pulmonary pleura the lung-tissue does 
not expand to its normal dimensions, but more or less retraction of the 
chest walls on the affected side takes place. The longer the fluid remains 
in the pleural cavity the more extensive will be the retraction. As the 
fluid disappears, the organs which have been displaced by its pressure re- 
turn to their normal positions. If the retraction is considerable they will 
be displaced upward, and the heart may be drawn from its normal position 
to the right or left. 

Etiology. — The causes of this form of pleurisy may be the same as those 
of plastic pleurisy. In a large proportion of cases it is secondary to some 
form of organic disease, as chronic Bright's disease of the kidneys, pulmo- 
nary phthisis, etc. Occasionally it seems to occur idiopathically, or at least 
from causes not well understood. It is a clinical fact familiar to every 
careful observer that sub-acute pleurisy is not infrequently the first step 
to the development of phthisis. It is claimed that serofibrinous pleurisy 
is always of tubercular origin. While it is undoubtedly often induced by 
tuberculosis of the pleura, it is at present not proven that such is its sole 
cause. The weak and enfeebled, rather than the strong and robust, are 
liable to attacks of sub-acute pleurisy. 

Symptoms. — This form of pleurisy may come on suddenly with active 
symptoms, or insidiously with very mild symptoms. In the majority of 
cases the symptoms are mild. There is no chill of invasion ; it comes on 
insidiously after exposure to wet, cold, and fatigue, in the enfeebled or in 
those who are suffering from some chronic disease. It is rarely attended 
by any noticeable pain in the side, or at least not by the severe pain which 
attends acute pleurisy. On close questioning the patient will state that 
some time before exposure an uneasy sensation in the affected side, attended 
occasionally by a sharp pain of short duration, was experienced. This 
form of pleurisy is often so insidious in its approach that the patient will 
be unable to tell when he commenced to be sick ; for a period of several 
weeks he will have gradually lost flesh and strength, yet will have been 
able to attend to bis ordinary avocations if they required but little physi- 
cal exertion. There will be slight dyspnoea on exertion, with slight febrile 
excitement at night. Sometimes there is an almost continual cough with 
a scanty muco-purulent expectoration ; at other times the cough will be 
entirely absent. Usually when this class of patients consult a physician 
the only subjective symptoms will be a frequent, small, feeble pulse, and 
slight heat and dryness of the skin, the temperature rarely rising above 
101° F. The countenance will be pale and anxious, and the breathing short 
and catching in character. On speaking, especially after exercise, the sen- 
tences are uttered in a broken, interrupted manner. The patient will be un- 
able to lie comfortably except on his back, or on the affected side with his 
head slightly elevated. The pulse, usually small and feeble, will vary from 
110 to 120 beats in the minute ; in fact, there will be no subjective symptom 
which will enable one to reach a positive diagnosis. 

In those cases which are ushered in by active symptoms the invasion will 



SEROFIBRINOUS OR SUB- ACUTE PLEURISY. 



181 



resemble that of acute pleurisy. There will be rigors followed by a tem- 
perature of 102° or 103° F.; the pulse will be full aud frequent, the pain 
on the affected side well marked and the breathing rapid and shallow. 
Patients will sometimes ascribe the pain to the lumbar region, as in ne- 
phritic colic, for which it is sometimes mistaken. After a few days the fe- 
brile symptoms abate, but do not entirely subside, and the serous effusion, 
which is much larger than that in acute pleurisy, for a time steadily in- 
creases, then remains stationary for a number of days or even weeks, and 
then there is a sudden renewal of the febrile symptoms, the dyspnoea is 
greatly increased, the cough becomes more constant and harassing, the pa- 
tient is unable to lie down, and the fluid rapidly increases ; in twenty-four 
hours the pleural cavity, — which previously has been only half full of 
fluid, — becomes entirely filled, and the dyspnoea becomes so urgent, and 
the danger from collateral congestion and oedema of the opposite lung so 
imminent, that immediate relief is demanded by paracentesis. With the 
rapid increase of the effusion the pain in the side subsides. However ill- 
defined the rational symptoms may be in acute pleurisy, its physical signs 
are more distinctive than in any other thoracic disease. 

Physical Signs. — The physical signs of pleurisy with effusion will vary with 
the amount of the fluid effusion. At its onset, before there is much fluid 
effusion, a friction sound will be heard over the affected side with more or 
less feebleness of the respiratory sound. After the pleural cavity partly fills 
with fluid, the vocal fremitus will be diminished or absent at the bottom 
of the pleural sac below the level of the fluid ; there will be flatness on per- 
cussion, and an absence of vocal and respiratory sounds. A change in the 
position of the patient will change the level of the fluid and the line of 
flatness. Above the level of the fluid the percussion resonance will be nor- 
mal or exaggerated, and in some cases tympanitic in quality. The respira- 
tory murmur will be exaggerated, and at the level of the fluid it may as- 
sume a bronchial character. The vocal sounds may be intensified, or a 
distinct bronchial voice may be heard. All of these physical signs are 
most marked posteriorly. 

When the pleural cavity is completely filled with fluid, and the lung is 
compressed backward against the spinal column, important modifications 
in the physical signs take place. 

Inspection will show an enlargement of the affected side, and a bulging 
of the intercostal spaces. The respiratory movements on the affected side 
will be changed from an up-and-out movement to a direct up-and-down 
motion, while on the unaffected side the expansive respiratory movements 
are increased. If the effusion is in the left pleural cavity the heart will be 
displaced to the right, and the apex beat may be noticed under the right 
nipple ; if it occupies the right pleural cavity the apex beat will be carried 
to the left, beyond its normal position. 

The circumference of the affected side at the end of expiration, will be 
one or two inches greater than that of the healthy side ; but at the end of 
inspiration the difference will be but slight. The expansive motion in in- 
spiration on the healthy side may be two or three inches greater than on 
the affected side. 



182 



DISEASES OF THE RESPIRATORY ORGANS. 



On palpation there is usually diminished or absent vocal fremitus over 
the affected side. In exceptional cases, however, the vocal fremitus persists 
and may he increased even token the cavity is filled with fluid. 

Upon percussion there will be flatness over the whole of the affected side ? 
and the flatness will extend below the normal limits of the lung. 

On auscultation there is usually entire absence of the respiratory sounds 
over the affected side, and the vocal sounds will be distant and indistinct. 
Not infrequently, however, at the upper and posterior portion of the 
pleural cavity distant bronchial respiration and bronchophony will be heard. 
The bronchial respiration and the bronchial voice are sometimes diffused 
and heard over the whole of the posterior portion of the affected side. 

As the fluid subsides in the pleural cavity, inspection shows that the en- 
largement of the affected side is decreasing, that the intercostal spaces 
are regaining their normal condition, and that the respiratory movements 
are returning. Mensuration shows a gradual diminution in the size of the 
affected side until it becomes smaller than the other. On percussion the 
pulmonary resonance will gradually return, first at the upper portion of the 
pleural cavity ; but it is not completely restored until some time after 
the fluid has disappeared, especially over the lower portions of the pleural 
cavity. 

On auscultation, as the fluid disappears, the vocal and respiratory sounds 
will gradually return. At first, the respiratory sounds are feeble and dis- 
tant ; gradually they become more and more distinct. As the two rough- 
ened pleural surfaces come in contact and move on each other, a creaking, 



Absent respiratorxj motion 

Diminished or absent vocal fremitus 



Flatness on percussion 



Absence of respiratory murmur in 
front, bronchial breathing behind. 

Vocal sounds distant or absent 



Fig. 40. 

Diagram showing Physical Signs in Pleurisy with Effusion ; pleural cavity filled with fluid. 

rubbing, friction sound is heard. These rubbing friction sounds are often 
audible for months after the fluid has disappeared. If, as sometimes hap- 
pens, the lower portion of the affected lung remains permanently imper- 
vious to air, the upper portion of the lung becomes emphysematous. Un- 
der such circumstances the emphysema is compensatory, and the percussion 




SEROFIBRINOUS OR SUB-ACUTE PLEURISY. 



183 



note in the infra-clavicular space on that side will have a tympanitic 
quality, and the expiration in this space will become prolonged, harsh, and 
blowing in character. 

Differential Diagnosis. — The diagnosis in uncomplicated cases of sub- 
acute pleurisy is usually very readily made. The diseases with which it is 
most likely to be confounded are 'pneumonic or phthisical consolidation of 
the lung, enlargement of the liver or spleen, cancer of the lung and pleura, 
and intra-thoracic tumors. It is hardly possible for a thoracic aneurism 
to be developed in such a manner as to be mistaken for sub-acute pleurisy. 
Pleurisy with effusion may be distinguished from phthisical and pneu- 
monic consolidation by the history of the case, by the absence of the charac- 
teristic expectoration, and by the lower range of temperature. Upon phys- 
ical examination it may be distinguished by the enlargement or retraction 
of the affected side, by the diminution or absence of vocal fremitus, and by 
the flat note of the percussion sound. If the cavity is partly filled, by 
the change in the line of flatness on change in the position of the patient, 
and by the feeble or absent respiratory sounds over the fluid. The bron- 
chial respiration which is sometimes heard over a pleural cavity filled with 
fluid differs from the bronchial respiration of pneumonic or phthisical con- 
solidation, in that it is more diffused and less tubular in quality. In 
phthisical consolidation the progress of the physical signs is usually from 
above downward ; in pleuritic effusion they advance from below upward. 
Phthisis of an entire lung rarely exists without the other lung being in- 
volved, while any -amount of pleuritic effusion may exist in one cavity, and 
the other remain unaffected. If doubt exists after considering all these 
points of difference, it may be removed by the use of an exploring 
trochar. 

Serous effusion into the right pleural cavity is distinguished from an 
enlargement of the liver upward, by the fact that when percussion is made, 
the patient being in a sitting posture, the line of flatness in liver enlarge- 
ments is higher in front than behind. The liver does not enlarge in such 
a manner as to fill the pleural cavity posteriorly and anteriorly to the same 
level. 

Sub-acute pleurisy of the left side will rarely be mistaken for enlarge- 
ment of the spleen, for when the spleen is sufficiently enlarged to encroach 
upon the left pleural cavity the enlargement will be downward as well as 
upward, the splenic tumor will be readily felt in the abdominal cavity, and 
the flatness on percussion at the lower portion of the pleural cavity will 
be continuous with the tumor in the abdomen. 

The diagnosis between pleurisy with effusion and cancer of the lung or 
pleura is often very difficult, and in some instances, if one relies only upon 
the rational symptoms and physical signs, it will be impossible. All such 
doubtful cases can only be decided by the use of the exploring trochar. 
The needle of the exploring trochar can be introduced into the thoracic 
cavity without the least danger, whether the needle enter a pleuritic effusion, 
a hepatizecl lung, a cancer of the pleura or lung, or an aneurism. 

Prognosis. — The prognosis in sub-acute pleurisy varies greatly in different 
cases. "While the majority will terminate in recovery, sudden death occurs 



184 



DISEASES OF THE RESPIRATORY ORGANS. 



in a limited number without lesions to account for it. A large serous effu- 
sion may take place suddenly, and cause death by its interference with res- 
piration and circulation. Cases may be protracted over a period of months, 
and finally a sero-fibrinous effusion may change into a sero-purulent one, 
and a sub-acute pleurisy may thus become an empyema ; in giving a prog- 
nosis it is to be remembered that in most cases that recover, more or less 
extensive adhesions result, which cause permanent crippling of the lung, 
and lead to the development of more or less extensive compensatory 
emphysema, chronic bronchitis, and fibroid induration of lung- tissue. 
When the new tissue formations are extensive, and the general health 
much impaired, in those who have a strong hereditary or acquired 
tendency to pulmonary phthisis, there is always danger that the new 
tissue may become tubercular, even when the pleurisy was not of tuber- 
cular origin. 

Treatment. — The main thing to be accomplished in the treatment of sub- 
acute pleurisy is to remove the fluid effusion as rapidly as possible, at the 
same time taking care to sustain the patient. The principal means which 
have been employed for the accomplishment of this object are hydragogue 
cathartics, diuretics, diaphoretics, and blisters applied in succession over 
different parts of the affected side. On account of the anaemic condition 
of the majority of these patients, general or local bleeding, as well 
as the use of mercury, is now very rarely employed ; for a like reason I 
very much question the beneficial effects claimed for cathartics, diuretics 
and blisters ; it is very questionable if the condition which favors the ab- 
sorption of the fluid in the pleural cavity can be reached by the employ- 
ment of any of the so-called depurative remedial agents. It is claimed that 
the use of hydragogue cathartics and diuretics quickly removes large quan- 
tities of fluid from the body, and consequently the fluid portion of the 
blood is greatly diminished, and that whenever a cavity contains fluid, the 
absorbents and blood-vessels of the part take it up to replace that lost by 
the blood, and thus fluid in the pleural cavity is absorbed. There is little 
doubt but that hydragogue cathartics and diuretics will hasten the absorp- 
tion of non-inflammatory serous effusion in simple hydrothorax, but there is 
no evidence that they have power to promote the absorption of inflammatory 
products from the pleural cavity in sub-acute pleurisy. It is certain that 
by the action of these depurative means the vital powers of the patient are 
greatly enfeebled and the processes of digestion and nutrition seriously in- 
terfered with. It is also well established that when the nutritive processes 
are going on most rapidly absorption takes place most rapidly. Conse- 
quently anything that interferes with these processes is contra-indicated in 
the treatment of this form of pleurisy. There are also other conditions 
which greatly impede the absorption of the fluid effusion in pleurisy. 
When the pleural cavity is distended with fluid, its absorption is impeded 
or prevented by the obstruction offered to the flow of blood through the 
pleural and sub-pleural vessels by the pressure. Under such circumstances it 
is useless to resort to diuretics and hydragogue cathartics. The mechanical 
withdrawal of a sufficient amount of liquid to relieve the tension of the cavity 
and remove the pressure from the lung and the sub-pleural veins is an abso- 



SEROFIBRINOUS OR SUB-ACUTE PLEURISY. 



185 



lute necessity before the processes of absorption can commence. If the surface 
of the pleura is covered by a thick layer of exudative material, this layer is 
interposed between the sub-pleural vessels and the fluid effusion, and must 
greatly interfere with the absorption of the liquid ; as it becomes thicker 
and thicker by successive deposits of fibrin, it is obvious that the longer the 
liquid remains in the pleural cavity the thicker the fibrinous deposit be- 
comes, and the less is the probability that the liquid will be absorbed. 
Against these conditions cathartics and diuretics are powerless. 

For many years I have rarely employed any depurative agents in the treat- 
ment of sub-acute pleurisy. The remedial agent which seems to me to have 
the greatest power in promoting the absorption of an effusion is the syrup 
of the iodide of iron. In connection with the administration of iron the 
patient should take the largest amount of the most nutritious food, with 
wine or some form of alcoholic stimulant. The principle of treatment 
is to employ all those remedial and hygienic measures which improve 
nutrition. 

As so little can be done by medication to excite or hasten the absorption 
of pleuritic effusion, the question of the employment of mechanical means 
for its removal presents itself. There is some difference of opinion in the 
profession upon this point. One class of observers claim that a single re- 
moval of the fluid is of little service, and that the danger of admitting air 
into the pleural cavity is so great that if the operation is frequently per- 
formed. a serous effusion is very apt to be changed into a purulent one, thus 
jeopardizing life. On the other hand, the advocates of the operation main- 
tain that if the fluid is permitted to remain in the pleural cavity it becomes 
purulent. The causes which impede or render impossible the absorption of 
the fluid seem to me reasons in favor of its early mechanical removal, es- 
pecially as the practice of aspiration has inaugurated a new era in the 
management of these cases, and has removed all objections to such early 
removal. When a perfect instrument is used and a small needle intro- 
duced into the pleural cavity, the entrance of air is impossible. In any 
case of pleurisy, when the accumulated fluid remains stationary for one 
week, or is increasing after the cavity has become half filled, and especially 
when the cavity is completely full, there should be no delay in aspirating. 
With every day that the lung remains compressed, and with every addition 
to the plastic deposit upon the pleural surfaces, the chances of its absorp- 
tion are diminished, and the danger that the lung will be permanently 
crippled is increased. 

The following rules should be observed in the performance of aspira- 
tion of the chest. Place the body of the patient in the erect posture, lean- 
ing somewhat forward, with the arm of the affected side thrown partly 
across the chest. This position of the arm is preferable to any other for 
the reason that the integument is not made unnaturally tense over the inter- 
costal spaces. Select a needle of small size for the first tapping, and in- 
troduce it to the depth of at least one inch into the fifth or sixth inter- 
costal space, at the junction of the axillary and infra-scapular regions. 
After the needle has been introduced the fluid may be permitted to flow 
through the instrument until the patient complains of a sense of con- 



186 



DISEASES OF THE RESPIRATORY ORGANS. 



striction about the chest, when the withdrawal of the fluid must bft 
stopped. The amount of fluid that can be withdrawn at the first aspiration, 
if the cavity is distended, will depend upon the length of time which the 
fluid has remained in the pleural cavity. If it has accumulated rapidly, 
the cavity may frequently be emptied without giving rise to any un- 
pleasant symptoms ; if, however, it has been slow in its accumulation 
and the pleural cavity has contained a large quantity of fluid for a consid- 
erable time, only a small amount can be withdrawn without producing a 
severe attack of dyspnoea. When this is the case the patient may be per- 
mitted to remain quiet for a few days, and then the operation should be 
repeated as often as it can be without producing unpleasant symptoms. 
The sense of constriction about the chest always indicates that no more 
fluid should be withdrawn at that time. It is claimed by some that aspira- 
tion of the chest in pleurisy may cause death suddenly or within twenty-four 
hours after the aspiration, and that the cause of death under such circum- 
stances cannot be accounted for, as there are no lesions found after death 
which are sufficient to produce it. I cannot understand how this is pos- 
sible if the aspiration is performed with sufficient care ; it certainly has 
never happened in any of my cases. I can conceive how the sudden with- 
drawal of a large quantity of fluid from the left chest might cause a severe 
attack of syncope from which a crippled heart might not rally. I have no 
hesitation in recommending this operation in all cases, provided it be done 
according to the rules just given, and I am not disposed to delay aspiration 
long after the pleural cavity has once become filled with fluid, for I am 
convinced that its early removal tends to promote a more rapid recovery, 
and prevents those changes in the pleura which lead not only to a tedious 
convalescence, but also to an incomplete ultimate recovery. 

SUPPURATIVE PLEURISY, OR EMPYEMA. 

{Pleurisy with a Sero-fibrinous and Purulent Effusion.) 

This is a suppurative inflammation of the whole pleura, usually confined 
to one side of the chest. It may be primary or secondary. When it is 
primary it usually commences as an acute affection ; when secondary, it is 
sub-acute or chronic from its commencement. 

Morbid Anatomy. — The pathological changes in this form of pleurisy are 
most extensive and best marked on the costal, diaphragmatic, and medias- 
tinal portions of the pleural membrane. In primary suppurative pleurisy 
there is poured out a large amount of plastic material which undergoes 
histological transformation into pus, and thus a large amount of thick pus 
is rapidly formed in the pleural cavity. In the secondary variety of sup- 
purative pleurisy a sero-purulent effusion will slowly accumulate in the 
pleural cavity, varying in consistency in different cases, sometimes being 
quite thin and mainly composed of serum, at others extremely thick and 
containing comparatively little serum. This purulent fluid usually occu- 
pies the most dependent portion of the pleural cavity ; it may, however, be 
confined either to the posterior or anterior half of the chest by old adhesions. 

The manner in which large purulent accumulations are formed in the 



SUPPURATIVE PLEURISY, OR EMPYEMA. 



18? 



pleural cavity is as follows : — in acute suppurative pleurisy with sero-fibri- 
nous exudation, a large number of pus cells form in the connective-tissue of 
the pleura and also on its surface, from which they are washed into the 
cavity, along with the fibrinous exudation, by the serous effusion. Some- 
times the accumulation is very large and takes place very rapidly. This is 
characteristic of the pleurisies which occur in connection with pyaemia. A 
sero-fibrinous exudation may become purulent when a fresh cause of in- 
flammatory irritation gives rise to an active cell-exudation ; the new irrita- 
tion may come from the admission of an* into the pleural cavity, or from 
some change in the fluid which has previously occupied the cavity, or, per- 
haps, from suddenly developed sepsis. Under these circumstances a variety 
of cell-formative processes are established. Some are produced in the plas- 
tic exudation, and some in the pleura itself. The clear serum becomes tur- 
bid, shreds of false membrane are loosened from their connection with the 
underlying tissue and undergo liquefaction, and the whole, or a large por- 
tion of the pleural membrane becomes a suppurating surface, and thus a 
large amount of pus is formed in the pleural cavity. If the pleural cavity 
is aspirated at the commencement of the purulent process in such cases, the 
first fluid removed will be found to contain a moderate number of cells ; at 
a second operation, a week or two later, a large number of cells may be 
found, and it is usual under such circumstances to attribute the increased 
number of cells to the effects of the first aspiration. This is not, however, 
a legitimate inference, for the increase in the cell development is the 
natural result of the morbid process which was in oj^eration at the first 
aspiration. 

Purulent accumulations in the pleural cavity may become so large that 
death may ensue in consequence of the depression caused by their pro- 
duction. The tendency of suppurative pleurisy is never toward convales- 
cence, unless by spontaneous openings. The inflammatory process is not 
limited to the pleura ; it may extend from the costal, pleura to the connec- 
tive-tissue underneath, to the periosteum of the ribs, causing necrosis, 
or it may perforate the walls of the chest and be discharged externally. In 
some instances the lung may be perforated and the discharge take place 
through a bronchial tube, or the diaphragm may be perforated and the pus 
find its way into the abdominal cavity. If the patient survives the empty- 
ing of the pleural cavity, repair is accomplished by the rapid and abundant 
formation of cicatricial tissue ; the pleural cavity is contracted in every di- 
rection like a huge cicatrix, the chest walls on the affected side retract to 
their fullest extent, and the thoracic and abdominal viscera are dragged out 
of their normal positions to help fill the space formerly occupied by lung- 
tissue. In some cases of circumscribed empyema the fluid portion of the 
pus is absorbed and the solid constituents undergo cheesy transformation, 
the salts of lime are deposited and the thickened pleura becomes calcified. 
The bony or calcareous plates which are occasionally found in the pleural 
cavity at post mortem examinations usually have their origin in an 
empyema. 

Etiology. — The cause of suppurative pleurisy is not always readily de- 
termined. It may be of traumatic origin. When it occurs spontaneously 



188 



DISEASES OF THE RESPIRATORY ORGANS. 



it is always associated with some vice of constitution, such as results from 
some exhausting disease, or the debility which attends chronic alcoholismus. 
It often complicates acute and chronic infectious diseases. In the en- 
feebled it is frequently developed from a sero-fibrinous pleurisy which has 
continued for a long time, but in most instances, under such circumstances, 
the occurrence of the suppurative process is due to some new infection, 
or to some new local excitement of pleuritic inflammation. Chronic 
tubercular pleurisies are very apt to be suppurative in character. It may 
be secondary to abscess of the liver, or to the opening into the pleural 
cavity of a vomica in the lung in chronic phthisis. An abscess in the 
abdominal cavity or in the chest walls may open into the pleura, and 
establish a suppurative pleurisy. 

Symptoms. — The rational symptoms of empyema will vary with its char- 
acter. Those cases in which the inflammatory processes are acute at the 
onset, accompanied by the rapid production of fibrin and pus, will be 
ushered in by chills, followed by a rapid rise in temperature, and a rapid, 
full pulse. There will be severe pain in the affected side, with the signs of 
great prostration. The prostration is greater than in acute fibrinous pleu- 
risy, and the countenance early assumes an anxious expression ; if the in- 
flammatory products become gangrenous the prostration is extreme, and the 
patient presents the appearance of one suffering from peritonitis ; typhoid 
symptoms manifest themselves very early ; and these cases usually termi- 
nate fatally within two or three weeks. In other cases the active symptoms 
subside after a week or ten days, and symptoms of the more chronic form 
of empyema are developed. The symptoms of chronic empyema are often 
very obscure ; the presence of pus in the pleural cavity in these cases can- 
not be determined either by the rational symptoms or by physical signs. 
The patient rarely suffers from local pain — there is simply a sense of un- 
easiness, or weight in the affected side ; there is a gradual loss of flesh and 
strength ; the countenance assumes a pale, anxious expression ; and there 
is an irregular diurnal chill followed by profuse sweats. Ordinarily the 
patient has a cough with a scanty muco-purulent expectoration, the voice 
becomes weak and there is more or less dyspnoea, and the patient gradually 
assumes the appearance of one in the last stages of pulmonary phthisis. If 
empyema occurs as a complication of septicaemia or pyaemia, its commence- 
ment is also, at times, very insidious. In these conditions patients some- 
times pass into a semi-comatose state. Not infrequently pyaemic patients 
make no complaints which would direct attention to the pleura, and the 
pleural cavity may be found two-thirds full of pus, without having given 
a single symptom of its presence. 

If an empyema is about to open externally, it will usually make itself 
manifest by a protrusion between the ribs, which gives a sense of fluct- 
uation, and after a time grows red, aud finally a valvular opening is 
formed and pus is discharged. If the opening takes place through the 
lung into a bronchial tube, the discharge of pus is ordinarily preceded 
by symptoms of pneumonia ; the patient will have a chill, followed by 
a cough and a more or less profuse expectoration containing blood, which 
will be followed by a profuse purulent expectoration, which will afford 



SUPPURATIVE PLEURISY, OR EMPYEMA. 



189 



marked relief. The profuse purulent expectoration will occur two or 
three times a day ; the chest walls gradually retract, and finally the ex- 
pectoration will cease altogether and the pleural cavity become obliterated. 
If the opening takes place into the peritoneal cavity, its occurrence is 
usually followed by a rapidly fatal peritonitis. If the communication 
is established with the intestinal canal, pus will appear in the discharges 
from the bowels. If the patient survives the establishment of either 
an external or internal opening, spontaneous or artificial, a connec- 
tive-tissue development takes place in the pleural cavity, and as the con- 
tents of the cavity are being discharged retraction of the chest and dis- 
placement of the abdominal and thoracic viscera take place ; this process is 
necessarily slow, and years may elapse before it is completed. 

Physical Signs. — The physical signs of empyema are essentially the same 
as those of pleurisy with effusion, except that the level of the fluid is not so 
readily changed by a change in the position of the patient ; if, however, 
the physical signs indicate the existence of fluid in the pleural cavity in 
one who is very much debilitated, who has a constant cough with muco- 
purulent expectoration, hectic fever with profuse sweats, and whose history 
indicates that the fluid has existed for a long time, one may be almost cer- 
tain that the fluid is purulent. 

Differential Diagnosis. — Unless a fistulous opening exist, a positive diag- 
nosis of empyema is impossible, except by an explorative puncture. 
When such a puncture has been made, and some of the contents of the 
pleural cavity have been drawn on* and subjected to microscopical ex- 
amination, it is not possible to confound an empyema with any other 
thoracic disease. 

Prognosis. — The prognosis in empyema is unfavorable. In acute sup- 
purative pleurisy death may occur at the end of one or two weeks. In the 
more chronic cases it may take place from gangrene produced by decompo- 
sition of the inflammatory products in the pleural cavity. Statistics show 
that in empyema of slow development, where spontaneous openings occur, 
about one in five recover, while in those in whom artificial openings are 
established the rate of mortality is greater. This class of patients die 
from the exhaustion produced by the accumulation of large quantities of 
pus, and from the exhaustion which attends a prolonged and abundant 
purulent discharge. A large number of these patients live for a year or 
more. The judicious use of the aspirator will tend to render the prog- 
nosis more favorable in the acute cases. I am confident that the early in- 
troduction of a drainage tube into the pleural cavity in chronic cases will 
save many lives. In estimating the prognosis in this disease, the treatment 
to which the patient is to be subjected must always be considered. 

The majority of empyemic children recover, while in adults, although 
for a time recovery seems almost certain, phthisis is sooner or later 
developed. 

Treatment. — In the treatment of this affection it is useless to attempt to 
produce absorption of the purulent accumulation by remedial agents. Its 
removal can only be accomplished by mechanical means — either by aspira- 
tion or by making a permanent opening in the chest walls. If aspiration is 



190 



DISEASES OF THE EESPIKATOEY ORGAN'S. 



resorted to a large-sized needle should be used, and no attempt should be 
made to empty the cavity at the first operation. Eemove only a small por- 
tion of the accumulation, being governed by the same rules which have been 
given for the removal of serous effusions, and allow from three to six days 
to elapse between successive aspirations. At each aspiration something in 
excess of the amount which was taken at the previous seance should be 
removed. Never continue the removal of pus in empyema after the patient 
complains of constriction in breathing, even though only three or four 
ounces have been removed. If the aspiration is to be successful the fluid 
will become thinner at each aspiration, and retraction of the chest wall will 
be noticed. If the fluid becomes thicker and emits an unpleasant odor, a 
permanent opening should immediately be made. In empyema occurring 
with septicemia and pyaemia the accumulation will exceed in quantity that 
removed, unless the aspirator is used daily. Under such circumstances a 
free opening should be made. If a permanent opening is to be made, let it be 
made in the axillary line in the seventh or eighth intercostal space. After 
a free opening has been made into the chest cavity, a quarter-inch rubber 
drainage tube should be introduced, and so fastened that it will remain. 
Often when there is little, space between the ribs a portion of bone should 
be removed, that the tube may not be compressed during respiration. A 
double drainage, by making two openings in the chest cavity, is rarely 
advisable. As regards the washing out of the pleural cavity after the intro- 
duction of the drainage tube, although it is strongly advocated by some, my 
recent experience is very positively against it, even when the purulent dis- 
charge has an offensive odor. Thrice have I had reason to believe that my 
patients have died from the direct effects of washing out the pleural cavity 
with a weak solution of carbolic acid. From the commencement empyemic 
patients must receive a most nutritious diet with moderate stimulation. 
Tonics, such as quinine and iron, are always indicated ; cod-liver oil will be 
of service if it does not interfere with stomach digestion. The patient 
must be kept in the open air as much as possible, and a change of climate is 
often attended by very marked improvement. The majority of cases of em- 
pyemic children will recover if aspiration is performed early and repeated 
at short intervals. In most adults it will be necessary to make a permanent 
opening in the chest wall. 

INTERSTITIAL OR ADHESIVE PLEURISY. 

Interstitial pleurisy may commence as a primary disease, or be the 
sequela of an acute, plastic, or a sub-acute effusive pleurisy. In any case 
there are more or less extensive new connective-tissue formations over a 
greater or less extent of the pleural surface. 

Morbid Anatomy. — The essential lesion in this form of pleurisy is the for- 
mation of new connective-tissue over the pleural surfaces. This hyperpla- 
sia may or may not have its origin in a pleurisy which gives fibrin, serum, 
or pus as its product. As a result the pleura becomes thickened sometimes 
to the extent of half an inch ; an equally important and constant lesion 
is adhesion between the costal and pulmonary pleurae. These adhesions, 



INTERSTITIAL OR ADHESIVE PLEURISY. 



191 



however they originate, are progressive, and, after a time, become very 
extensive. In some cases the two surfaces may become closely agglutinated 
to each other throughout their whole extent, and then the entire space be- 
tween them may be obliterated. As a result of these adhesions the expan- 
sive motion of the lungs is interfered with, and sometimes to such an extent 
as to cause constant dyspnoea. The heart may be displaced to the right and 
backward. In one case where the adhesions were extensive over both lungs, 
the heart cavities were much dilated, and, a loud ventricular murmur always 
being heard, valvular disease of the heart was diagnosticated by good ob- 
servers who saw the case during life. This form of pleurisy often leads to 
the development of fibrous phthisis. 

Etiology. — It occurs most frequently in rheumatic and gouty subjects. It 
is often associated with general fibroid degeneration. When it occurs as 
a sequela of sero-plastic pleurisy it is developed with the disappearance of 
the sero-plastic effusion. 

Symptoms. — Its development is always slow and often intermittent. Its 
most constant early symptom is a dull pain over the affected part, accom- 
panied by a sense of constriction. An early symptom is dyspnoea on exer- 
tion, which steadily increases with the advance of the disease, and becomes 
so severe that even slight exertion, such as going up stairs, will give rise 
to such severe paroxysms that signs of collapse sometimes follow. There 
is usually a dry, hacking cough, frequently attended by free bronchial 
hemorrhages. I have frequently found these pleuritic adhesions the only 
apparent cause of quite profuse bronchial hemorrhage. As the adhesion 
becomes extensive, the patient loses flesh and strength, and in some cases 
the ordinary symptoms of chronic phthisis are present. If there is much 
displacement of the heart the patient will be troubled with cardiac palpita- 
tion on slight excitement or physical exertion, so that his dyspnoea and 
cough are often supposed to be clue to some obscure cardiac lesion. 
Often after this class of patients have suffered much and seem to be stead- 
ily getting worse, periods of remission occur, during which for months and 
perhaps years they will seem to be recovering. The appetite returns, they 
gain flesh and strength, the dyspnoea becomes less, and then, while they are 
apparently recovering, they suddenly get worse, all their aggravating symp- 
toms return greatly exacerbated, and they rapidly pass into a decline. 

Physical Signs. — Inspection shows diminished expansive motion of the 
affected side, or of the entire chest if both pleurae are affected. 

Palpation shows diminished vocal fremitus over the seat of the adhesions. 

Careful mensuration of the chest will often establish the diagnosis when 
doubt exists as to the exact character of the changes. 

On percussion there will be slight dulness, which will be most marked 
at the part where the adhesions are most extensive. 

On auscultation the respiratory sound will be feeble, sometimes scarcely 
audible even during a full inspiration ; friction sounds will be heard. These 
friction sounds are creaking or crepitating in character, very loud, and 
often resemble mucous rales and gurgles, for which they are sometimes mis- 
taken, but the loss of chest expansion and the feebleness of the respiratory 
sounds will readily correct the mistake. 



192 



DISEASES OF THE RESPIRATORY ORGANS. 



Prognosis. — The prognosis in this form of pleurisy varies with its dura- 
tion and extent. If the adhesions are not extensive and are of recent date, 
the process may be arrested and complete recovery is possible ; but if they 
are extensive and the inflammatory process has continued for a long time, it 
is generally progressive and recovery is impossible. If it is attended by 
great emaciation and progressively failing health it may cause death with- 
out complications. The majority, however, die from the complication of 
chronic bronchitis, emphysema, and chronic interstitial pneumonia ("fibrous 
phthisis "). In some cases the disturbance of the general circulation from 
dilatation of the right ventricular cavity leads to general dropsy and all 
the conditions which result from heart insufficiency. 

Treatment. — The first and most important thing to be accomplished in 
the treatment of this affection is to improve the nutrition of the patient. 
In accomplishing this the diathesis of the patient must be carefully consid- 
ered. The diet must be regulated according to the indications ; the diet of 
gouty subjects must be very different from that of the enfeebled, broken- 
down alcoholic subject. While iron and the mineral acids will be indicated 
in one class, cod-liver oil and the hypophosphites will be indicated in the 
other. In all cases, the bichloride of mercury in minute doses will be found 
of service. Climatic conditions are very important in its successful man- 
agement ; as a rule high altitude with a warm, dry atmosphere, such as is 
obtained in New Mexico, will be found most favorable. The external ap- 
plication to the chest which has seemed to me to have a desired effect in 
arresting its progress and removing its results, is the oleate of mercury — 
its use must be continued for a long time, care being taken not to bring 
the patient under the constitutional effects of the mercury. 

CANCER OF THE PLEURA. 

Cancer of the pleura and sub-pleural tissue is never primary, and is only 
met with in advanced cancerous infection. It appears either as circum- 
scribed grayish thickenings of the pleura or in the form of distinct papular 
elevations on the pleural surface. As the papules enlarge, they form pe- 
dunculated outgrowths, which vary in size from a pea to a small orange. Ac- 
companying these developments there is interstitial pleurisy, which causes 
extensive thickening, adhesion, and induration of the pleura, attended by 
the effusion of fluid into the pleural cavity. 

Etiology. — It most frequently complicates cancer of the mamma, medi- 
astinum, and lungs. 

Symptoms. — The signs of pleural cancer are always obscure. The history 
of the case is always important. If the tumors are large, or the fluid effu- 
sion abundant, so as to cause compression of the lung, there will be dysp- 
noea, cyanosis, and vertigo, with the physical signs of fluid accumulation 
and the slow development of solid tumors in the pleura. Should the evi- 
dence of a tumor with slow accumulation of fluid in the pleural cavity oc- 
cur in a case of long standing cancer of the breast, accompanied by gradual 
emaciation and dyspnoea on slight exertion, cancer of the pleura may be 
suspected. If a cancerous tumor is developed in the pleura posteriorly, with 



PYOPNEUMOTHORAX. 



193 



the aorta in front, there may be a pulsation and bruit which will cause it 
to be mistaken for thoracic aneurism. The prognosis is always unfavora- 
ble, and the treatment is only palliative. 

PYOP^EUMOTHOKAX. 

This a condition characterized by the presence of both air and fluid m 
the pleural cavity. The entrance of air into the pleural cavity is usually 
promptly followed by the effusion of liquid, for it excites suppurative in- 
flammation of the pleural membrane. 

Morbid Anatomy. — The morbid changes which may occur in the pleural 
membrane and in the pleural cavity in pyopneumothorax very nearly cor- 
respond to those described as occurring in empyema ; they are increase of 
tissue, granular appearance of the surface of the pleura, and the development 
of pus. By the entrance of air into the pleural cavity, the lung is allowed to 
collapse, to contract toward its base near the spinal column, in the same 
manner as when the cavity is filled with fluid, although the opening (as from 
rupture in an emphysema) may be no larger than a pin-hole. 1 The heart 
may be considerably displaced. The quantity of fluid varies in different 
cases ; at one time the cavity will be nearly filled with fluid and contain 
little air; — again it will be distended with air and contain little fluid. 
When extensive and firm adhesions of the pleural surfaces exist prior to the 
entrance of air into the pleural cavity, collapse of the entire lung does not 
take place, but the escaped air is contained in a small space enclosed by ad- 
hesions on all sides. This condition is usually present when pyopneumo- 
thorax is developed from the perforation of an empyema, or suppurative 
pleuritis. The air in the cavity is always deoxidized and rich in carbon 
dioxide ; it may also contain sulphuretted hydrogen. 

Etiology. — Regarding the source of the air in the pleural cavity different 
views have been entertained. Some have claimed that gas escapes into the 
pleural cavity from the tissues or blood, in the same manner as it is claimed 
to escape into the intestines from the mucous membrane ; this may be pos- 
sible, but it is by no means probable. Others, again, have claimed that 
it is the product of decomposition of fluid in the pleural cavity ; this is 
rarely, if ever, the case, for fluid effused into closed cavities resists de- 
composition in a surprising manner, although when taken from such cavi- 
ties or exposed to the contact with air within them, it rapidly decomposes. 
Pus or serum will resist decomposition in a pleural cavity so long as it is not 
exposed to air. 

There can be little question but that in pneumothorax and pyopneu- 
mothorax there is always an opening between the air-passages of the lung 
and the pleural cavity, an opening which is the result of an ulcerative proc- 
ess which may begin within the lung and work outward, or in its pleural 
surface and work inward. In rare instances air enters the pleural cavity 
through an external opening in the chest wall. Hydatids sometimes rupt- 
ure into the pleural cavity. In most cases of traumatic pneumothorax 



1 But there need be vo pleurisy : although a secondary pleuritis may light up around the opening and close 
it, thus effecting a cure. 

13 



194 



DISEASES OF THE KESPIKATORY ORGAKS. 



air does not enter the pleural cavity through the opening in the chest wall, 
but comes from the lung through an opening in the pulmonary pleura, the 
lung being torn at the same time that the opening is made through the 
walls of the chest. The commonest example is in connection with fracture 
of the ribs, in which the lung is sometimes torn by the broken end of the 
bone, and air escapes through the rent into the pleural cavity. Entrance of 
air into the pleural cavity usually occurs either in connection with pulmo- 
nary phthisis, gangrene of the lung, empyema, or pulmonary emphysema. 
It is most frequently met with in connection with pulmonary phthisis. Ab- 
scess of the bronchial glands, and ulceration of the oesophagus or stomach, 
may lead to it. When an empyema has existed for a long time an opening 
may be established by ulceration through the lung into a bronchial tube, 
thus permitting the fluid to be expectorated, and air to enter the pleural 
cavity. In pulmonary emphysema, a sac containing air which has been 
formed upon the surface of the lung may rupture, and air enter the pleural 
cavity and develop pneumothorax ; the consequent pleurisy will rapidly 
develop a pyopneumothorax. At the post-mortem examination of one who 
has died of pyopneumothorax, it is often difficult, and sometimes impos- 
sible, to find the opening in the pulmonary pleura, for the reason that in 
some instances it becomes covered with a fibrinous deposit, and in others the 
opening has been closed some time before death by an inflammatory process 
in the lung substance about the opening. 

Symptoms. — The symptoms which attend perforation of a lung, and the 
escape of air into a pleural cavity, are usually well marked, but they are 
somewhat variable. First, there is a class of cases in which the symptoms 
are severe in character, the patient is suddenly seized with a sense of faint- 
ness followed by hurried respiration and great dyspnoea. Pain may or may 
not be a symptom ; its existence indicates inflammation. The dyspnoea is 
in part mechanical, in part reflex. It is extreme, comes on suddenly, is 
soon followed by well-developed cyanosis, the patient passes rapidly into a 
state of collapse, and, in some instances, death occurs in a few hours. 
Usually, however, the patient survives the shock of the perforation, and, 
after a time, becomes comparatively comfortable, suffering, however, from 
more or less dyspnoea. He is unable to lie down, able only to recline upon 
the affected side. Some say they experienced a sense of "tearing," and 
felt as if a fluid "were being poured inside the chest." 

As the pleural cavity becomes filled with the fluid effusion (which may re- 
sult from the attending pleuritic inflammation), the dyspnoea and cyanosis 
increase, and general dropsy gradually develops. Aseptic air alone will not 
cause inflammation or rise in temperature. It is a purulent accumulation 
in the pleural cavity which proves fatal, and not the pneumothorax, for with 
its development the temperature rises and the patient becomes more mani- 
festly hectic, if hectic has previously existed. When the purulent accumu- 
lation becomes very abundant the patient dies from the exhaustion produced 
by the intensity of the fever or from collateral hyperemia and oedema of the 
opposite lung. In some cases the symptoms which attend the entrance of 
air into the pleural cavity come on more insidiously. The difficulty of 
breathing may be gradually developed, and the existence of air in the pleu- 



PYOPNEUMOTHORAX. 



195 



ral cavity may not be recognized until after considerable fluid has collected 
in the pleural cavity. When pneumothorax occurs in connection with pul- 
monary phthisis, its occurrence is marked by very active symptoms, pain 
being prominent, followed by all the evidences of collapse. When oc- 
curring in connection with pulmonary emphysema its development is very 
insidious. 

Physical Signs. — The physical signs of pyopneumothorax are very charac- 
teristic, and, if properly appreciated, will always enable one to recognize its 
existence. By inspection there will be noticed a bulging of the intercostal 




Tympanitic resonance 

Amphoric respiration 

Metallic tinkling 

Succusswn sound 

Absent vocal fremilvs 

Flatness *. 

Absent voice 

Absent respiration 



Diagram illustrating the Physical Signs of Pyopneumothorax. 




Fig. 41. 



space and an increase in the size of the affected side, which becomes more 
prominent than in sub-acute pleurisy and has a "rounded" look. There 
will be the displacement of viscera seen in sub-acute pleurisy when the pleu- 
ral cavity is distended w T ith fluid, and there will be absence of motion on the 
affected side, while upon the unaffected side the respiratory movement will 
be also decreased in force and frequency, but to no such great extent, the 
breathing being almost wholly abdominal. 

Upon palpation there will be entire absence of vocal fremitus upon the 
affected side, unless there are old adhesions. The heart, at the same time, 
is felt pushed from its normal site. Thus far there is no difference between 
the physical evidences of pyopneumothorax and sub-acute pleurisy. 

On percussion, when the patient is sitting or standing there will be tym- 
panitic resonance from the summit of the affected side to the level of the 
fluid. Below the level of the fluid there will be complete flatness. 1 A 
change in the position of the patient will change the level of the fluid, and 
also, of course, the character and site of the percussion note. 

Upon auscultation there will be found an entire absence of all respiratory 
and vocal sounds below the level of the fluid ; but, as soon as its level is 
reached, if the opening from the bronchial tube which admits the air into 
the pleural cavity still remains pervious, amphoric respiration or " echo " 
will be heard, and it will be metallic in character. Metallic tinkling is al- 
most uniformly associated with amphoric respiration, and is produced in a 



1 Except in pyopneumothorax it is rare to find an exactly horizontal line of demarcation with pleural 
effusions. 



196 



DISEASES OF THE RESPIRATORY ORGANS. 



variety of ways. It may be produced by agitation of the liquid from the 
vibration of the voice, or by coughing and full inspiration, or by dropping 
of liquid from the walls of the cavity upon the surface of the fluid. It is 
more frequently produced by agitation of the fluid from speaking and 
coughing. The characteristic physical sign of this disease is the succussion 
sound, which is a metallic, splashing sound, produced by abruptly shaking 
the chest while the ear is resting upon the surface. Over the affected side 
no vesicular breathing can be heard, while over the healthy side the vesicu- 
lar breathing is exaggerated. 

Differential Diagnosis. — When pyopneumothorax is fully developed, it is 
scarcely possible to confound it with any other disease, but it is possible to 
confound pneumothorax with some other conditions. The only physical 
evidences of a perforation which permits the entrance of air into the pleural 
cavity, are tympanitic percussion, absence of all respiratory sounds on the 
affected side, and intense dyspnoea ; the same development of signs might 
occur in connection with complete obstruction of a large bronchus. Again, 
it is said that pneumothorax maybe confounded with extreme pulmonary 
emphysema. Patients suffering from these diseases present a somewhat 
similar appearance ; in both classes there is tympanitic percussion, but in 
the emphysematous patient the tympanitic percussion is present over loth 
lungs, while in a patient suffering from pneumothorax it is present only 
upon the side on which the perforation has occurred. Besides, there is a 
vesicular element to the tympanitic note in emphysema never found in 
pneumothorax. In emphysema there will also be heard some respiratory 
sounds. The expiration is prolonged and low pitched in emphysema ; not 
so in pneumothorax. The breathing is broncho-vesicular in emphysema ; 
not so in pneumothorax, where respiratory sounds are absent. Succussion 
is present in pyopneumothorax ; not in emphysema. If errors in the dif- 
ferential diagnosis of these two conditions are possible, they will be made 
at the commencement of the attack. 

A large cavity in the lung substance may be mistaken for pyopneumo- 
thorax. I have never met with a pulmonary cavity of sufficient size and 
with the conditions to produce the succussion sound. Amphoric res- 
piration and metallic tinkling maybe developed in a large cavity, but the 
succussion sound will be absent ; on the other hand, when amphoric res- 
piration and metallic tinkling are present in hydropneumothorax the sue 
cussion sound will also be present. In a cavity rales would be loud and 
numerous ; vocal fremitus is very of ten exaggerated ; the chest wall above it 
would probably be slightly depressed, and finally, the heart, etc., would not 
be displaced. 

With a knowledge of the history of the patient and a proper appreciation 
of the physical signs, it is hardly possible to confound pyopneumothorax 
with any other form of disease. In no other disease are the physical signs 
so characteristic and unequivocal, and in a large proportion of cases the 
rational symptoms are equally diagnostic. 

Prognosis. — The prognosis in pyopneumothorax is always unfavorable. 
All authorities agree that when it occurs in connection with advanced pul- 



HTDKOTHORAX. 



197 



monary phthisis or gangrene it generally proves fatal within five or six days ; 
but in pneumothorax without pleurisy the prognosis is favorable. Every 
day the patient lives betters the outlook ; the majority of fatal cases 
die within two days, the period of survival in the remainder rarely extend- 
ing beyond the sixth day. When recovery has taken place in cases of 
pyopneumothorax, either they have been of traumatic origin, the result 
of great muscular strain in connection with extensive pulmonary emphy- 
sema, or an empyema has discharged itself through a bronchus. There is 
record of a few recoveries where the rupture occurred in the early stage 
of phthisis. When recovery does take place it is reached in the following 
manner : — plastic material is poured out in the tissue surrounding the open- 
ing in sufficient quantities to completely close it ; the air and fluid are thus 
imprisoned in the pleural cavity ; the air is rapidly absorbed by the pleural 
membrane, and if the closure is sufficiently firm to persist after the air has 
been removed, the case will be thus changed from one of pyopneumo- 
thorax to one of empyema. Cases have been related in which perforation 
of the lung and pneumothorax were present without any fluid collecting in 
the pleural cavity. Such cases are of such rare occurrence that they can 
hardly be taken into consideration as regards prognosis. 

Treatment. — The treatment of this affection is almost necessarily pal- 
liative. At the very onset of the attack, when the patient is suffering from 
the shock of the perforation, a full hypodermic injection of morphine 
will be found of service, aud it may be repeated once or twice a day for 
the first few days. If the patient survives for a few days, stimulants 
may be advantageously administered, and he must be sustained by a 
most nutritious diet. Among drugs, musk and chloroform are recom- 
mended by so good an authority as Dr. Walshe. Hot poultices and sooth- 
ing fomentations give relief when applied over the chest. The que- 
bracho bark is now given for relief of the dyspnoea. When the dyspnoea 
is extreme and the distress of the patient is very great, and a considerable 
quantity of fluid has accumulated in the pleural cavity, the question will 
arise whether a free opening shall be made through the chest walls. As a 
rule, this must be regarded as a palliative measure, and should be resorted 
to only in extreme cases. If it be resorted to, a fine trochar should be in- 
serted into the chest, and the air permitted to escape through a connecting 
tube under water, until an equilibrium has been established. It may give 
relief for a time, and it is justifiable to resort to it when the fluid collec- 
tion is abundant and the febrile excitement is intense. It may delay the 
fatal termination. Walshe recommends general bleeding or dry cupping. 1 

HYDKOTHOKAX. 

Hydrothorax is anon-inflammatory fluid effusion into one or both pleural 
cavities ; it often accompanies general dropsy. The fluid is generally clear, 
of a yellowish-green color, and may be sufficient in quantity to compress to 
a considerable extent one or both lungs. It may occur in any chronie 



1 Dis. of Heart, etc. 



198 



DISEASES OF THE EESPIEATOEY ORGAN'S. 



exhausting disease which causes general hydrsemia. It rarely occurs as the 
sole morbid process in the human body. In a large number of autopsies 
a small amount of clear or bloody serum will be found in the pleural cavi- 
ties, which is merely the result of post-mortem changes ; such conditions 
should not be regarded as evidence of hydrothorax. 

Etiology. — Any disease or condition (e. g., mitral disease especially) that 
impedes, and raises the pressure in, the venous circulation will cause it. 
Thus it may be caused by the pressure of enlarged glands ; tumors and 
venous thrombi may induce it ; also diseases of the heart and kidneys, the 
cancerous and other cachexia?. Hydrothorax generally occurs in connec- 
tion with general anasarca, such as is developed in Bright's disease. 

Symptoms. — It generally comes on insidiously, and its development is 
attended by no febrile symptoms. Its occurrence is marked by steadily in- 
creasing dyspnoea, until the patient reaches a condition of extreme distress, 
and orthopnea ; the lips become livid, the finger-ends blue, and the res- 
piration gasping. He is unable to lie down and can speak only in mono- 
syllables. On physical examination there will be found the signs of fluid 
in both pleural cavities. There may be a short, dry cough. If the effusion 
is large, the action of the heart will be embarrassed, as shown by a small, 
feeble pulse. All the phenomena which attend this condition are due 
to mechanical pressure caused by the presence of fluid in the pleural cavi- 
ties, and patients die cyanosed as the result of diminished breathing 
capacity. 

Differential Diagnosis. — Ordinarily the diagnosis of hydrothorax is readily 
made. It may be confounded with sub-acute pleurisy, but generally the 
history of the case will determine the character of the effusion. Then, its 
simultaneous occurrence on both sides in connection with general dropsy, 
without any irritant or attendant fever, will be sufficient to enable one to 
make the diagnosis of hydrothorax. It may be mistaken for pulmonary 
oedema ; the two conditions are very likely to occur together, but in pul- 
monary oedema a crackling sound will be heard over the ©edematous lung, 
which sound is not present in hydrothorax, and there will be copious, 
watery (perhaps blood-stained) expectoration, which is absent in hydro- 
thorax. In emphysema the increased resonance, and in bronchitis the 
sputum and rales, will suffice to differentiate the three conditions. An 
enlarged (painless) liver will not be mistaken for dropsy of the chest. The 
physical sign of hydrothorax is fluid in both pleural cavities which is freely 
movable by a change in the position of the patient, and is not attended by 
friction sounds or vocal fremitus. The introduction of a trochar and with- 
drawal of the fluid will decide the case. 

Prognosis. — The danger attending hydrothorax will depend to a great 
extent on the general condition of the patient at the time of its occurrence. 
When it occurs in connection with general anasarca in Bright's disease, or 
in extensive heart disease, it may prove the direct cause of death. The 
majority of cases yield readily to treatment, and life may be prolonged, 
months, even years, by judicious management. 

Treatment. — The general treatment of hydrothorax corresponds to that 



HEMOTHORAX. — PULMONARY PHTHISIS. 



199 



for the removal of dropsical accumulations in other parts of the body. It 
is a simple dropsical effusion, and can be removed by the administration of 
remedies which diminish the quantity of water in the blood. Such reme- 
dies are the hydragogue cathartics, diuretics and that general class of 
agents employed for the removal of fluid from the areolar tissue. Elaterium 
is the best. Digitalis should be given (F. Anstie), and as soon as its effects 
show, the muriated tincture of iron (gtt. xx every six or seven hours) should 
be given. In many cases it will be impossible to wait for the effects of diu- 
retics and hydragogue cathartics, as the patient will die unless immediate 
relief from the pressure of the fluid is afforded. Under such circumstances 
the aspirator may be used with advantage. Those remedies may be em- 
ployed which are of service in the treatment of general anasarca. 

HEMOTHORAX. 

HcBmotliorax is the escape of blood into the pleural cavity ; it is never a 
primary affection. The escape of any considerable quantity of blood into 
the pleural cavity may occur in connection with syphilis, cancer of the lung 
or pleura, from the bursting of an aneurism, the rupture of the pleura fol- 
lowing an extensive pulmonary apoplexy and accompanied by escape of 
blood from the lung, and the rupture of a vessel. It may be due to trau- 
matic causes, a vessel being injured, as in fracture of the ribs. Sometimes 
blood is mixed with pleuritic effusion, the product of pleuritic inflamma- 
tion in those of a scorbutic or purpuric diathesis. Fluid blood in the 
pleural sac soon excites inflammation, whose products are usually serum 
with a variable admixture of pus. 

The symptoms of hemothorax are those of liquid accumulation in the 
pleural cavity, with the accompanying evidences of internal hemorrhage, 
pallor, syncope, etc. In hemothorax, dyspnoea is sometimes greatest at 
the onset, diminishing gradually. 

In those cases where there is no appreciable traumatic cause for the bleed- 
ing, all that can be done is to keep the patient at rest. Opiates are not 
contra-indicated. Stimulants may be necessary. In some instances relief 
may be obtained by the performance of paracentesis. 

PULMONARY TUBERCULOSIS. 

(Phthisis.) 

Recent investigations have established a pathological unity in the morbid 
processes of pulmonary phthisis, based on the development of tubercle 
tissue. 

While all forms of tubercular disease must be considered identical in 
their origin, and the primary lesion in each to be tubercle, the wide varia- 
tions in the morbid changes which are found in the lungs of phthisical 
subjects, as well as the marked differences in their clinical history, compel 
us to recognize clinically two distinct varieties of pulmonary tuberculosis : 



200 



DISEASES OF THE RESPIRATORY ORGANS. 



I. Acute tuberculosis. 

II. Chronic tuberculosis. 

The pathological changes which characterize pulmonary tuberculosis 
depend upon the following factors : 

1. The amount of infective material received, and the rapidity with 
which it enters the lung. 

2. The channels by which it reaches the pulmonary tissue. 

3. The inherited or acquired predisposition of the affected person to the 
development of tubercular tissue. 

4. The constitutional diathesis predisposing to either suppurative or 
fibroid changes in connection with inflammatory processes. 

When large numbers of bacilli enter the lung through the blood-vessels, 
the resulting disease is usually part of an acute general miliary tuberculosis. 

When moderate numbers are received more gradually, or through the 
air-passages, the resulting tubercular development is composed, in vary- 
ing proportions, of gray miliary tubercle and foci of caseous (tubercular) 
pneumonia. The succeeding phthisical processes may be rapidly necro- 
tic, (acute phthisis) ; gradually destructive, with suppuration and varying 
amounts of fibroid development, or largely fibroid in character (chronic 
phthisis). As the bacilli make their way through the air-passages to the 
alveoli, they may become fixed at any point on the epithelial surfaces or 
within the pulmonary tissues. The more frequent seats of their primary 
location are (1) the junction of the terminal bronchioles and the alveolar 
walls, (2) the bronchial, and (3) the alveolar surfaces. Many remain at 
these points, others make their way, or are carried by the leucocytes, to 
the substance of the tissues, becoming finally fixed in the perivascular 
lymph channels, or the interstitial spaces of the bronchial and alveolar 
walls. 

The primary changes induced by their presence are hyperplasia of the 
fixed cells, and round cell infiltration. These result, within the lymph 
channels and interstitial spaces, in the formation of gray miliary tuber- 
cle, and, in the alveolar cavities, in the development of larger masses of 
tubercular tissue, forming the tubercular pneumonia, which, under later 
changes, becomes caseous pneumonia. In both cases the round cell infil- 
tration affects the adjacent tissue to a greater or less degree, and is the 
first indication of subsequent inflammatory processes. 

It is this secondary inflammation which largely determines the morbid 
anatomy in the several forms of phthisis, and which, in connection with 
the tubercular tissue, results in that pulmonary consolidation so charac- 
teristic of all phthisis. 

The second effect of tubercle bacilli is manifested in the marked tendency 
shown by all tubercular tissue, as well as the products of the associated 
inflammation, to undergo "coagulation necrosis," granular and caseous 
degeneration, so that only the newly formed products show the translucent 
appearance so characteristic of gray tubercle, while all older tubercular 
tissue has become necrotic or converted into caseous foci. Degenerated 
miliary tubercle may not be distinguished from that which was primarily 



PULMONARY TUBERCULOSIS. 



201 



pneumonic or disseminated. The tubercle bacilli themselves are found 
disseminated throughout the tubercle tissue and less abundantly in the 
inflammatory products. When caseous foci become exposed to the air, 
their development is rapid. 

The mechanical effects of the tubercular developments have an especially 
important bearing upon the nutritive changes in the lung. Direct com- 
pression of the parenchymatous elements is associated with obstruction of 
the lymph channels and vessels, and occlusion of the smaller bronchioles, all 
of which increase the necrotic tendency. The vascular obstruction is 
augmented by thrombosis, by endothelial proliferation, and by endarteritis 
and eudophlebitis obliterans. 

The inflammatory changes of phthisis are prominently necrotic, suppu- 
rative, and fibroid. They affect all the tissues of the lung. The fibroid 
changes, which are present in greater or less degree in all cases, cause 
thickening of the vascular w r alls, induration, and subsequent weakening 
of the bronchial tubes, and a development of fibrous tissue in and about 
tubercular foci and throughout the pulmonary tissue. Extreme degrees 
of fibroid change result in fibroid phthisis. 

Necrosis and suppuration are associated processes. When necrosis is 
acute, it precedes marked suppuration ; when more gradual, it follows a 
diffuse or localized purulent infiltration of the tubercular and inflamma- 
tory products. 

Necrotic masses seldom remain long intact. They break clown gradually 
or in sloughing masses, leaving, as they are thrown off in the sputa, the 
typical cavities. When fibroid changes have been slight, these cavities will 
have soft, sloughing, pus-infiltrated walls, and will continue to enlarge by 
ulceration. If fibroid developments have been more abundant, the walls 
will be firmer, and granulation may take the place of ulceration and the 
cavity be healed, or its walls converted into a firm, smooth, pyogenic 
tissue. 

Cavities by dilatation may be formed at points in the bronchial walls 
where tubercular fibroid degeneration has occurred. These bronchiectatic 
cavities are more abundant in fibroid phthisis. Aside from the purely 
tubercular lesions, adjacent parts of the lung may present the evidences 
of simple bronchitis and catarrhal pneumonia. Secondary infection may 
occur in other parts of the lung, the bronchi, larynx, or intestinal canal, by 
direct contact of the tuberculous secretions ; while ulceration of a caseous 
focus into a vein may be followed by a general infection, and an irruption 
of gray tubercle throughout the body. 

A tubercular pleurisy is always present when phthisical processes are 
near the surface. It is plastic in form and results in adhesions. If a 
tubercular nodule ulcerates into the pleural cavity, a sero-purulent exuda- 
tion will be rapidly developed. 

Two stages can be recognized in the anatomical changes in the lungs : 

1. The stage of consolidation, corresponding to the primary tubercular 
developments and the infiltration of the lung by inflammatory products. 

2. The stage of softening and excavation ; beginning with the lique- 



202 



DISEASES OF THE RESPIRATORY ORGANS. 



faction and removal of the necrotic tissues, including formation of cavi- 
ties. 

A consideration of the j>athology of the disease makes it patent that 
these two stages will always be found side by side in the same lung when- 
ever cavities have formed. 



ACUTE PULMONARY TUBERCULOSIS. 

(Acute Phthisis.) * 

Morbid Anatomy. — The development of tubercle in acute pulmonary 

tuberculosis usually occurs at the 
apex of the lung, either in front or 
posteriorly. 

. When resulting from a rapid in- 
fection, as the rupture into a bron- 
chus of a caseous gland, the consoli- 
dation assumes the form of a caseous 
broncho-pneumonia. In most cases, 
however, while the pneumonic con- 
solidation is prominent, more or less 
miliary tubercle is formed. The in- 
flammatory processes are acute ; but 
little fibrous tissue is formed, and a 
coagulation necrosis may break down 
the affected parts even before caseous 
changes are prominent. The vascu- 
lar as well as the less resistant tis- 
sues may be included in the necrotic 
change, and profuse hemorrhages fol- 
low removal of the affected mass. In 
less acute conditions, caseous changes 
are more prominent, and may include 
the areas of coagulation necrosis as 
well as other tubercular tissue. Ow- 
ing to the slight amount of fibrous 
change, the cavities formed usually 
have soft sloughing walls. The atten- 
dant pleurisy is usually well marked 
and plastic in character. 

On removing the lungs of acute 
phthisis, the surface over the affected 
portion may appear normal, or mot- 
tled by yellow-gray areas, correspond- 
Fig 42 ing to points of solidification. More 

Lung in Acute Pulmonary Tuberculosis. frequently it will be covered by a 

Shoiving areas of consolidation and cavities. plastic pleuritic exudation. The Con- 




ACUTE PULMONARY TUBERCULOSIS. 



203 



solidated portions may include an entire lobe of one lung, or be scattered 
in smaller masses throughout one or both lungs. On section, the con- 
solidated portions are better marked. The cut surface has much the 
appearance of the red hepatization of lobar pneumonia. Scattered here 
and there, more or less abundantly, on the dark reddish-gray background, 
may be seen gray miliary tubercles ; yellow, or yellowish-white masses of 
varying size, representing degenerated gray tubercle or caseous pneumonic 
foci ; sharply outlined areas of coagulation necrosis, which are still dark 
reddish-black or a dirty yellow, from caseous change ; and finally, here 
and there a dirty sloughing cavity with ragged, pus-infiltrated walls, and 
containing remnants of the dead tissue or soft clots. Under the micro- 
scope the alveoli are seen distended by fresh or degenerated tubercle, 
which may extend into the smaller tubes. Smaller bits of the same 
tissue stud the bronchial walls, and in the vascular lymph spaces are 
seen obstructing the lumen of 
the vessel. Round cell infiltra- s 
tion is present throughout the 
affected lung. 

In the peripheral zones the 
primary changes of epithelial 
proliferation and cellular infil- 
tration may be the only evidences 
of bacillary activity. Less fre- 
quently than in chronic phthisis, 
bronchial ulcers and sub-epithe- 
lial abscesses may mark the 
points of proliferation in lymph 
follicles, or softening and rupture 
of tubercle nodules, but cica- 
trices and fibrOUS-tisSUe forma- Acute Pulmonary Tuberculosis, 
tions are never prominent and Section of lung shoiving a single alveolus in stage > of hepa- 

.-it tization. 
Seldom appreciable. A. Wall of alveolus, with infiltration of pus at B, B. 

— ,. . mi t ■ •!• C' Cavity of alveolus nearly filled with changed epithelia 

EtlOlOgy. — Ihe direct exciting and a few pus-corpuscles. 

Cause Of acute as of all forms of ^ Millar inesh enclosing the cell elements, x 300. 

tuberculosis is the bacillus tuberculosis. This bacillus is received directly 
or indirectly from some other tuberculous subject. 

The channels of communication are numerous and varied. The most 
frequent are by particles of dried sputa floating in the air ; by the use of 
dishes, napkins, handkerchiefs, and other personal belongings of phthisi- 
cal subjects ; by the use of milk of tuberculous women or cows, and 
possibly by tuberculous meat. Other unique methods of contagion are 
occasionally noticed. 

Although the bacillus is accepted as the sole exciting cause of phthisis, 
its omnipresence, and the impossibility, under the present social condi- 
tions, of avoiding a more or less intimate contact with it, render the pre- 
disposing causes of its development, without which it is inactive, of 
paramount clinical importance. These causes are general and local. The 




204 



DISEASES OF THE RESPIRATORY ORGANS. 



most important general causes are an inherited or acquired feebleness of 
constitution, anti-hygienic influences, climate, and soil. 

The local causes are found in inflammatory conditions of the pulmonary 
tissues. 

Inherited Tendency. — At present proof is wanting that the bacillus is 
ever conveyed to the foetus in uter o, although some observations appear to 
show that such may exceptionally be the case. The supposition that the 
bacilli are present in the tissues at birth, and remain latent, to become 
active later in life, is based upon the frequent development, in children, of 
tuberculous lesions of the joints without previous disease of the lung. 
The fact of an inherited vice of constitution, and its influence in deter- 
mining tubercular growth, are so decided that many observers have claimed 
that phthisis can never be developed by those who have no such tendency. 
Every-day experience disproves such sweeping statements. We have no 
knowledge of what constitutes the tubercular diathesis, although it is 
grossly manifested by certain well-marked signs to which we give the 
name "scrofulous." 

My own statistics show that such a predisposition is inherited in more 
than eighteen per cent. 

Mothers transmit phthisical tendencies more certainly than fathers. 
But when one parent alone is affected, the mother is more apt to transmit 
to the daughters than to the sons, and vice versa. The stronger the 
hereditary predisposition, the earlier will be the development of the disease, 
and the more acute its course. A phthisical vice of constitution may be 
inherited by the children of the aged, of drunkards, of those enervated by 
excesses, and of those who at the time of the birth of their children were 
suffering from some form of constitutional disease, such as cancer, syphilis, 
or gout. It is therefore necessary, in order to fully determine the influence 
of an hereditary tendency in any given case, to know the condition of the 
parents at the time of the individual's birth. Children of consanguineous 
marriages are especially liable to pulmonary phthisis. 

Anti-hygienic Surroundings. — Second only to hereditary influence are 
anti-hygienic surroundings. Impure air, improper quality and insufficient 
quantity of nutritious food, are among the most prolific of this class of 
causes. Bad ventilation and impure air, an indoor life, especially when 
large numbers are crowded into a small space, are strong predisposing 
causes. The frequency of phthisis in clerks, printers, tailors, milliners, 
seamstresses, factory employees — who live in a hot, close, dust-laden atmos- 
phere — proves this. Of indoor workers those are most liable to phthisis 
who exercise least at their vocations. Compositors surfer oftener than the 
press-hands in the same room. Prison and cloister statistics show a mor- 
tality from phthisis of from forty to fifty per cent., while that among the 
people at large is only fifteen per cent. Careful examinations of the dust 
and air of prisons for bacilli have shown that this difference cannot be 
accounted for on the theory of contagion alone. The moister the air and 
the higher the temperature of the apartment, the more liable is phthisis to 
be developed. If, in addition to these anti-hygienic conditions, are added 



ACUTE PULMONARY TUBERCULOSIS. 



205 



insufficient and improper clothing, want of cleanliness, alcohol drinking, 
prolonged lactation, and repeated miscarriages, it is evident that the feeble- 
ness of constitution which predisposes to phthisis can be acquired as well 
as inherited. 

I am convinced, from a careful analysis of my records, that the phthisi- 
cal developments depend as much upon the anti-hygienic influences under 
which childhood has been passed as upon hereditary tendencies. These 
predisposing anti-hygienic influences embrace the important problem of 
infantile diet. Few mothers, especially among the wealthier classes, are in 
a condition properly to nourish their own offspring. The habit which pre- 
vails of .feeding children until they are one, two, or even three years of 
age upon barley-water and pap, has a great influence upon the future 
physical development of the child. In determining the influences which 
have predisposed to phthisis in any case, it is important to consider not 
only the condition of the parents at the time of the birth of the individ- 
ual, but also the hygienic influences under which his childhood and early 
life were passed. One of the great objects of early physical training should 
be to overcome hereditary physical tendencies ; this can be accomplished, 
in the majority of cases, by good hygienic surroundings and systematic 
physical training during infantile and early life. It is especially important 
that the children of phthisical parents should be placed under such influ- 
ences, during iufancy and childhood, as shall ensure the greatest physical 
vigor. All these predisposing influences tend to arrest physical develop- 
ment. 

Climate has long been regarded as an important factor in the develop- 
ment of phthisis. We know of no climatic condition which renders its 
development a necessity, or that makes its development impossible ; yet 
there is no question but that it occurs with greater frequency in one climate 
than in another. It is rare in the torrid and frigid zones, and frequent 
in the temperate. Altitude is more important than climate, for most high 
elevations are antagonistic to its development. The condition of the soil 
of a region or locality favors, or is antagonistic to, phthisis : light, sandy, 
porous soils are antagonistic ; while heavy, hard, clayey, and impermeable 
soils are favorable. A damp, cold atmosphere, an impermeable soil, and 
sudden changes in temperature, are the most favorable conditions for devel- 
oping phthisis. Want of sunlight acts also as a strong predisposing cause. 
It seems probable that the climatic and telluric conditions influence both 
the resisting power of the individual, and the vitality of such bacilli as 
are distributed through the air. 

Local Causes. — One who carefully studies the clinical features of a large 
number of cases of phthisis must be convinced that bronchitis of the 
smaller tubes and chronic lobular {catarrhal) pneumonia are the starting- 
points of a large number of cases of phthisis. Some call these "excep- 
tional " catarrhs. 1 That an apparently simple catarrh leads to the devel- 
opment of tuberculosis in one case and not in another may be explained by 



1 Williams found in 1,000 cases of phthisis that bronchitis was the origin in 12 per cent. Niemeyer 
regards bronchitis tis the primary and essential developing cause in the majority of cases. 



206 



DISEASES OF THE RESPIRATORY ORGANS. 



the fact that one individual is in a condition to resist the bronchitis, while in 
another all the predisposing causes of tuberculosis are in operation, and the 
catarrh then furnishes the favorable soil for the development of bacilli, 
while it decreases the resisting power of the tissues. The relation which 
pneumonia bears to the development of phthisis has been sufficiently con- 
sidered under the head of its morbid anatomy. From a clinical standpoint 
there seems to be no question but that a non-resolved pneumonia is the 
starting-point of phthisis in quite a large proportion of cases. The ques- 
tion which it seems difficult to decide is, Are such pneumonias tubercu- 
lar ? 

That pulmonary phthisis not infrequently dates from a pleurisy is evi- 
dent to every careful observer. Phthisis which is preceded by pleurisy is 
often attended by an extensive development of fibrous tubercular tissue, 
and it may be assumed that the 'primary pleurisy in all such cases is also 
tubercular. Bronchial hemorrhage is frequently the first and only sign of 
phthisical developments. It is claimed that tuberculosis precedes and 
causes the hemorrhage. Unquestionably such bronchial hemorrhages indi- 
cate a vice of constitution which favors phthisical developments ; but it 
requires no argument to prove that the hemorrhage is not of necessity an 
evidence that tubercles exist in the lung at the time of the hemorrhage. 
The connection which exists between phthisical developments and bron- 
chial hemorrhage is not always clear. 

The mechanical irritation of the bronchi produced by the constant inha- 
lation of an atmosphere laden with dust leads to phthisis. The phthisis 
of knife-grinders, stone-cutters, potters, and coal-miners, are examples 
of this. It must be stated, however, that the primary fibroid changes 
in the lungs of such persons do not always become tubercular. The 
constant inhalation of noxious gases, such as are generated in over- 
crowded, badly ventilated apartments, is a frequent predisposing cause 
of phthisis. 

Pregnancy, instead of preventing phthisis, as was at one time supposed, 
predisposes to it, and renders its course more rapid in those who are already 
phthisical. 

Emphysema and goitre have been by some supposed to afford an immu- 
nity against phthisis, but my observations lead me to the conclusion that 
it is a very frequent attendant of both these conditions. The notion that 
malaria and marsh fevers are antagonistic to phthisis is disproved by every- 
day experience. The relation between diabetes mellitus and pulmonary 
phthisis is not well understood, but that one complicates the other very 
frequently is a clinical fact. 

The factors which determine whether a particular pulmonary tubercu- 
losis shall result in recovery, or acute or chronic phthisis, are found in the 
manner of the infection and the diathesis of the patient. Sufficient quan- 
tities of infective material may be received by those of high resisting power 
to develop an acute phthisis, and small amounts in those of strong tuber- 
cular tendency may induce a similar condition. Patients in whom all 
inflammatory processes tend to necrosis and suppuration are more liable 



ACUTE PULMONARY TUBERCULOSIS. 



207 




to acute phthisis, while those of a strong fibroid diathesis are not only less 
liable to tubercular disease, but, even when infected, quite certainly develop 
chronic forms of the disease. 

Symptoms. — A young adult who for some time 
has had a dry, hacking cough, with a gradual 
but steady emaciation, is suddenly seized with a 
sharp pain in the side ; the pulse becomes rapid 
and feeble, and the temperature rises to 104° in 
the evening, while the morning temperature may 
be normal. With increase in pulse-rate and 
temperature the skin becomes pungently hot. 
The fever alternates with night chills and pro- 
fuse sweats. The cough is soon accompanied 
by an opaque, purulent expectoration, in which Tubercle Bacim from Pht hisicai 
are found numerous tubercle bacilli and yellow s P utum - stained with Fuchsia, 
elastic fibres. There is rapid loss of flesh and f Gmupfo/m^same 
strength; the patient becomes extremely anae- ^ — VaT^Xn 
mic ; and the constant harassing cough causes famtly at c, &. x 500. 
loss of sleep and extreme exhaustion. The expectoration is usually not 
abundant until after the breaking down of the lung-tissue has occurred. 
Patients ascribe the emaciation and weakness to the profuse sweats. The 
respirations and the pulse-rate increase in frequency with the fever. The 
pulse ranges from 120 to 135. Cardiac palpitation and sudden accelera- 
tion of the pulse-rate follow excitement. In some cases the chill, fever, 
and sweat occur with such regularity that malarial fever is suspected, or a 
malarial element is regarded as the prominent feature. Nausea, vomiting, 
and diarrhoea are often prominent symptoms, and greatly add to the ex- 
haustion which is so marked a feature of the disease. The skin assumes 
a pearly pallor, the hectic flush is present, and the eyes are bright and 
glistening. Haemoptysis may mark the advent of the disease and recur 
at intervals during its course. It is rarely absent during the entire course 
of the disease. Anorexia is always a marked symptom. Not infrequently 
the destructive processes are so rapid as to cause pneumothorax. Acute 
phthisis usually pursues a steadily progressive course, but it may assume an 
intermittent character, and have periods of arrest and apparent amend- 
ment followed by periods of exacerbation and rapid progress. 

Physical Signs. — The physical signs will vary with the seat and extent of 
pulmonary consolidation, and with the rapidity with which destructive 
processes are established. 

Inspection, during its early stage, shows rapid respiration and imperfect 
expansion of the upper part of the chest during a deep inspiration ; as the 
disease advances, the loss of expansion becomes more and more apparent, 
but there is no infra-clavicular retraction. 

On palpation the loss of motion in the infra-clavicular spaces is more 
apparent ; and if the pleuritic changes are not extensive, there will be 
increased vocal fremitus. 

On percussion there will be more or less dullness over the infra-clavicular 



20S 



DISEASES OF THE RESPIRATORY ORGANS. 



spaces. If there are large superficial cavities which contain little fluid; 
there will be amphoric or cracked-pot resonance. 

Upon auscultation, in the early stage, expiration is notably prolonged 
and high-pitched, and fine mucous rales with fine crepitation will be 
heard over the affected district. The respiration is wavy and interrupted. 



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Fig. 45. 

Temperature in a case of Acute Phthisis. Patient set. 25. The larger falls of temperature, on the 5th, 9th, 
16th and 24th clays followed the administration of sulphuric ether. Falls of a degree and a degree and 
a half were induced by large doses of the sulphate of quinine. 

Death occurred after a steady rise in temperature for a week preceding. 

There may be distinct bronchial breathing and bronchophony over a 
circumscribed space posteriorly in the scapular region. Excavations take 
place rapidly in the consolidated portions of the lung ; they are of varying 
size and are situated at varying distances from the surface of the lung. 
Deeply-seated cavities, when filled, give deep-seated dulness, and, when 



CHROMIC PULMONARY TUBERCULOSIS. 



209 



empty, an exaggerated percussion resonance. Over small cavities with 
lax walls low-pitched, puffing, cavernous respiration will be heard. This 
is very frequently heard in acute phthisis where soft yielding walls result 
from rapid pulmonary necrosis. Amphoric breathing, gurgles, and 
metallic tinklings will be heard over large cavities which communicate 
freely with bronchial tubes. The sub-clavian murmur (discussed in 
chronic phthisis) is not so liable to be heard in acute as in chronic phthisis. 

Differential Diagnosis. — Acute phthisis may be mistaken for croupous 
'pneumonia, bronchiectasis, and acute general capillary bronchitis. 

In pneumonia the prolonged ushering-in chill, the continuous high 
temperature, the characteristic sputum, the dulness limited to a lobe, and 
the pneumonic countenance, are symptoms which readily distinguish it 
from acute phthisis. In some cases the differential diagnosis cannot be 
made during the first week. Bronchiectasis accompanied by wasting, 
fetid expectoration, haemoptysis, and night sweats, with the physical signs 
of consolidation, may well be mistaken for the advanced stage of acute 
phthisis. In phthisis the signs of consolidation precede those of cavities ; — 
in bronchiectasis they follow them. Fever and emaciation are always 
greater in phthisis than in bronchiectasis, and the symptoms are more 
steadily progressive. In capillary bronchitis there is no dulness on per- 
cussion, subcrepitant rales are heard on both sides of the chest, and there 
is no bronchial character to the respirations. The temperature range is 
lower than in phthisis. Emaciation is rapid in phthisis, and the signs of 
the formation of cavities occur early. 

Prognosis. — The prognosis in acute phthisis is always unfavorable. Its 
average duration is from five weeks to five months. A sudden ameliora- 
tion of the symptoms may occur before the cavities are formed, but the 
amelioration is one of short duration, and is usually followed by a more 
rapid progress of the disease. It may be complicated by pleurisy, pneu- 
mothorax, hydrothorax, peritonitis, and, rarely, by pericarditis. Death 
may occur from exhaustion, asthenia, or complications. Acute capillary 
bronchitis and pulmonary oedema and congestion often lead to a rapidly 
fatal termination. 

Treatment. — Most cases are hopeless ; the dietetic and climatic methods 
employed in chronic phthisis have no place in the management of acute 
phthisis. 1 Morphia in small doses — one-twentieth of a grain hypoder- 
mically every six or eight hours — has, in my hands, been more satisfactory 
in staying the progress of the disease, prolonging life, and keeping the 
patient comfortable, than any other plan. 

CHROXIC PULMONARY TUBERCULOSIS. 

{Chronic Phthisis.) 

Chronic pulmonary tuberculosis presents, both clinically and anatomi- 

1 Dr. McCall Anderson (in London Lancet, June, 1877) takes a more hopeful view of these cases, and 
claims that subcutaneous injections of atropia check the exhausting sweats ; and that quinine, digitalis, 
and opium reduce the temperature, and if they fail, ice-cloths to the abdomen will accomplish the desired 
result. His reported results are exceedingly encouraging, but the failure of his treatment as tried by others 
causes many to doubt his diagnosis. 
14 



210 



DISEASES OF THE RESPIRATORY ORGANS. 



cally, three well-marked varieties, dependent upon the form of the tuber- 
cular development and the character of the secondary inflammation. 
They may be designated as : 

1. Pneumonic tuberculosis, caseous pneumonia, or catarrhal phthisis. 

2. Disseminated tuberculosis. 

3. Fibrous tuberculosis, or fibroid phthisis. 

Aside from these distinctive forms, many cases will be seen in which the 
several tubercular developments are variously commingled. 
Morbid Anatomy. — Pneumonic tuberculosis. 

The primary tubercular developments occur in the bronchi and alveolar 
cavities, and not only may be, but often are, preceded by localized bron- 
chitis or catarrhal pneumonia. 

The tubercular tissue fills the air-cells in one of two ways : (1) by poly- 
poid outgrowths from the alveolar 
walls, consisting of round and polyg- 
onal cells in a basement substance ; 
(2) by masses of similar cells — with or 
without giant cells — not in connection 
with the alveolar walls, which partially 
fill the vesicles of the affected lobules, 
the intervening space being filled with 
inflammatory products. These masses 
vary in size. They may be limited to 
a single lobule, or may attain the size 
of a walnut. 

After a time masses of cells obstruct 
the bronchioles. The nutrition of the 
bronchial walls at the seat of the ob- 
struction is interfered with, and they 
become attenuated, or a peribronchitis 
is developed. This peribronchitis is 
primarily tubercular, and secondarily 
necrotic and suppurative or fibrous. 
Early in the process lymphoid cells 
infiltrate the alveolar septa, the bronchial walls, and the alveolar contents. 
Pressure on the vessels in connection with endothelial proliferation in their 
lumen, and thrombosis, as well as the direct action of the bacilli, induce 
caseation of the tubercular and inflammatory products. As caseation 
advances, all the elements become granular and are agglutinated by a 
slightly transparent substance which glistens like fibrin upon the addition 
of acetic acid. These cheesy masses are found in patches ; they are fri- 
able, and present a gray homogeneous appearance, forming the so-called 
yellow tubercle, and contain bacilli. Before distinctly necrotic processes 
supervene, ulcerations may occur in the bronchioles. Ulcers thus formed 
in the tubes are usually sharply defined and shallow : sometimes they 
involve adjacent lung tissue as well as the bronchial tubes. 

The gross appearance of lung-tissue involved in this form of phthisis, 




Fig. 46. 
Pneumonic Tuberculosis. 

Section- of lung shoiving two alveoli. 
A, A. Wall of alveoli covered with changed epithe- 
lium. 

B. " Polypoid outgrowth " from the alveolar 
wall, nearly filling the air-vesicle— composed 
of a delicate, gran ular basement substance in 
which are imbedded round and polygonal 
cells. 

C, C. Epithelial cells betiveen the last and wall of 
the air-vesicle. 
D. Alveolus partly filled with epithelial and 
lymphoid cells in the basement substance. 
x 280. 



PNEUMONIC TUBERCULOSIS. 



211 



before necrotic changes supervene, varies. It may be of a gray color, hard 
and glistening, described by Laennec as "gray infiltration" 1 or it may 
appear as a colloid jelly-like mass (" gelatin if or m infiltration" of Laennec, 
or the "colloid caseous pneumonia " of Thaon). 

When a few lobules only are involved, they may become encapsulated, 
or may undergo resolution. It is rare, however, for a lung to return to 
its normal condition unless the nodules are small and few in number. 
Even should the masses be removed, obliteration of the alveoli which they 
occupied is apt to occur. If a cheesy nodule is encapsulated, cretaceous or 
chalky material is found in the centre of the fibroid tissue. The lung- 
tissue between these nodules may be anaemic, hyperaemic, (Edematous, or 
emphysematous, or the seat of atelectasis. The larger the noclule and the 
more rapidly it has formed, the more liable is it to soften. Cheesy masses 
may soften, and by a process of ulceration be removed through the bronchi. 
Absorption of caseous matter by the lymphatics is attended by more or less 
adenoid hyperplasia, and a group of miliary granules may be developed 
about a caseous centre, the remainder of l^he lung not being involved. 
Sometimes softening and ulceration are so rapid that the process becomes 
distinctly gangrenous. 

Cavities. — The walls of a phthisical cavity are always irregular. At first 
they are soft and friable ; later they become tough, smooth, and fibrous. 
Bands of dense connective-tissue traverse them, sometimes covered by 
a layer of granulation- 
tissue, and vessels and 
large bronchi often 
extend across them. 
Sharply "cut-off" stubs 
of bronchi often project 
half an inch from their 
walls ; portions of the 
wall may stand out like 
the columnar carneae of 
the heart ; or the sur- 
face may be uneven or 
ragged. The connec- 
tive-tissue trabecular ex- 
tending across a cavity 
frequently contain 
blood-vessels, whose 
rupture may cause fatal 
haemoptysis. When 
cavities are formed, the 
lung-tissue around the 
cavity will be indurated, 
and the cavities will be separated from one another by bands of firm 

1 The infiltrated tubercle of Laennec is considered as desquamative pneumonia by Buhl, and scrofulous 
inflammation by Eindlieisch. 




Fig. 47. 
A Lung Cavity. 

A. Stump of sm.aU bronchus.— B, B. Bands of fibrin.— C. Loon of 
blood-vessels in bed of cavity.— I). Smaller cavities opening into a 
larger one. 



2VZ 



DISEASES OF THE RESPIRATORY ORGANS. 



fibrous tissue, arid the peri-bronchial and peri-vascular connective-tissue 
sheaths and the thickened pleura will all be involved in an indurative 
process. Cavities increase in size by peripheral disintegration, or several 
small ones may coalesce and form one large, irregular excavation. Phthis- 
ical cavities contain air and a grumous purulent fluid of a yellowish or 
greenish color, with which shreds of lung-tissue may be mingled. If the 
growth of a phthisical cavity becomes arrested, a "limiting membrane 
forms on its inner surface." The purulent secretion from it at first is 
abundant, later it diminishes, and the case becomes one of a " quiescent 
cavity." A large cavity may, by contraction of the fibrous tissue around 
it, have its walls approximated, but not united. True cicatrization of a 
chronic cavity which has a distinct lining membrane rarely if ever occurs. 

Ulcerating cavities are those which, having been long quiescent, take on, 
for some reason, an ulcerative process. A small cavity at the surface of the 
lung, after having caused a localized pleurisy and a thinning of the friable 
wall of consolidated lung- tissue which separates the pleura from the cavity, 
may break through into the pleural cavity and cause pyopneumothorax. 
Pleurisy is rarely absent in this variety of chronic phthisis ; firm adhesions 
form, and the pleura may be from three-quarters of an inch to one inch 
thick. These changes — pulmonary and pleuritic — are best marked at the 
apices. 

The bronchial glands may be softened, cheesy, chalky, pigmented, and 
enlarged. The right heart is frequently hypertrophieel or dilated. 

Disseminated tuberculosis is characterized by gray tubercle granules 
scattered more or less abundantly throughout the affected portion of the 
lung, or by masses of them agglomerated by fibrous tubercle-tissue. 

The lungs are large, emphysematous, and pale, unless pneumonia, con- 
gestion, or oedema is present. The surface of the lungs is often marbled. 
The apex of the lung is studded with firm, hard, gray, or cheesy nodules, 
varying in size from a pin's head to that of a pea. 

Upon section of a lung which shows these changes, muco-pus flows from 
the cut bronchi. Peribronchitic and inter-alveolar interstitial pneumonia 
is developed to a greater or less degree around these nodules, with irregular 
dilatation of the alveoli. These nodules originate chiefly in the lymph- 
sheaths of the arterioles, in the peribronchial adenoid tissue, or in the 
small masses of cytogenic tissue in the alveolar walls. 1 These bloodless 
nodules are incapable of suppuration, resorption, or organization.. As the 
tubercle-tissue about the vessels increases, it causes occlusion of their 
lumen. The lumen of the occluded vessel is occupied by granular fibrin, 
and on transverse section a row of white blood-corpuscles and of endothe- 
lial cells is often seen between the coagulum and the vessel wall. In recent 
cases the walls of the vessels are very easily distinguished. But if the 
centre of the tubercle has become caseous, the vessel wall is also altered 
and is very indistinct. Thickening of the alveolar walls may also result 

1 Rindfleisch states that the points at which the smallest bronchioles become continuous with alveolar sacs 
are the situations of tltt first eruption of the tubercles, and that the first lesion is a tuberculous infiltration of 
all the angles and projections situated at these points. 



DISSEMINATED TUBERCULOSIS. 



213 




Fig. 48. 



Section 



lung showing a small miliary tubercle, with 
surrounding pulmonary alveoli. 
A. Cheesy centre of tubercle. 

B. B. Trabecule? of the basement tissue of the tubercle, 

containing lymphoid elements, large cells, etc. 

C. C. Divided arteries with in filtration of their vail 

with tubercular tissue. 
D B.B. Lung alveoli filled with catarrhal products, x 50. 



from the development of tubercle-tissue in them. Many claim that 
the commencement of the process is a small cellular projection on one 
side of an alveolus, which, as 
it grows, pushes the capillaries c.\ * a J.<* 
and the epithelium with it into 
the alveolar cavity. The bron- 
chioles are thickened and di- 
minished in calibre; sometimes 
there are complete peribronchial 
cylinders of new embryonic or 
tubercle-tissue. The alveolar cav- 
ity may be filled by the new 
formation, the walls remaining 
intact ; or the wall may be de- 
stroyed by the growth of the pro- 
jecting nodule, and thus com- 
munication opened between 
adjoining air- vesicles. 1 

After coalescence of masses of 
tubercle-tissue, anaemic necrosis 
occurs ; the cellular elements become granular, atrophied, and fatty, and 
form cheesy yellow masses. These caseous masses are easily removed from 
the parenchyma in which they are imbedded. Surrounding these masses 
are found groups of gray miliary tubercles. The mode of the formation of 
cavities and their appearance are the same as already described. Between 
the ulcerous cavities the lung-tissue may be emphysematous, engorged, or 
pneumonic. The bronchi are filled with muco-pus ; their mucous mem- 
brane is the seat of a catarrh, and is congested and trabeculated. Their 
walls are thickened, tubercle-tissue is found in them, and ulcers are not 
infrequent. 

The pleura is congested, and covered with fleshy, soft vegetations over 
the parts involved in the chronic phthisical processes. Organized adhe- 
sions are common ; in them tubercles maybe found, and also in the pleura. 
Tubercles may be found in the larynx, trachea, mesenteric and lymphatic 
glands, and in the mucous surfaces of the alimentary tract, the perito- 
neum, spleen, kidney, liver, brain, bladder, and testes. Fatty heart is not 
uncommon. Thus a chronic local disease of slow and seemingly inter- 
mittent progress is found associated with evidence of general infection. 
The recent dictum is that chronic tubercular growths may heal. Many, 
however, believe that, once established, the process can never become 
quiescent. 2 Ulceration, dilatation of the bronchi, and the formation of 
large cavities are not infrequent attendants on this process. 3 

1 Hamilton states that this appearance, which so resembles the condition of the lobules in catarrhal 
pneumonia, has caused the mistake of regarding tubercle and catarrhal pneumonia as identical. 

2 Rindfleisch advances a new doctrine of the " healing processes in tuberculosis of the lung,' 1 viz. : it 
consists in a shrinkage of the infiltration, combined with a formation of new vessels. These vessels do not 
penetrate deeply into the infiltration, but surround it and supply it with constant, though scanty, nourish 
ment. It is a " fibrinous shrinkage : " the capsule not only encloses, but nourishes. 

3 In a variety called by O. Clark and Rindfleisch "Broncho-phthisis Pulmonalis" the central feature 
of the change is an extensive ulceration of all the bronchi of medium size down to the intra-lobular 



214 



DISEASES OF THE RESPIRATORY ORGANS. 



Fibrous tuberculosis, or interstitial tubercular pneumonia, is char- 
acterized by the diffuse development, in the lungs, of dense fibrous tissue 
associated with tubercles. The fibrous changes may be primary, an inter- 
stitial pneumonia, with subsequent tubercular infiltration, or the in- 
flammation secondary 
to tubercular develop- 
ment may assume the 
fibrous character, and 
involve not only the 
tubercle, but the pul- 
monary tissue as well. 

T b e affected lung 
is diminished in size. 
The pleural surfaces 
are adherent and 
greatly thickened. A 
Hf section of a portion of 
lung that is the seat 
of this variety of 
phthisis presents a 
smooth or granular sur- 
face, or it has a stri- 
ated appearance. If 
granular, the granules 
. . S™- 49 - . . . are imbedded in the 

Section of lung showing a small tubercular nodule loith surrounding 

alveoli. fibrous mass. The n- 

A. Cheesy centre of 'nodule. , ,. , . 

B, B. Fibrillar basement substance containing cells and nuclei. DrOUS tl SS U e Contains 

C, C. Giant cells. i • , 

d. vacuoles. more or Jess pigment 

E, E, E. Alveoli, surrounding thetubercle, containing pneumonic products, vv , n (.„„;.,i - t T 7 T-,;«'K Tr ,r, 
F. Part of wall of an artery infiltrated with tubercle-tissue, x 250. material, WHICH gives 

to the cut surface a 

bluish or gray color. If the process is old, the lung will be tough ; if 
recent, it is less resistant and less leathery. When the disease has existed 
for a long time, the apex, and sometimes the whole lung, is converted 
into fibrous tissue, all traces of the normal lung-tissue being obliterated. 
The indurated tissue may be studded with nodules. The nodules may be 
small masses of dense fibrous tissue containing a few cells at their centre, 
masses of tubercular tissue, granulation -tissue enveloping tubercles, or 
cheesy masses with tubercles and interlacing fibrous bands. Giant cells 
may or may not be present in the nodules. The connective- tissue growths 
may begin in the walls of the bronchi, alveoli, or blood-vessels, in the 
septa, or in the pleura. The alveoli are at times dilated, at times nar- 
rowed ; they are always deformed. The alveolar epithelium undergoes 
slight multiplication and swelling. New cells also form in the walls. 
Cheesy masses, specks of cretaceous material, and cavities of varying size, 
are found in the hard lung. 

branches. Spaces of all sizes are seen — on section— connected with one another. Rindfleisch states 
that a " desquamative pneumonic process 11 accompanies this peculiar form of tuberculosis of the lung-. 




CHRONIC PULMONARY TUBERCULOSIS. 



215 



The bronchi are at times thickened, at times thinned. Bronchiectatic 
cavities (cylindrical, fusiform, or sacculated) are found, chiefly in the apex. 
The appearance of these cavities is similar to that described in chronic 
interstitial pneumonia. Through ulcerative processes, cavities, often of 
large size, result from these bronchiectases. As the disease progresses, 
more and more of the tubercle-tissue is changed into connective-tissue. 
But while the growth of connective-tissue is extra-alveolar, the tubercle- 
tissue is both extra- and infra-alveolar. The early stage of connective- 
tissue development consists in the accumulation of a large number of small 
cells looking like granulation-tissue and lymphoid cells ; while, in the later 
stages, we find dense fibrillated tissue containing a few T cells — and those 
spindle-shaped — and an abundant supply of irregular blood-vessels. Tuber- 
cles may also be found in the pleura. 

Etiology. — The same factors are concerned in the development of chronic 
as of acute tuberculosis. Local inflammations, however, play a more 
prominent part in rendering the pulmonary parenchyma less resistant to 
bacillary invasion. 

Some authorities state that bronchitis, catarrhal pneumonia, or pleurisy 
do not predispose to phthisis. My own experience is to the contrary. 
The only possible inference to be drawn from the fact that, of two per- 
sons living under similar conditions, one surfers from phthisis and the 
other does not, is that the failure of the bacilli to develop in the one case, 
and their success in the other, depends upon the vital power of the tissues 
to resist their invasion and to prevent their growth. 

It is well determined that inflammatory processes decrease the power 
with which the tissues resist the invasion of other bacteria ; and not only 
analogy, but all the well-established principles of pathology as well as clin- 
ical facts, prove beyond question that inflammatory, and particularly sup- 
purative processes, favor the development of tubercle bacilli. 

Pulmonary irritants which lead to fibrous formations are not only less 
liable to be attended by tuberculosis, but tend to prolong its course, and 
even to result in arrest or cure of the disease. Anthracotic changes show 
but little tendency to become tubercular, and when infection does occur 
fibrous phthisis results. 

Symptoms. — There are certain symptoms which characterize the early 
stages of each variety of tuberculosis. 

Pneumonic tuberculosis usually commences as a bronchial catarrh. The 
cough is paroxysmal and accompanied by tenacious muco-purulent sputa, 
now and then blood-stained. There is a gradual but steady loss of flesh 
and strength ; the patient grows pale and has an occasional night-sweat. 
These symptoms are accompanied by the physical signs of slight consolida- 
tion at the apex of one or both lungs, with those of localized bronchitis, 
of the small tubes. A localized pleurisy is very certainly present in these 
cases. Sometimes this variety begins with more acute symptoms, and the 
physical signs of apical lobular pneumonia are present. In such cases the 
pneumonia does not resolve, and the fever takes on a distinctly remittent 
type, with a more rapid loss of flesh and strength, and a copious purulent 



216 



DISEASES OF THE RESPIRATORY ORGANS. 



expectoration, often blood-streaked. Night-sweats become profuse and 
exhausting, and there are the physical signs of progressive consolidation of 
lung-tissue. At any time during the early stage the physical processes may 
be arrested, and during the period of arrest there may be a great improve- 
ment in the general condition of the patient, and complete recovery is 
possible. But in a large proportion of cases a return to the anti-hygienic 
conditions in which its primary development occurred, or a fresh bron- 
chitis, lights up anew the phthisical process. 

Disseminated tuberculosis may for a ]ong period give no distinctive signs ; 
for interstitial pleurisy, chronic bronchitis, and emphysema nearly always 
accompany it, their prominent symptoms masking those of tuberculosis. 
Patients with this form become emaciated ; their dyspnoea resembles that 
of emphysema. The expectoration is in the earlier stages mucous, and 
later it becomes muco-purulent. Haemoptysis is common ; and hectic 
fever is more pronounced than in any other variety. There are no periods 
of improvement, though there may be periods during which the disease 
remains stationary. Pleurisy, laryngitis, and intestinal catarrh are more 
marked than the pulmonary symptoms. As the disease advances, its symp- 
toms resemble those of fibroid phthisis. 

Fibrous tuberculosis — or fibroid phthisis — comes on very insidiously ; it 
may be ushered in by one or more attacks of haemoptysis. In most cases 
it commences with the physical signs of a localized bronchitis and pleurisy 
at the apex of one lung. Cough, and a muco-purulent expectoration with 
more or less pain in the affected lung, may exist for a long time before there 
is any marked impairment of the general health. After a variable period 
the patient begins to lose flesh and strength, the cough increases, and the 
expectoration becomes more abundant. There is a progressive loss of 
appetite, but at no time is the temperature high or the pulse rapid. Dysp- 
noea becomes more and more marked, especially on exertion. Eetraction 
of the chest walls under the clavicle commences quite early and is steadily 
progressive. The limited play of the chest walls is the most distinctive 
early sign. This variety of phthisis rarely occurs in young persons, and it 
is often associated with a rheumatic, gouty, or syphilitic taint, or is the 
result of mechanical irritation. 

Of the symptoms which are common to all varieties of tuberculosis, the 
significance which is to be attached to the presence or absence of bacilli in 
the sputa is of paramount importance. 

Without entering upon a discussion of this question it may be stated 
that single examinations of the sputa cannot determine either the presence 
or absence of tuberculosis. The presence of small numbers of bacilli may 
be possible after prolonged exposure to infection, when tubercle has not 
formed. Persistent absence or presence of bacilli, or large numbers in the 
sputa, however, are almost positive evidence of the character of any pul- 
monary disease. The number of bacilli in any given specimen has little or 
no diagnostic significance, since the rupture of a caseous focus may have 
filled the sputa temporarily when there is little actual disease in the lung. 
Few of those who rely least upon the presence of bacilli for prognosis 
would care to find their ow T n sputa persistently loaded with them. On the 



CHRONIC PULMONARY TUBERCULOSIS. 



217 



other hand, bacilli may be absent for a considerable period from the sputa 
of those who are unquestionably suffering from extensive pulmonary tuber- 
culosis. They may be present at one time, and absent at another in any 
given case. We are often able to recognize phthisical consolidation before 
bacilli appear in the sputa. 

In analyzing the symptoms which are common in all varieties of chronic 
phthisis I shall first consider the cough. It is the earliest and most con- 
stant of all the phthisical symptoms. It is present early and continues 
throughout the whole course of the disease. At first it is dry and hack- 
ing. It may exist before there are any physical signs, and then there is 
little or no expectoration; it may amount only to a "clearing of the 
throat." The severity of the cough without expectoration is a measure of 
the extent to which the pleura is involved. The younger and more excit- 
able the patient, the more paroxysmal is the cough. It is usually worse in 
the morning on rising, or just after lying down at night. Lying on the 
affected side often brings on violent paroxysms. Some cough after the 
slightest exertion ; others have a varying number of paroxysms during the 
day, and can estimate how long an interval of rest they will have between 
the paroxysms. The loss of sleep occasioned by the cough may add much 
to the discomfort and wasting of the patient. In advanced phthisis, when 
cavities have formed, the cough becomes " hollow " in character. Expec- 
toration may accompany cough from its commencement. At first it is 
tenacious, glairy, frothy, and mucous ; then yellow purulent spots are 
found in it. It is always important to ascertain whether pallor, fever, and 
emaciation have been preceded by cough and expectoration, or whether 
emaciation was the primary symptom. The sputa are gelatinous and 
faintly pink when , the infiltration is extensive. Vitreous, gelatinous, 
rounded masses may be mingled with yellow catarrhal expectoration, and 
these are evidences of a recent pneumonia. Dots and streaks of blood in 
catarrhal sputa indicate a lobular pneumonia ; and when this occurs, fatty, 
swollen, and granular bronchial and alveolar epithelium will be found 
intermingled in the mass. The sputa in the earlier stages — often for 
months — are muco-purulent. When shreds of elastic tissue are found, it 
indicates softening and destruction of lung-tissue. Elastic fibres are gen- 
erally found in compact, airless, uneven masses, which readily sink in 
water. As cavities form, the sputa become more purulent, sometimes 
being wholly composed of fluid pus, which may be fetid and greenish, and 
contain elastic fibres coming from the alveolar wall, organic matter, fat- 
crystals, pigment, young cells, and small masses of cheesy matter, and the 
tubercle bacilli ; the latter are present in the sputa of all varieties of 
advanced phthisis. The quantity of matter expectorated varies with the 
extent of the bronchial catarrh and the number and size of the cavities. 
It may be expectorated readily, or only with difficult}'. Usually, the more 
feeble the patient the more difficult the expectoration. In rapidly formed 
cavities the expectoration may contain fragments of bronchioles and blood- 
vessels, w T ith shreds of lung-tissue. 

Haemoptysis is a very important symptom of phthisis, and may occur 
during any stage of the disease ; the blood may simply streak the sputa, 



218 



DISEASES OF THE EESPIRATORY ORGANS. 



or a pound or more may be expectorated at one time. Hemorrhages that 
occur in the early stage of pulmonary phthisis are, in the majority of 
instances, bronchial, and the blood expectorated is arterial in color. When 
streaks of blood appear in the sputa, the bleeding usually comes from the 
vessels of the alveolar walls. Profuse hemorrhages in the later stages of 
phthisis have their origin in cavities in the lung substance. Hemorrhages 
that occur in the early stages may be profuse, but they are rarely danger- 
ous ; hemorrhages in advanced phthisis may be the immediate cause of 
death. Haemoptysis usually comes on with coughing. There is a sen- 
sation as if a fluid were trickling underneath the sternum, and there may 
be violent cardiac palpitation, oppressed breathing, and a peculiar sweetish 
taste in the mouth. In profuse hemorrhage the rapid flow of blood into 
the mouth may excite vomiting and be mistaken for haematemesis. For 
some time after the primary hemorrhage blood is coughed up, and the 
color of the spitting becomes darker and darker. Sometimes without 
warning there is sudden filling of the mouth with hot arterial blood. 

Many English writers describe a hemorrhagic phthisis. In this variety 
an apparently healthy man has a sudden and profuse hemorrhage, recurring 
daily for some time, and followed by cough and slight expectoration for 
a few days, with no physical signs of consolidation. These cases often 
continue for years without any other phthisical symptoms, but sooner or 
later phthisis is developed. 1 Haemoptysis often occurs in those who have 
no physical or rational signs of phthisis at the time of its occurrence, and 
who do not become phthisical afterward. Although haemoptysis occurs 
more frequently in phthisis than in any other pulmonary affection, and 
there are few phthisical subjects who do not have one or more hemorrhages, 
yet its occurrence is by no means a certain indication that an individual 
afterward will develop phthisis. 

Fever. — Rise in temperature is so constant a symptom of phthisis that 
it has led to the expression, "there is no consumption without fever;" 
but in no two cases is the fever course exactly the same. In some cases 
the temperature in the morning may be subnormal, only reaching normal 
in the evening; in others the rise commences at 2 p.m., continues until 
8 p.m., and then falls until 5 in the morning. Between 10 and 11a.m. 
the temperature is nearly normal. As cavities form, the post-meridian 
rise occurs later ; i. e., 10 to 12 at night. Toward the end of the disease 
the fever type resembles that of pyaemia. Night-sweats temporarily lower 
the temperature. When the alveoli are involved in tubercular pneumonic 
processes, the temperature rises rapidly to 103°-104° F. Hectic fever may 
occur in any stage of phthisis, but is usually confined to the stage of soften- 
ing and excavation. It has three stages : first, at some time during the 
day there is a well-marked chill or chilly sensation, which may last from 
half an hour to an hour, followed {second) by a dryness and heat of the 
surface, the temperature rising from 102° F. to 104° F., the face assuming 
a peculiar brilliant appearance, and the cheeks having a peculiar rosy tint 
called the " hectic flush." After a time the fever gradually subsides, and 
some time in the night (it may be toward morning), the third or sweat- 

1 Tubercular disease of the vascular walls is the primary and chief event in such cases. 



CHROMIC PULMONARY TUBERCULOSIS. 



219 



ing stage comes on. The night-sweats are usually profuse and exhausting, 
and always indicate the existence of hectic fever. The chilly feeling may 
be absent, the subsequent fever may be so slight as to be overlooked, but 
sweats are constant. A steady and continuous low temperature indicates 
that the phthisical processes are retrogressive ; a steady and continuous 
high temperature indicates that they are progressive. In fibroid phthisis 
the temperature rarely rises more than a degree or two above the normal. 
In the absence of local symptoms, the thermometer alone may detect pul- 
monary phthisis in the aged. 1 An intermittent temperature indicates a 
milder process than a remittent or continuous febrile action. 

The pulse in chronic phthisis bears no uniform relation to the temper- 
ature ; it is always feeble. It varies greatly in frequency and force, but 
rarely in rhythm ; it is accelerated by slight exciting causes. In the early 
stages its excitability is one of its most characteristic features. The 
arterial tension is below the normal. In the early stage of fibroid phthisis 
it is rarely over 100. In a few cases it is abnormally slow. An improve- 
ment in the other symptoms is not always accompanied by an improvement 
in the pulse. In the last stage of all varieties of phthisis the pulse becomes 
Tery rapid and feeble. 

The respirations are more or less accelerated, and after exertion there 
is dyspnoea. When the patients are quiet, unexcited, and resting in bed, 
the respirations may be normal or but slightly increased. But on ex- 
ertion the breathing becomes accelerated and labored. The accelerated 
breathing is due to the fever, the diminished breathing area, to bronchial 
obstruction, and to pain in the chest. Anaamia and heart failure may also 
contribute to it. In the absence of fever the dyspnoea and accelerated 
breathing diminish. The extent to which the lungs are involved influences 
the frequency of the respirations. In young subjects the dyspnoea is fre- 
quently periodical. During the whole course of fibroid phthisis, shortness 
of breath on exertion is a constant symptom. 

Pain in the chest is not a prominent or constant symptom of chronic 
phthisis, except in connection with pleuritic changes. Dry and inter- 
stitial pleurisies are common ; yet they seldom cause severe pam, but 
rather a sense of tightness and constriction on taking a full inspiration. 
Intercostal neuralgia is frequent and may be confounded with the pain 
of a localized pleurisy. Dragging pains in the side are most marked in 
fibroid phthisis. Pain on swallowing should always cause one to carefully 
examine the larynx. It usually announces the co-existence of laryngeal 
phthisis. 

Emaciation is an early and constant symptom of phthisis ; but it is 
not always progressive. Fever is the chief cause of the wasting and pallor 
that are so common in all varieties of phthisis. The higher the average 
range of temperature, the more rapid the emaciation. The pulmonary 
change may be preceded by progressive emaciation, but in all such cases 

1 Sir William Jenner makes three clinical types of chronic phthisis in reference to temperature— the 
insidious, the active febrile, and the adynamic. In the first the morning temperature is normal ; in the 
second, the morning temperature will be about 100° or 101°, and the evening temperature 103°-lO4°. In 
thethinl, morning and evening temperatures are both high and not very different; but between these 
times irregular fluctuations occur. 



220 



DISEASES OF THE RESPIRATORY ORGANS. 



the average temperature is a degree above the normal. Emaciation may 
be a part of the constitutional tendency of the individual, but such 
emaciation forms no part of the phthisical wasting While emaciation, 
loss of strength, and progressive anaemia are recognized premonitory 
symptoms, they cannot be regarded as diagnostic. Emaciation may not 
be continuous in all cases ; there are periods when the patient may even 
regain lost weight and muscular strength. The anorexia, dyspepsia, 
diarrhoea, profuse expectoration, and haemoptysis are all causes of the 
emaciation. Phthisical wasting occurs not only in the fat and muscle, 
but in the organs and blood as well. 1 Slow, gradual wasting belongs to 
the history of fibroid phthisis. 

The symptoms indicating disturbances in the alimentary tract are 
important. Anorexia is often for a long time one of the most promi- 
nent symptoms. It may be accompanied by nausea, vomiting, and pain in 
the stomach, due either to reflex causes or subacute or chronic gastric 
catarrh. At the autopsy we often find a normal gastric mucous membrane 
in one who during life gave the symptoms of acute gastric catarrh. The 
most common cause which acts in a reflex manner to produce vomiting is a 
violent fit of coughing. It is important to distinguish between the vomit- 
ing due to reflex causes and that due to gastric catarrh. With dyspeptic 
symptoms the tongue and pharynx are frequently covered with aphthae. 
The most important interference with digestion which occurs during the 
progress of phthisis is due to changes which take place in the small and large 
intestine. These intestinal changes are marked by more or less tympani- 
tis and by diarrhoea which is often very troublesome and difficult to relieve; 
few altogether escape these symptoms. Diarrhoea may occur in any stage, 
but it is more likely to occur during the later stages ; in some cases 
it alternates with hectic fever. It is usually most severe at night. The 
profuse watery diarrhoea which comes on late in phthisis is called colliqua- 
tive diarrhoea. Hemorrhoids and fistulm in ano are frequent trouble- 
some complications of phthisis, and should always be relieved by surgical 
interference in the early stages of the disease. The cure of a fistula in 
ano or the healing of an old ulcer is often followed by phthisical de- 
velopments ; and scrofulous joint disease, psoas and lumbar abscesses in 
children are often followed by phthisis in early adult life. 

Cerebral symptoms are rarely pronounced in any stage of phthisis; there 
is no chronic disease in which the mind is so clear. The hopefulness and 
buoyancy of spirits which attend its development are remarkable. The 
least improvement is hailed by the patient as an indication of commencing 
recovery. He speaks lightly of his unpleasant symptoms, and is very 
reluctant to admit that his disease is of a serious nature ; rarely will a 
phthisical patient admit that recovery is not possible. 

Laryngeal symptoms of phthisis have been considered under the head of 
Chronic Laryngitis. The pharynx is sometimes the seat of tuberculous 
processes. Arrest of menstruation is a very frequent occurrence in females 

1 Malassez states that the red discs are diminished in number. The haemoglobin is also diminished. 
Leucocytes, fibrin, and calcic phosphate are in excess. Granular masses agglomerate into patches vary- 
ing greatly in size ; and, on a warm stage, they appear to develop into or give rise to organisms which 
move about in the blood. 



CHKO^IC PULMONAEY TUBEKCULOSIS. 



221 



who are consumptive. In young females this is sometimes the first 
noticeable symptom. Its occurrence in advanced phthisis indicates extreme 
exhaustion, and it is often followed by a more rapid progress of the disease. 

The skin is pale, and traversed by prominent blue veins. Sudamina and 
pityriasis versicolor are often observed. The nails curve and become claw- 
like. The terminal phalanges of the fingers become "clubbed/' and this 
is by some regarded as an important diagnostic symptom, but it occurs fre- 
quently in other chronic thoracic affections. It has been regarded as (1) a 
form of scleroderma beginning in the phalanges and extending centrally 
over the body ; (2) as due to interference with peripheral return circu- 
lation ; and (3) as an hypertrophy of connective-tissue. 1 The hair becomes 
thin, dry, gray, and falls out. (Edema of the feet and legs is not an infre- 
quent symptom during the last stage, and its gravity is well recognized by 
the non-professional. Its occurrence indicates that a fatal issue is not far 
distant. It may be due to secondary changes in the vessels, but in a large 
proportion of cases it is due to thrombosis of the veins of the lower extrem- 
ities, the result of an enfeebled heart. 

Physical Signs. — There are two recognized stages in chronic phthisis : a 
stage of consolidation, and a stage of softening and excavation. 

As the disease advances, evidences of the two stages will be found in 
close juxtaposition, areas of consolidation surrounding cavities and points 
of commencing softening. 

The physical signs of the stage of consolidation vary with the extent of 
the consolidation according as it involves large areas or small disseminated 
patches. 

Inspection reveals diminished expansion — on inspiration — in the supra- 
and infra-clavicular regions of the affected side. If there are extensive 
pleuritic thickenings and adhesions, or if extensive fibroid changes exist, 
flattening and retraction, most marked at the end of a full inspiration, 
will be found on the affected side or over the seat of the phthisical devel- 
opment. 

Palpation shows more distinctly the loss of expansion on the affected 
side. Vocal fremitus is slightly increased over the affected lung, although 
extensive pleuritic changes may render the vocal fremitus less distinct. 

Percussion. — The percussion sound will vary with the extent of the 
consolidation and the condition of the lung-tissue surrounding the con- 
solidated portion. There is always more or less pulmonary resonance. If 
the consolidation is slight, the percussion sound may remain normal, and 
localized emphysema may give rise to exaggerated resonance even when 
consolidated lung-tissue exists. When practising percussion, to recognize 
a slight consolidation at the apex of the lung, it is important to percuss 
from the trachea rather than toward it. In all cases percussion should be 
performed at the end of a full inspiration and at the end of a full expi- 
ration. Dulness usually appears first under the scapula, next over the 
sternal end of the clavicle, and gradually extends down, being limited, for 
a long time, to the apex of the lung. If the dulness is slight at first, it 
gradually increases and may reach complete flatness. 



1 In 1.773 cases Pollock found clubbing of the finger-ends in about 25 per cent. 



2'22 DISEASES OF THE RESPIRATORY ORGANS. 

Auscultation. —The auscultatory signs vary greatly in different cases, 
and at different times in the same case. Over the affected portion the res- 
piratory sounds may be feeble or exaggerated, interrupted, " cog-wheeled," 
or wavy. The breathing may be rude or bronchial; or, when rude in 
character, it may be rude and wavy, rude and interrupted, at the same 
time being exaggerated, or it may be feeble and rude. At the commence- 
ment, there may be only a loss in the vesicular character of the inspira- 
tions, with a slight rise in the pitch of the expiration. 

The pitch of expiration as compared with that of inspiration indicates 
the extent of the consolidation. 

Prolonged expiration, ivhen high-pitched, is very significant. The expi- 
ration is prolonged in emphy- 
sema, but low-pitched. Wavy or 
jerking respiration is regarded 
by some as a friction sound, by 
others as the result of a narrow- 
ing of the bronchi which inter- 
feres with the entrance of air into 
the lung substance. Accom- 
panying or preceding changes in 
the respiratory murmur, crepitat- 
ing sounds are heard ; they may 
be crumpling or creaking in 
character. Small mucous and 
sub-crepitant rales, if present, 
are heard loudest after cough- 
ing, and, if the consolidation is 
extensive, they have a metallic 
ring. It is claimed by some that all the rales that are heard in this 
stage of phthisis are produced upon the surface, and not in the sub- 
stance of the lung. This statement is too sweeping, for these sounds 
are usually circumscribed. They can be changed by coughing, and are 
often entirely removed by violent coughing, and can be heard before 
the inspiration is completed. If they were pleuritic, they would remain 
after coughing, and would retain their distinctly crepitating character at 
different examinations. Pleuritic sounds are present in a large proportion 
of cases, but they can be very readily distinguished from rales produced 
in lung substance. Carefully conducted post-mortem examinations show 
that, in a large proportion of cases of phthisis, the pleuritic changes are 
secondary to the changes' in the lung substance. Besides, by inflating 
phthisical lungs after they are removed from the body, sounds similar to 
those heard during life arc distinctly audible if a stethoscope is pressed 
firmly upon their surface. A systolic murmur over the subclavian artery 
of the affected side, heard loudest during expiration, indicates that 
the pleural surfaces at the apex of the lung on that side are adherent, 
Vocal resonance is usually increased in proportion to the percussion 
clulness. 

In the second stage, or stage of softening and excavation, the physical 




Fig. 50. 

Diagram illustrating Physical Signs of the First Stage of 
Chronic Phthisis. 

Partial infiltration at the apex of tJie lung. 



CHROMIC PULMONARY TUBERCULOSIS. 223 



signs of consolidation become more marked, and new auscultatory signs 
are developed. 

Inspection shows a greater frequency of respiration and a more marked 
depression above and below the clavicle on the affected side, as well as an 
increased difficulty in local expansion. In fibroid phthisis the retraction 
is more marked than in any other variety. 

Palpation shows a more marked diminution in expansion of the affected 
side. On forced inspiration — both hands being placed on the chest equally 
far from the median line — the fingers that rest over the affected lung will 
move but slightly compared with those on the opposite side. Vocal frem- 
itus is increased. 

Percussion elicits more uniform and widely-spread dulness, which 
assumes a wooden or tubular character. 

Auscultation. — Bronchial breathing and broncophony become more dis- 
tinct ; numerous moist, crackling rales, unchanged by coughing, are heard 
over a circumscribed space, and have a distinct, sharp, metallic character, 
unlike the crepitation and bubbling sounds which were heard during the 
first stage. 

As excavation becomes more marked, inspection shows greater depres- 
sion in the infra-clavicular region than existed in the preceding stage, and 
there is more complete absence of expansive movements during the respi- 
ratory acts. 

Palpation gives results similar to those of the early part of the second 
stage. Over large cavities containing air and communicating with a bron- 
chus, vocal fremitus is intensified. 

Percussion. — The percussion sound will vary according to the condition 
of the cavities and their surroundings ; over large superficial cavities partly 
filled with liquid there will be amphoric or "cracked-pot" resonance, if 
there is a free communication with a bronchial tube. Deeply- seated cavi- 
ties, when filled, will give deep-seated dulness, and, when empty, an exag- 
gerated percussion sound. A metallic amphoric note is obtainable only 
from a cavity whose transverse diameter is at least to 14- in. 1 Occasion- 
ally, cracked-pot resonance will disappear and remain absent for some 
time, and no evidence of a cavity can be found where one was known to 
have previously existed. This happens when the bronchial tube which has 
communicated with the cavity becomes obstructed in such a manner as 
to prevent the ingress of air and the egress of fluid. 

Auscultation. — Over small cavities with lax walls, low-pitched, puffing, 
cavernous respiration will be heard. When cavities are surrounded by 
firm, tense walls, and are of large size, communicating freely with a larger 
bronchus and are situated near the surface, a musical, or amphoric, res- 
piration is heard. The amphoric echo is sometimes most marked on inspi- 
ration ; at other times on expiration. The clearness of the amphoric 
note is no Avay influenced by the presence of a moderate amount of 
fluid in the cavity. But when the fluid in the cavity has its level at or 
above the opening of the bronchus, the incoming air may bubble up and 
cause gurfjles. These have a metallic quality, and vary according to the 



1 Merbach and Leichtenstern. 



224: 



DISEASES OF THE KESPIRATORY ORGANS. 



character of the fluid, 
bubbling the sounds : 



—the thinner and more watery the fluid, the more 
the thicker the fluid, the more crackling are the 



Cracked-pot resonance 
Cavernous respiration. 

Cavernous whisper . . . 




Fig. 51. 

Diagram illustrating Phvsical Signs of Cavities in the Third 
Stage c'f Chronic Phthisis. 



sounds. Gurgles are always most distinct and abundant during and after 

cough. When very large cav- 
ities with rigid walls contain 
thin liquid, metallic, tinkling 
sounds may be produced by 
coughing and speaking. The 
vocal sounds over large cavi- 
ties have a metallic or musi- 
cal quality. Whispering pec- 
toriloquy is a diagnostic sign 
of a cavity. 

Differential Diagnosis. — The 
early stage of chronic phthisis 
may be confounded with bron- 
chitis, pulmonary infarction, 
pleurisy, acute lobar 'pneu- 
monia, ancemia with cough 
and expectoration, and cancer 
o f the lung. The evidence of consolidation of lung-tissue is essential to the 
diagnosis of phthisis. So long as bronchitis is accompanied by a tem- 
perature of 100° F., and the physical signs show that the bronchitis is 
general, phthisis is readily excluded ; but if the temperature rises to 103° 
F., and localized crepitant rales develop at the apex of either lung, accom- 
panied by dulness on percussion over the seat of the rales, with a bronchial 
character to the respirations, then there is reason to believe that phthisis is 
being developed. If, with these signs, there is gradual loss of flesh and 
strength, the cough becoming hacking in character, and the expectora- 
tion containing fine yellow streaks and blood-stains, it is almost certain 
that phthisis is developing. The diagnosis between chronic bronchitis 
and fibrous phthisis rests upon the evidences of consolidation and retrac- 
tion in phthisis, and their absence in bronchitis. 

Infarctions are attended by haemoptysis and localized areas of dulness. 
Their etiology, however, is very different from phthisis, heart disease being 
their chief cause. The blood expectorated in phthisis is of a bright scarlet 
color ; in infarctions it is dark and in the form of coagula. Infarctions are 
most frequently situated in the lower lobes ; in phthisis the dulness is 
apical. The temperature in infarction is usually lower than in phthisis, 
seldom exceeding 102° F. 

In pleurisy with effusion, flatness will exist from the base of the lungs 
to the level of the fluid ; the line of flatness will change with a change in 
the position of the patient ; the breathing will be exaggerated above the 
line of dulness ; the range of temperature is lower and does not undergo 
such marked diurnal changes as in phthisis. The cough is more hacking 
and is not accompanied by expectoration, and vocal fremitus is dimin- 
ished or absent. If, after the disappearance of the fluid, the lung remains 
compressed and bronchial, or broncho-vesicular breathing is present, with 



CHRONIC PULMONARY TUBERCULOSIS. 



225 



feebleness of the patient, hacking cough and " short breath," the differen- 
tial diagnosis between it and fibrous phthisis is difficult. A localized 
pleurisy afc the apex of the lung, not the result of a general pleurisy, 
is indicative of tubercular developments. 

AncBmia with cough and expectoration is attended by no febrile symp- 
toms, and. by none of the physical evidences of pulmonary consolidation. 

In cancer of the lung there is usually bulging of the chest at the seat of 
the cancerous development; in phthisis there is retraction. In cancer 
the temperature is often sub-normal, in phthisis it is more or less elevated. 
The currant-jelly expectoration of cancer is diagnostic. Pain is constant in 
cancer and intermittent in phthisis. The cancerous cachexia and swollen 
lymphatic glands also aid in the diagnosis of cancer. 

Whenever cavities have formed in phthisis the diagnosis is not difficult 
if the physical signs are properly appreciated ; they can be confounded only 
with those of bronchiectasis. The rules for the diagnosis of bronchiectatic 
cavities are given under the head of chronic bronchitis. In any case the 
presence of bacilli in the sputa renders the presence of phthisis probable, 
and their persistence establishes the diagnosis. 

Prognosis. — Chronic pulmonary phthisis is not necessarily a fatal disease. 
Its morbid processes may be arrested in their early stage in a large propor- 
tion of cases. In the advanced stage, or stage of cavities, proper treatment 
will prolong life, and in some cases permanently arrest the progress of the 
disease. Kecovery has occurred in one-sixth of my recorded cases during 
the past ten years. Its duration depends on the variety and treatment. 
In Laennec's and Bayle's statistics, its average duration is from one to two 
years. My records of chronic phthisis give an average duration of three 
years and four months. The younger the subject, the shorter its dura- 
tion. Phthisis can in no sense be regarded as a self-limiting disease. 
Some cases, after a period of activity, become stationary and then slowly 
recover ; others slowly but steadily progress to a fatal termination ; others, 
again, pursue a more rapid and fatal course. The course that any case will 
take is determined more by the conditions under which it is developed than 
by the natural history of the disease. If an individual has suffered from 
phthisical developments from which he has apparently recovered, his chances 
for recovery from a second attack are greatly diminished. The history of 
phthisical manifestations in early life renders the prognosis unfavorable 
when the disease develops during middle life. 

The prognosis is unfavorable when there is a strong hereditary tendency, 
when phthisis develops early in life, when scrofulous or glandular disease 
has existed in childhood, when the patient is narrow-chested, when the 
ordinary pulse-rate is high, and when there is great variation in weight 
without any apparent cause. Opinions in regard to haemoptysis vary. 
Many think its occurrence renders the prognosis favorable, and that there 
is a larger percentage of recoveries when frequent haemoptysis occurs. 
My own experience leads me to the opinion that frequent haemoptysis in an 
early stage of the disease is not unfavorable. When oedema of the feet and 
lower extremities comes on in advanced phthisis, the prognosis is very 
unfavorable, and a fatal issue is not far off. The following complications 
15 



226 



DISEASES OF THE RESPIRATORY ORGANS. 



render the prognosis unfavorable : pleurisy, pneumothorax, emphysema, 
pneumonia, secondary irruptions of miliary tubercles, pericarditis, menin- 
gitis, diarrhoea, intestinal ulceration, peritonitis (with or without perfora- 
tion), sub-acute gastric catarrh, amyloid degeneration of liver, intestines, 
spleen, or kidneys, chronic laryngeal catarrh, and bronchitis. 

But there is no general law that can be applied to all cases. The general 
condition of the patient, the rapidity of the emaciation, the pulse-rate and 
temperature, the amount of consolidation, the age of the patient, a knowl- 
edge of the progress of the disease in other members of the family, and the 
character of the phthisical process, will indicate the probable course of the 
disease. In chronic phthisis of long standing the future course may be 
determined in some degree by the past history of the case. It must be 
remembered that phthisical patients who seem to be progressing favorably 
may suddenly develop some complication which rapidly terminates the case. 
Again, a case that presents symptoms which indicate a rapid course may 
suddenly be arrested and a retrogressive process be established. Advanced 
cases may die suddenly from heart failure or syncope. The majority waste 
to a skeleton, but the mind is perfectly clear and the patient is hopeful of 
recovery, and makes plans for the future as if perfectly well. 

Treatment. — I shall consider the treatment of pulmonary phthisis under 
three heads, viz. : 

(1) Prophylactic ; (2) Medicinal — internal and local (as inhalations); 
and (3) Hygienic, including the climatic treatment. 

Prophylactic. — During the period when prophylaxis can be successfully 
employed it is possible to prevent the development of phthisis. In one 
whp is delicate and leads a sedentary life, or is engaged in an occupation 
where the surroundings are unhealthy and depressing, or whose family 
history strongly predisposes him to phthisical developments, the occurrence 
of emaciation or loss of strength should immediately lead to such a change 
in habit of life, occupation and surroundings as shall arrest defective nutri- 
tion, invigorate his constitution, and thus counteract his marked tenden- 
cies. Children born of phthisical or decrepit parents should not be nour- 
ished in infancy by their own mothers, but should be placed with healthy 
wet-nurses. During childhood they should be fed chiefly on good cow's 
milk, and the greatest care should be taken in their exercise and general 
hygiene. Change of climate and surroundings is often of the greatest pro- 
phylactic importance in this class of children — let the child be removed 
from the city to the country. There is no other agent so powerful in 
correcting phthisical tendencies in childhood as systematic physical exer- 
cise in the open air. This training should be commenced in infancy and 
continue to adult life. All those agencies which tend to develop pulmo- 
nary hyperemia and bronchial catarrh should be avoided. Individuals with 
phthisical tendencies should not breathe air laden with foul vapors or fine 
particles of dust. Sudden changes in temperature must be avoided, also 
hot crowded apartments. They should have the largest amount of fresh 
air, not only during the day, but also at night ; their sleeping apartments 
should be large and well ventilated. Pulmonary hyperaemia may be the 
result of speaking a few hours in a crowded and badly ventilated apart- 



CHRONIC PULMONARY TUBERCULOSIS. 



227 



ment, and then may be followed by broncho- or lobular pneumonia and 
phthisis. Flannel should be worn next the skin the whole year. It is 
important that such individuals should not engage in excessive physical 
exercise — as jumping, running, and violent gymnastics. 

The diet should be simple and nutritious, and taken with regularity ; 
and the digestive process should never be overtaxed by taking a large quan- 
tity of food into the stomach at one time. Alcohol is not to be taken, 
except after severe mental or physical work, when there is a sense of 
exhaustion, or after the body has been chilled. The functions of the skin 
must be most carefully preserved. The soil on which the dwelling-house 
is built must also be carefully chosen ; a sandy, porous earth is the best. 
All bronchial catarrhs must be carefully and promptly treated until com- 
plete recovery is reached. I know of nothing so certain to assist in the 
removal of bronchial catarrhs, in this class of subjects, as a change of 
climate. Those living in the mountains should go to the sea ; those at 
the sea to the mountains. The " milk-cure " and (i grape-cure," so strongly 
advocated by some for the arrest of early phthisis, will often be useful in 
those who have feeble digestive powers. The primary object of prophy- 
laxis is to sustain and improve the nutrition, and to guard against bron- 
chial, pleuritic, or pulmonary complications. 

At present we are unable to assure absolute immunity from the recep- 
tion of the bacillus, but all possible means should be employed to avoid 
contact with sources of infection. Unless its source is known to be abso- 
lutely free from contagion, all milk fed to children should be boiled, and 
they should not be allowed to come in contact with phthisical parents, 
except under the most guarded conditions. For older persons the air of 
crowded public places not only induces pulmonary hyperemia, but is 
peculiarly liable to be loaded with bacilli when dust is stirred up. A 
persistent use of a respirator by persons of a phthisical tendency is theo- 
retically desirable, but clinically it is found that only a few of those sub- 
jected to the worst forms of dusty occupations can be induced to submit 
to the annoyance. 

It may be remembered that the bacillus is not found in the breath of 
phthisical patients in appreciable numbers, or thrown off from moist sputa. 
The possibility of tubercular inoculation by wounds of the skin at once 
suggests the proper prophylactic measures. When a patient becomes 
affected, the face (in men) should be cleanly shaved, the expectoration 
received in paper cups or old cloths, and both burned after use. The dis- 
charges from the bowels should be disinfected, and the utmost cleanliness 
observed in every particular. 

Medicinal Treatment. — The most constant symptom of phthisis is fever, 
and its reduction is therefore one of the most important things to be ac- 
complished in the management of the disease, for the wasting, the cough , 
the expectoration, and the rapidity of the phthisical processes, are closely 
connected with the fever. In some cases sulphate of quinine is one of the 
most reliable and satisfactory anti-pyretics. I have often found that when 
quinine had little anti-pyretic power while the patient was "taking exer- 
cise," a reduction of temperature was effected by the same dose if he were 



228 



DISEASES OF THE RESPIRATORY ORGANS. 



put to bed. Even when cavities are forming, its administration will often 
be followed by a lower temperature. One-tenth of a grain of morphine 
combined with quinine increases its anti-pyretic power, so much so that 
now I rarely give quinine as an anti-pyretic to phthisical patients without 
it. Eecently it has been my practice to give phthisical patients, whose 
temperature ranges much above the normal, five grains of anti-febrin two 
or three times in the twenty-four hours. I find that their appetites are 
improved during its use, and that they suffer very much less from those 
nervous symptoms which usually distress such patients. Digitalis exer- 
cises no anti-pyretic power, and only temporarily increases heart-power in 
phthisis. Salicylate of soda is recommended as an anti-pyretic by English 
physicians, but my experience does not favor its use. Arsenic will act as 
an anti-pyretic in some mild cases when all others fail, but it is mainly of 
service in combination with cod-liver oil as a tonic. Aconite, veratrum, 
gelsemium, and antimony I seldom use, on account of the disturbance of 
digestion which they cause. In many cases, after the disease has passed 
the first stage, the fever cannot be controlled. 

Another medicinal agent which has been extensively employed in the 
treatment of phthisis, and which, for the past twenty years, has enjoyed 
the reputation of curing this disease, is cod-liver oil. It has been claimed 
that if this remedy is commenced very early it has the power of arresting 
the phthisical processes. I am not among those who advocate its indis- 
criminate use. I doubt if it exerts any specific influence upon the disease ; 
it is more than probable that all its beneficial influence is due to the fact 
that it furnishes some element essential to the digestion and assimilation 
of certain nutritive elements. In very many cases the exact manner in 
which it acts remedially is not well understood. There are three facts 
which seem to me to afford some clue to the mode of its action : first, 
unless the patient gains in weight while using the oil, it seldom or never 
proves remedial : secondly, flesh and weight may be gained during its 
administration, and still the phthisical processes steadily progress ; and 
thirdly, when it does act remedially, the weight gained is far greater 
than would result from the oil as a mere element of nutrition. A great 
gain in weight will sometimes immediately follow the administration of a 
small quantity of oil. It always acts remedially with more certainty in 
young persons and children than in the aged ; generally, old persons are 
not much benefited by its use. Those patients who improve under its 
use take more food than they have been accustomed to previous to its 
employment, and digest it more perfectly. In some instances diarrhoea 
will be arrested by its use, and also vomiting of food after eating. In other 
cases the oil itself will be rejected and its administration rendered impos- 
sible. If possible, it should be given in connection with an alkali. At 
first small doses should be given, not often repeated. A teaspoonful once 
or twice a day is sufficient to commence with, the dose being gradually 
increased to a tablespoonful three times a day. No special benefit is to be 
derived from the administration of large doses. Most patients take the oil 
best immediately or soon after meals. If it disagrees with the stomach, 
lying down a short time after taking it will often prevent any disagreeable 



CHRONIC PULMONARY TUBERCULOSIS. 



229 



sensation. Some can better take it upon going to bed at night. It should 
not be administered in connection with stimulants unless the patient cannot 
take it in any other way. Regularity and perseverance in its use are essen- 
tial in order to obtain the full benefit it is capable of producing. If, at 
times, it seems to disagree with the digestive organs, it may be tempora- 
rily omitted, especially during the summer months. The best oil in the 
market is " Moller's," or what is termed Norwegian oil. Fish-oils of 
various kinds, cream, glycerine, oils from vegetables, koumyss, malt 
extracts, pancreatic and pepsin emulsions, etc., have all proved inferior 
to the simple cod-liver oil. Phosphorus, sulphur, the hypophosphites 
of lime, soda, and iron, sulphurous acid, the sulphites, are all excel- 
lent adjuvants to the oil, but cannot take its place. When intestinal 
digestion is imperfect, the hypophosphites are especially beneficial. When 
phthisical subjects become anaemic, iron may be given at each meal if 
the temperature is below 100° F. ; it may be combined with quinine, 
arsenic, and the mineral a'cids as tonics. 

There is a great diversity of opinion as regards the use of alcohol in 
the treatment of phthisis. Some claim for it a curative power ; others 
maintain that its daily use does harm. The question, therefore, arises, 
Under what circumstances has experience taught that it is of service, and 
when it is hurtful ? I am convinced that benefit may be expected from 
the use of alcoholic stimulants only when they increase the desire for food 
and assist digestion, or when their use is followed by an increase in strength 
and a disposition to take exercise. On the other hand, if their use causes 
a rise in temperature and an acceleration of the pulse, followed by a feel- 
ing of increased weakness and nervous depression, they will certainly do 
harm. The belief that alcohol has the power of arresting phthisical 
development is one which experience does not sustain. The daily use of 
alcohol for a time may mask phthisical symptoms, and the patient and his 
friends may fancy that the progress of the disease is stayed ; but soon he 
reaches a condition in which the disease will make rapid progress, and in 
which a large quantity of stimulants will not give relief. It is unfortu- 
nate for a phthisical patient to become addicted to the daily use of stimu- 
lants. If an individual with developed phthisis reaches complete recovery 
while taking alcoholic stimulants freely, I am confident that he would have 
reached it more rapidly and safely without them. The quantity and kind 
of stimulants to be used must be determined by the effects ; no rule can 
be given ; each case is a law unto itself. Malt liquors and wines do less 
harm than whiskey and brandy, and are usually more serviceable. Phthisi- 
cal patients tolerate alcohol to a marked degree. 

Cough-mixtures are prescribed by physicians to phthisical patients more 
frequently than any other medicinal agents. Such mixtures are usually 
composed of substances which are more or less nauseating ; and as the 
future well-being of every phthisical patient depends upon his powers of 
digestion, everything that may interfere with the healthy performance of 
this function must, as far as possible, be avoided. Although a distressing 
symptom may temporarily be relieved by a cough-syrup, its administration 
will certainly cause digestive disturbances which will do positive harm. 



230 



DISEASES OF THE RESPIRATORY ORGANS. 



The relief obtained by cough-mixtures is due, for the most part, to the 
anodyues which they contain. 

This brings us to the question, Should opium be given to phthisical 
patients ? In answer to this question I would say that opium should 
never be given in any stage of phthisis, except as already noted in con- 
nection with quinine, unless the cough is distressing and the patient is 
unable to obtain the required amount of sleep. Under such circumstances 
the milder narcotics should first be tried. Opium should be reserved for 
the later stages of the disease. Its use should be commenced with the 
smallest dose that will give rest. In the majority of instances I have 
found that more speedy and satisfactory relief will be obtained from the 
cough and restlessness during the early stages of phthisis by the inhala- 
tion of a few drops of chloroform than from the use of opium ; besides, 
chloroform is less liable than opium to disturb digestion. One must be 
careful in the use of chloroform ; there is danger that phthisical patients 
may become addicted to its excessive use. Codeia, chloral hydrate, hydro- 
bromic acid, " cblorodyne," creosote, stramonium, and belladonna some- 
times act better than opium. All narcotics act only as palliatives, and 
should be employed only when the symptoms become sufficiently distress- 
ing to demand relief. In those cases where a constant hacking or violent 
paroxysmal cough is excited or kept up by an inflamed or irritable condi- 
tion of the fauces or larynx, the topical application of sedative or astrin- 
gent remedies by means of sprays will be found of great service. Of all 
topical applications for the relief of this condition, a solution of cocaine 
will be found the most efficacious. It is sometimes imperative to give a 
stimulating expectorant. Ammonium carbonate in the infusion of wild 
cherry bark is one of the best. It never nauseates. 

Night- sic eats are a part of hectic. When quinine does not control 
them, quinine with opium may do so. Oxide of zinc (gr. ij-iv), gallic or 
sulphuric acids, arseniate of iron (gr. }-^), ext. of belladonna or sulphate 
of atropia (hypodermically), muscarine, picrotoxine, ergot, — all may be 
tried at different times. Atropia is the most reliable. Cold spongings 
and sponging with acidulated or astringent waters (alum in alcohol) are 
always agreeable and sometimes efficacious. Capsicum in the sponging 
water is sometimes serviceable. 

Gastric and intestinal disturbances are a part of the history of nearly 
every case of phthisis, and there are two conditions upon which the diar- 
rhoea and distress after eating may depend; viz., either upon a hyperagmic 
condition of the gastro-intestinal mucous membrane, produced by indigesti- 
ble food, or upon ulceration of the large or the small intestine. If it depend 
upon gastro-intestinal hyperemia, the quantity and quality of the food 
must be carefully attended to, and a mild saline laxative rather than an 
astringent must be administered ; this should be followed by the daily use 
of the lacto-phosphate of lime. If the diarrhoea is dependent upon catarrh 
with or without ulcerations in the small intestine, cod-liver oil and the 
hypophosphites of lime and soda will often be of service. Five grains of 
pancreatine given two hours after eating will often relieve the intestinal 
pain even in the later stages of the disease. If these fail to give relief, 



CHEOXIC PULMOXAEY TUBEBCULQSIS. 



231 



ten grains of bismuth, combined with the twelfth of a grain of morphine, 
after each movement, will almost certainly control the diarrhoea for a 
time. If the diarrhoea depends upon ulceration of the large intestine, 
all that can be done is to give temporary relief by opium suppositories. 
When diarrhoea is persistent and accompanied by rapid emaciation, it is 
tubercular. Vomiting after meals is often a troublesome attendant of 
phthisis. Champagne with the food, hydrocyanic acid, pepsin, and a long 
list of other remedies are recommended for its relief. The most certain 
relief is obtained by giving the patient a glass of hot water every two 
hours, followed in half an hour by a teaspoonful of raw scraped beef 
made into a sandwich, at the same time keeping him absolutely quiet in 
a recumbent posture. 

The most valuable remedies for the arrest of liaimoptijsis are rest and 
opium. Lead, ergot, ice, and a long list of astringents are recommended, 
Ergofin hypodermically is much employed. Turpentine is more relia- 
ble than any remedy except opium. Local pains in the chest may be re- 
lieved by blisters and counter-irritants; strapping the chest so as to render 
the chest walls immovable often gives marked relief from the pains caused 
by the circumscribed pleurisies which attend phthisical processes. Dry 
cupping often gives marked relief from the dyspnoea which accompanies 
acute phthisical processes. 

The antiseptic treatment of phthisis has not thus far given satisfactory 
results, although the recognition of its specific cause has led to the trial 
of innumerable remedies of this class. Carbolized inhalations have been 
quite extensively employed, with very favorable results, according to the 
statements of some observers ; but, after quite an extensive trial, my 
experience is decidedly against their use. The internal or hypodermic 
use of antiseptics, notwithstanding the strong statements made in their 
favor by some of their enthusiastic advocates, I have found to fail not 
only in counteracting the sepsis of advanced phthisis, but in reducing the 
high temperature which so rapidly exhausts the phthisical patients. The 
injection of cavities through the chest walls has not been followed by 
satisfactory results. 1 More recently, favorable results have been reported by 
careful observers from the use of creosote, both internally and by inhala- 
tion. I believe that it is utterly futile to attempt to reach the bacilli 
imbedded in tubercular or caseous products. It is quite possible that 
antiseptic inhalations may decrease the infective power of the secretions, 
and retard secondary inoculations of adjacent lung, and thus be slightly 
adjuvant to other measures, but their use must be guarded. When used 
freely they have seemed to me to increase the tendency to hemorrhage. 
When employed, they are carried more deeply and applied more evenly 
by the vaporizer and the pneumatic cabinet than any other method of 
inhalation. The pneumatic treatment has also seemed to me to be of 
value in relieving pulmonary congestion, assisting the general circu- 
lation and promoting general nutrition. It is also an efficient measure 

1 Dr. Pepper, American Journal Med. Science. The modus operandi of washing out lung-cavities and 
the use of drainage tubes in such cases, are fully discussed by Mosler in the October number of the Ber. 
Klin. Woch.,187S. 



232 



DISEASES OF THE RESPIRATORY ORGANS. 



for arresting haemoptysis and freeing the bronchial tubes from accumula- 
tions. 

The Hygienic Treatment of Phthisis. — The quantity and quality of the 
air habitually respired is a most important consideration in the hygienic 
treatment of phthisis. Phthisical patients should sleep in large, well- 
ventilated and well-lighted rooms with a southerly or westerly exposure. 
Flannels should be worn next the skin, and the surface must never be 
exposed to sudden changes of temperature ; cold sponging or baths often 
act as tonics when judiciously employed. 

The patient must live as much as possible in the open air, and should 
avoid sedentary occupations, taking systematic daily exercises, but never 
to fatigue. It is a very great mistake for a phthisical subject to exercise 
when his temperature is ranging from 102° F. to 104° F. 

The dietetic treatment is usually delayed, like most measures, until forced 
upon the attention by failing digestion. The most absolute rules should 
be given upon the earliest recognition of the disease, and a system of forced 
feeding instituted, in which the digestion may be aided by artificial fer- 
ments if necessary. 

The diet should be varied, and phthisical subjects should become accus- 
tomed to drink from one to three quarts of milk each day. The quan- 
tity of food taken should be determined by the power of digestion ; a 
phthisical subject should never take more food at a time than can be 
easily digested. Peptonized foods and preparations of pancreatin will aid 
a feeble digestion, in the later stages as well as earlier. 

The climatic treatment of phthisis is a subject which has recently 
received much attention, but it is to be remembered that its usefulness is 
confined almost exclusively to the first stage of the disease, and that no 
absolute rules can be laid down in regard to it. It is well known that 
some consumptives thrive best in a warm, moist air, others in a cool, dry 
atmosphere ; some are most vigorous in winter, others in midsummer. 
Each year's experience impresses on me the conviction that while climate, 
more than any other agent, has a controlling influence over phthisical 
developments, 1 each case must be carefully analyzed before any definite 
directions can be given as to the climate best suited to it. Although we 
know of no climatic conditions which render phthisis a necessity or an 
impossibility, still there are conditions which are known to be antagonistic 
to its development as well as those which favor its development. Scarcely 
twenty years ago the great desideratum was thought to be a warm, dry 
atmosphere, but we now know that a cold climate not only does not hasten, 
but often arrests phthisical processes. The statement has been made that 
"the higher the altitude the less prevalent is phthisis," but the altitude 
at which such immunity exists varies with the latitude, and with the idio- 
syncrasy of the individual. 

Mountains and elevated districts were thought to be beneficial on account 
of their elevation alone. But recent investigations show that the absence 
of atmospheric impurities is the chief element, and that the purity of the 



1 Laennec long ago wrote : " Of all the means hitherto recommended for the cure of phthisis, none have 
been followed more frequently by complete cessation of the disease than change of climate." 



CHROXIC PULMONARY TUBERCULOSIS. 



233 



air is the chief reason that elevated regions are so beneficial in phthisis. 
Prof. Tyndall's experiments are of special interest in this connection. 1 
Organic germs are more abundant in the air in the city than in the coun- 
try. Eain and ozone free the air from them, the latter by oxidation. Rain 
cleanses the atmosphere of solid particles and purities it by washing down 
ammonia and carbonic acid. The presence of ozone in the air is presump- 
tive evidence of its purity. The air of high mountains and plateaux and 
along the shore of the ocean is richer in ozone than that of the plains. 
Prof. Tyndall's experiments show that in early summer the mountains, 
and in late summer and fall the seashore, have their purest air. The 
benefit which phthisical patients derive from living near pine forests has 
long been known. Turpentine exhaled from pine or hemlock forests con- 
verts oxygen into ozone, and thus the air of pine forests becomes pure. 
Direct inhalation of ozone has little power over phthisis ; hence it is not 
the ozone, but the purity of air it induces, that renders the air of certain 
localities so salubrious. It was formerly thought that resorts where no 
rain fell for weeks and months were the best suited to phthisical subjects, 
but experience has taught the reverse. Long-continued rains are certainly 
unfavorable, but cleansing showers act beneficially. The amount of rain- 
fall is not a sure indication of the amount of moisture in the air of any 
region, the latter depending more upon the dampness of the soil. The 
atmosphere of a region with a loose, porous, sandy soil, through which the 
water filters, and whose surface dries quickly, is never damp ; but hard, 
compact, rocky, or clayey regions, that drain but slowly and imperfectly, 
hold the moisture and cause a dampness which is a strong predisposing 
cause of phthisis. 2 

Atmosjjlieric temperature is an important element in the climatic treat- 
ment of phthisis. Some patients thrive best in a warm sedative climate, 
others in a cool, stimulating climate. Extended clinical observation leads 
one to believe that it is neither the heat nor cold of a certain locality, but 
the absence of sudden and frequent changes, which makes it so beneficial 
to phthisical invalids. 

Altitude is regarded by many at the present time as of more importance 
than any other natural element. As a rule, the atmosphere at elevations 
of 1,500 or 1,800 feet is purer than on the plains ; yet all high altitudes 
are not thus pure ; experiment has shown the atmosphere of some elevated 
regions to be impure, and that consumptives on such elevations do badly. 
Something more than altitude is needed to make a given locality suitable 
to phthisical subjects. Eecent investigations show that the similarity in 
the composition of sea and mountain air at certain times of the year is far 
greater than was at one time supposed. Mountain air is less dense, less 



1 After boiling, filtering, and evaporating a vegetable in r usion, he hermetically sealed it in flasks, which 
he transported to the Alps, 7,000 feet above sea level. Some ot the flasks were opened during transporta- 
tion, and in these millions of organisms developed in the fluid while the fluid in the flasks that were 
opened on the mountain remained free from such organisms. By further experiments he showed that 
dust-laden air was necessary to the procreation of these organisms, and they are diffused through the 
atmosphere, although the air in different localities may be infected in different degrees. 

2 Laennec states that the dampness arising from such a condition of soil is one of the most certain devel- 
oping causes of phthisis, and he makes mention of a locality having such a soil, in which the dampness 
was so constant and of such a character that two thirds of the resident population died of phthisis. 



234 



DISEASES OF THE RESPIRATORY ORGANS. 



humid, and lower in temperature than sea air, but in both we find excess of 
ozone and freedom from organic impurities. Both sea and mountain air 
are cooler and less subject to frequent variations in temperature than the 
air of the plains. A slight diminution in atmospheric pressure produces 
no palpable changes. But a great diminution (say one quarter) produces 
serious disturbances of nutrition, developing a condition which favors 
rather than retards phthisical developments. The effects of diminished 
atmospheric pressure vary so greatly in different individuals that no prac- 
tical deductions can be made. 

The question arises, Will this patient be benefited by sea or by mountain 
air ? Beneke's experiments show that tissue changes take place more rap- 
idly on or by the sea than in the mountains. Hence those in whom the pro- 
cess of tissue change needs no hastening, and those with exhausted nervous 
systems, with an overtaxed brain from excessive mental labor or an all- 
absorbing business, and who still retain considerable muscular power, 
should go to the mountains ; while those past middle life, who have devel- 
oped phthisis late, who are incapable of much muscular activity, and who 
therefore require stimulation for the production of tissue change, do best 
in sea air. Sea air is better suited than mountain air to those who can- 
not bear sudden changes of temperature, while the susceptibility to such 
changes is greatly lessened by mountain air. 

On our own continent is found every variety of climate. Permanent im- 
provement only occurs after a prolonged residence in the place which experi- 
ence proves best suited to each case. A change of climate should not be 
made every year. The limited space which can be devoted to the con- 
sideration of the localities best suited to phthisical patients in this and 
other countries will only allow of mention of the most important ones. 
Every stage of fibroid tuberculosis, no matter how far advanced or where 
the fibroid developments began, is benefited in the high altitudes found in 
Colorado and about the Kocky Mountains. But there is one grave objec- 
tion to Colorado as a winter refuge : the enormous monthly, and also the 
diurnal, range of temperature must severely try any invalid. It is impor- 
tant that every phthisical patient who visits Colorado or any high altitude 
should place himself under the direction of an intelligent physician before 
he attempts any exercise. 

It is during or before the stage of consolidation that persons with 
pneumonic phthisis are to be benefited by climatic influences, 'and a care- 
ful analysis of each case is important before directions can be given as to 
the region most likely to suit his special requirements. The patient must 
not wander around till he hits upon the place which suits him ; much 
valuable time is thus lost. Except in those who are convalescing from 
some acute lung disease, a sojourn in a southern climate during the winter 
seems, after a time, to hasten the degenerative processes. My favorite 
resorts in the winter, for those recovering from acute pulmonary diseases, 
are Aiken, S. C, Palatka, Enterprise, and Gainsville, Fla., Thomasville, 
Ga., and Nassau. These localities are also favorable for those in whom 
there are evident phthisical tendencies, but in whom, as yet, no physical evi- 
dences of pulmonary consolidation exist. My best results, when the evi- 



CHROXIC PULMOXARY TUBERCULOSIS. 



235 



dences of consolidation were present, have been obtained in those who have 
stayed from one to three years in mountain regions 1,500 to 2,000 feet above 
the sea. My most decidedly beneficial and permanent results have been 
obtained in Asheville, X. C, in New Mexico, and in the Adirondack region 
of New York State. The temperature, rainfall, and surroundings of the 
latter region are all at variance with preconceived notions of a proper "re- 
sort for consumptives," but results are strong in its favor. A camp or tent 
life in the open air is best for those who can enjoy such life. Excursions 
and cheerful social intercourse in the open air should always be an object. 
A dreary spot, even with the best hygienic conditions, will not give favora- 
ble results. 

I would advocate sanitariums for the phthisical. Not overcrowded hos- 
pitals, but cottages and pavilions in sheltered spots, in appropriate climates, 
and at a given elevation, where privacy and quiet are possible, and where 
all shall be supervised by a capable and intelligent physician. Minnesota 
has a dry, cool, exhilarating climate. Southern California, Georgia, and 
South Carolina have a dry, warm atmosphere. The Bermudas, Bahamas, 
Florida, Turk's Island, Santa Cruz, and St. Thomas have a warm, moist, 
and usually healthy climate. The extraordinarily dry belt of country which 
runs northward from San Antonio, Texas, has begun to endanger the su- 
premacy of Florida as a winter health resort for the consumptive. That 
this belt offers some climatic advantages for weak lungs over the mild but 
rather humid air of Florida cannot be doubted. Nassau, the capital of the 
Bahamas, is a noted resort and one that suits most phthisical subjects past 
middle life ; Matanzas, Cuba, has a dry, warm climate, suitable for a win- 
ter home for the enfeebled, but not for those who have developed phthisis. 
It may be that, for various reasons, a phthisical patient prefers a residence 
abroad. Dry climates near the sea are Malaga, Eiviera, and Algiers. Egypt 
and South Africa are highly recommended by the English physicians for 
phthisis. Sea voyages to Australia and New Zealand are recommended in 
cases of "hemorrhagic phthisis." J. Hughes Bennett finds the lakes of 
Scotland the best resorts for consumptives in the summer. The Engadine 
has been strongly advocated by many. 

Within the past ten years, Davos am Platz, in the Swiss Alps, has been 
most extensively visited. Williams, Albutt, and other English physicians 
give very favorable reports of it, and from my limited experience I can 
fully indorse their statements. It is 5.200 feet above the sea, very dry, but 
not windy, and not changeable. 1 Davos possesses, also, the unique climatic 
characteristic of freedom from high winds (the records showing that from 
October 1, 1880, to March 31, 1881, there were one hundred and thirty- 
four days with "no wind"), while its "sun temperature" rises even in 
January, as Dr. Franklin notes, as high as 150° — conditions which admit 
of much invaluable outdoor exercise by invalids. Some points in Colorado 
and New Mexico offer all the favorable climatic conditions which are to be 
found in Davos. 



1 Lancet, 1878, i. 834. 



SECTION II. 



DISEASES OF THE DIGESTIVE SYSTEM. 



{Including Diseases of the Liver, Spleen and Pancreas.) 



DISEASES OF THE MOUTH. 



The following classification may be made of the diseases of the mouth { 



Catarrhal stomatitis is an inflammation of the whole, or a portion of the 
mucous membrane of the buccal cavity and tongue. It may be acute or 
chronic. 

Morbid Anatomy. — At its onset the mucous and submucous tissue of the 
tongue and inside of the mouth becomes tumefied, much redder than nor- 
mal, and dry. Later, the mucous and salivary secretions are very much 
increased. The swelling is greatest over those parts disconnected with 
bone, as the tongue and cheeks. The tongue becomes covered with a 
whitish coating, and the red papillae are visible through it. A copious 
glairy secretion, slightly acid in its reaction, containing pus and epithelial 
cells, covers its surface. This secretion has a sourish, but not a fetid odor. 
In some cases the changes are slight and superficial, in others the tongue 
is so swollen that it presses on the teeth and becomes indented by them, and 
the mucous membrane of the cheek and gums fills the space outside of 
them. The whole surface becomes covered with a tenacious, opaque secre- 
tion. 

If the process becomes chronic, the glands of the mouth become 
swollen and tender, the filiform papillae become elongated and pale, and 
give what is called the " hairy tongue." The tongue is less swollen than 
in the acute stage ; the secretions have a fetid odor. Occasionally, 
patches of exudation form over the tongue and sides of the mouth, which 
tend to collect about the teeth. Large diffuse ulcers sometimes occur in 
adults. 

Etiology. — The acute form occurs almost exclusively in children during 
the period of dentition. The chronic occurs mainly in adults. Decayed 



I. Stomatitis. 



c. Gangrenous, 

d. Ulcerative. 



a. Catarrhal, 
fa Follicular. 



II. The "thrush." 

III. The tongue-diseases. 

a. Glossitis. 

b. Cancer. 

IV. Inflammation of the parotid 

' gland or "Mumps" 



CATARRHAL STOMATITIS. 



CATARRHAL STOMATITIS. 



23? 



and ulcerated teeth, acid ingesta, and the taking frequently of too hot or 
too cold fluids, often excite it. The prolonged administration of mercury 
and preparations of iodine for their specific effect, causes a form which is 
termed mercurial stomatitis. The excessive use of tobacco is a frequent 
cause. Gastric catarrh may precede or follow it. It may be an ex- 
tension of inflammation from wounds of the tongue and fauces. More or 
less severe catarrhal inflammation of the mucous membrane of the mouth is 
present in most of the specific fevers, especially in scarlatina. Improper 
food, bad air, and bad hygienic surroundings will induce it in children. 

Symptoms. — The acute form commences with a burning, smarting pain 
in the mouth. The child refuses to take food, or allow the finger to 
be put in its mouth ; it will take freely of cold drinks, is fretful and sleep- 
less, and there is usually a slight rise in temperature. Vomiting and diar- 
rhoea often accompany it. The salivary secretion is increased, and flows 
from the corners of the mouth, excoriating the parts with which it comes 
in contact. It may extend into the larynx and cause laryngeal catarrh. 
When it occurs in adults, there is a slight rise in pulse and temperature, a 
general feeling of malaise and much difficulty in swallowing. The patient 
is constantly trying to get rid of the slimy coating on the tongue and mouth, 
by hawking and spitting. The sense of taste is blunted, and there is usu- 
ally an unpleasant bitter taste in the mouth. These symptoms are usually 
accompanied by a dull frontal headache. 

In chronic stomatitis the breath in the morning has a fetid odor, the 
taste is vitiated, and there is often great depression of spirits. Rarely is 
the digestion interfered with. 

Differential Diagnosis. — Catarrhal stomatitis may be mistaken for the 
changes which take place in the tongue and mouth in some of the specific 
fevers. In catarrhal stomatitis the coating of the tongue is soon followed 
by a copious salivary secretion ; while in fevers the tongue becomes dry, 
and the detachment of brown crusts leaves a glassy, smooth surface. In 
catarrh, the appetite for solid food and the digestive functions are not 
much changed, while in fevers there is great thirst and repugnance for 
food. There are slight, if any, constitutional symptoms in catarrh, while 
in incipient fever there are marked constitutional symptoms. 

Prognosis. — The acute form generally terminates in recovery within a few 
days. Chronic oral catarrh is very persistent and stubborn, and rarely yields 
to treatment. 

Treatment. — In young children the diet should be cold milk with lime- 
water. The mouth should be washed with a slightly alkaline wash, and 
chlorate of potash given internally. In all cases the cause should be re- 
moved, and the bowels regulated with rhubarb and soda. 

In chronic catarrhal stomatitis, after the removal of its exciting causes, 
moderately strong alkaline washes should be frequently used, and in obsti- 
nate cases a weak solution of nitrate of silver will be found most effica- 
cious. Carbolic acid sprays relieve the offensive odor and other unpleasant 
symptoms. 



238 



DISEASES OF THE DIGESTIVE SYSTEM* 



FOLLICULAK STOMATITIS. 

Follicular, aphthous, sometimes called croupous, stomatitis is a vari- 
ety of inflammation of the mouth, in which the mucous follicles are pri- 
marily and chiefly affected. 

Morbid Anatomy. — On the anterior portion of the tongue, and on the 
mucous surfaces of the gums £nd cheeks, there appear small vesicle-like 
elevations, semi-transparent, and having a red zone about their base ; these 
are called "aphtha? some regard them as a peculiar deposit, others as a 
local croupous exudation. They are often numerous ; after they have rupt- 
ured they leave an irregular gray surface, resembling a small ulcer, which 
heals slowly. Occasionally a number of aphthae coalesce and form irregular 
ulcer-like or excoriated patches. In the majority of cases the ulcers soon dis- 
appear, new crops appear and the disease may run a tedious course. Dirty 
white or yellow sloughs cover the ruptured aphthae, and gradually separate, 
leaving no scar. Follicular ulcers on the inner side of the lips sometimes 
occur at the menstrual epoch, or during pregnancy and lactation ; ulcers 
like these rarely occur in men. 

Etiology. — Aphthae may accompany any disease of the tongue or mouth. 
It is, like most oral diseases, chiefly prevalent among children during den- 
tition, and is rare after five years of age. It is idiopathic, or a sequela of 
one of the exanthemata. Unripe fruit, candy, and indigestible food re- 
maining in the child's mouth will cause it. Bad hygienic surroundings 
and a weakly, badly nourished state of the body, are its principal predis- 
posing causes. It sometimes prevails epidemically. 

Symptoms. — Aphthous stomatitis shows itself in very young children by 
pain on taking the breast and in swallowing. Older children have pain on 
talking and masticating. There is a slight febrile excitement and enlarged 
and tender sub-maxillary glands. Salivation occurs, and the parts about 
the mouth and chin become excoriated by the saliva, which continually 
runs over them. Feculent diarrhoea is common, and there is more or less 
interference with digestion. 

Differential Diagnosis. — This cannot be confounded with any other dis- 
ease. 

Prognosis. — It is never fatal ; it generally disappears as soon as the causes 
that produced it are removed. 

Treatment. — Correct any intestinal disturbance that may exist with small 
doses of rhubarb and magnesia, or mild salines ; restrict the diet to milk. 
Wash the mouth with a weak solution of glycerine and borax, or chlorate 
of potash. In severe cases the mouth should be washed every few hours 
with a dilute mineral acid, or nitrate of silver. In weak children, when the 
general health is impaired, stimulants may be given with benefit. 



GANGRENOUS STOMATITIS. 



239 



GANGRENOUS STOMATITIS. 

Gangrenous stomatitis, "cancrum oris/' or sloughing phagedena of the 
mouth, is a formidable disease of childhood, in which the tissues of the 
cheek are prominently involved. 

Morbid Anatomy. — There is first a hard swelling developed in the cheek, 
the skin over it being red, shining, tense, and brawny. In the mouth, at 
the side of the indenture, there is a deep, ragged, angry, unhealthy ulcer 
covered with a dark, ashy, or brown colored slough. The adjacent tissue is 
cedematous, and hemorrhage from the livid and swollen part sometimes 
occurs. The ulcer in the cheek rapidly extends and deepens, emits a 
very fetid odor, and often perforates the walls of the buccal cavity. The 
slough may occupy the whole of one side of the mouth, the teeth may 
become loosened, and caries, or necrosis of the inferior maxilla, result. If 
the ulcerative process is not extensive, separation of the slough may occur, 
and the ulcer heal by granulation and cicatrization. The facial vein may 
be implicated, and then pyaemia, with multiple abscesses, may result. 

Etiology. — This is a very rare disease. It occurs principally in debilitated 
children between two and five years of age who are convalescing from some 
form of acute disease, such as scarlet fever. Whether it is contagious or 
not has never been determined. It sometimes follows the prolonged use of 
mercurials. Bad air, insufficient food, and anti-hygienic surroundings, 
predispose to it. 

Symptoms. — It commences with pain in the mouth, which is increased by 
movement of the jaws. Then the local changes already described appear 
on the cheek and gums, and an abnormal quantity of saliva, mixed with a 
putrescent fluid, often with blood, flows from the affected side of the 
mouth. The breath has a peculiarly offensive odor. The adjacent glands 
become enlarged and tender. As the disease advances, the constitutional 
symptoms of septicaemia are developed. In most cases the child after a 
time becomes drowsy, passes into coma, and dies. 

Differential Diagnosis. — Cancrum oris maybe mistaken for "malignant 
pustule." Malignant pustule attacks the skin and exposed parts first, 
while gangrenous stomatitis begins in the mucous membrane of the cheek 
or about the gums, involving the skin secondarily. Malignant pustule is 
at once accompanied by constitutional symptoms, and soon followed by the 
phenomena of a septic or typhoid fever, while cancrum oris is without 
pyrexia or loss of appetite at its onset, and severe general symptoms do not 
come on till late. 

Prognosis. — This is an exceedingly fatal disease — nineteen out of twenty 
die. In the few cases where the process has been mild, recovery has 
occurred within two weeks from its commencement. The complications 
are pneumonia, bronchitis, and pyaemia. Death may occur from exhaus- 
tion or from one of the above named complications. 

Treatment. — Prompt measures are indicated at the onset of this affection. 
Nitrate of silver, and even strong nitric acid, should be thoroughly applied 



240 



DISEASES OF THE DIGESTIVE SYSTEM. 



to the slough, and the mouth frequently washed with solutions of carbolic 
acid and chlorate of potash. The best internal remedies are quinine and 
hydrochloric acid. The diet should be highly nutritious ; stimulants may 
be freely given, if indicated. When the child cannot swallow, beef tea and 
brandy enemata should be administered. 

ULCERATIVE STOMATITIS. 

Ulcerative stomatitis, or noma, is a variety of inflammation of the mouth 
chiefly affecting the gums and spreading over a large extent of surface. 

Morbid Anatomy.— The gums are hyperaemic and tumefied. Sometimes 
they assume a purplish color, separate from the teeth, and are covered with 
a pulpy gray-white material which disintegrates, becomes soft and dark, 
and gradually spreads to the lips and side of the cheek. This gangrene- 
like slough may gradually extend until the gums are destroyed. In some 
few instances little vesicles precede the slough. If the slough is removed 
as soon as it appears, the gums underneath will be found red, bleeding and 
granular. The teeth become loosened and often drop out, the tongue 
enlarges and has a sodden appearance, and the mucous membrane of the 
cheek swells so that it often receives the impression of the teeth. Some- 
times the bones about the face lose their periosteum and exfoliate. When 
recovery takes place deep cicatrices may remain and cause more or less 
distortion of the face. 

Etiology. — Noma, or ulcerative stomatitis, is met with only in children 
from one to ten years of age. It occurs among those who inhabit filthy 
localities, who are badly fed and compelled to breathe unwholesome air. 
Dampness seems to exert a predisposing influence, and the disease is most 
prevalent during the autumn months. It is probably contagious, for well- 
marked epidemics of it are recognized. It is common after asthenic in- 
flammation and the eruptive fevers. The prolonged use of mercurials will 
cause ulcerative stomatitis. 

Symptoms. — The mouth is hot and painful for some time, and then ap- 
pear the changes already described. There is pain on chewing or speaking, 
and there may be slight febrile excitement, although constitutional symp- 
toms are not prominent. There is an increased flow of saliva which has 
a very offensive odor, and is mixed with blood and shreds of the pulpy 
mass. There is enlargement and tenderness of the sub-maxillary glands. 
In some cases the child will pick at its mouth and throat, and very often 
loosens and swallows some of the shred-like sloughs. The appetite may 
not be impaired, though the bowels are disordered, and the child is restless 
and sleepless. The upper lip becomes swollen, dark-red, and projects out- 
ward, while the mouth is kept widely open to prevent painful contact with 
the lips or tongue. The excessive salivation soon decreases, but the un- 
pleasant fetor of it and of the breath persists. Late in the disease the adja- 
cent glands become enlarged and tender. 

Differential Diagnosis. — Ulcerative stomatitis maybe mistaken for " can- 
crum oris/' or gangrenous stomatitis. It is a local disease, while cancrum 



THRUSH. 



241 



oris is attended by constitutional symptoms ; it begins in the gums, while 
gangrenous stomatitis begins in the cheek. The progress of noma is slow 
compared with the very rapid extension of cancrum oris. The livid red- 
ness, the dark swelling, and the ashy slough of cancrum oris are absent in 
ulcerative stomatitis. 

Prognosis. — This is good. Its duration is about eight days, but slough- 
ing about the gums may continue for weeks. 

Treatment. — The treatment is the same as in aphthous stomatitis. The 
chlorate of potash may be used as a wash or gargle and internally, and will 
usually arrest it. In many instances, fresh, air, cleanliness and a restricted 
diet are all that is necessary to effect a cure. If the ulceration spreads, 
the application of nitric acid, and sometimes the employment of the ac- 
tual cautery, must be resorted to. For the profuse salivation which is 
sometimes so troublesome, belladonna has proved efficacious. 



THKUSH. 

Tlirush, sprue or muguet is an aphthous disease of the epithelium of 
the mouth and tongue, due to the growth of the germs of the thrush-fun- 
gus, the oidium albicans. It was formerly classed as an exudative inflam- 
mation. 

Morbid Anatomy. — The mucous membrane of the mouth assumes a dark 
red color, and upon the most superficial layer of the epithelium there ap- 
pear numerous small, round whitish spots, — " aphthae," — which give to it a 
flocculent or curdy appearance. These spots are often aggregated in 
groups of two or three ; at first, as they enlarge, they fall off or can be 
readily removed, but are soon reproduced and run 
together in patches. The development in thrush 
of the oidium albicans and of its frequent parasitic 
companion, the leptothrix buccalis, in and between 
the epithelial cells may continue until the mucous 
tissue is invaded. The epithelium becomes swollen 
and loosened, the tongue and inside of the mouth 
are covered with, a yellowish pultaceous, creamy 
mass, underneath which the mucous membrane is 
of deep red color, and the papillae are enlarged. In 
the new-born it occurs most abundantly about the 
boundary line between the hard and soft palates 5 
in adults, on the mucous membrane of lips, cheek 
and end of tongue. It may invade the pharynx, 
oesophagus and stomach. It has been found in the 
\ungs and air-passages and about the breasts and 

genitals of infants. A microscopic examination of a patch shows it to con- 
tain mucous and epithelial cells, fat spherules, and the spores and filaments 
of the oidium albicans. The spores are round or ovoid and form masses of 
varying sizes, while the filaments coming out of the spores are cylindrical, 
curved or branched, and consist of long cells, which are constricted where 
they join one another, each cell being filled with granules. 
16 




Fig. 52. 

Oidium Albicans, 
tongue in a case of ' 
A, A. Sj)ores.—B, 



Hal threads. 



3o;i 



From the 
"Thrush." 
B. Myce- 



242 



DISEASES OF THE DIGESTIVE SYSTEM. 



Etiology. — In children this disease occurs from birth to the second year, 
and is very rare after that time until adult life. These parasitic plants 
grow best in the presence of acids, hence the acid secretion of the mouth 
for the first six or seven months predisposes to it. All food or drink that 
will produce irritation of the stomach or intestines, and make the intestinal 
contents acid, predisposes to it. Want of cleanliness in the care of nursing- 
bottles, spoons, etc., is one of its principal causes, consequently it is more 
frequently met with in children brought up on the bottle, especially in asy- 
lums. In adults thrush occurs toward the end of any long exhausting 
disease, such as cancer, or consumption. 

Symptoms. — In children the mouth becomes hot and painful. The child 
will not allow its mouth to be touched. An examination shows the mu- 
cous membrane to be drier than natural ; soon after, the peculiar thrush 
aphthae appear, and there is salivation, which is always markedly acid. 
The lips swell and become everted. Diarrhoea is frequent and the passages 
are often green and smell of fatty acids ; so acid are they at times that 
they cause an erythema about the anus. If this condition persists, the but- 
tocks and parts around the genitals become excoriated. Besides this diar- 
rhoea, vomiting and purging give additional evidence of gastro-intestinal 
disturbance. In adults suffering from exhausting disease, the mouth be- 
comes hot, dry and painful before the thrush appears, and there is diffi- 
culty in swallowing, after which the mouth and tongue soon present the 
characteristic appearance of the disease. 

Differential Diagnosis. — The presence of the parasite establishes the diag- 
nosis. 

Prognosis. — In vigorous children the average duration of this affection 
is from eight to ten days, but in feeble infants it often lasts for months. 
Its only serious complication is gastro-intestinal catarrh. Death may result 
from the exhaustion of the diarrhoea. 

Treatment. — The most important thing to be accomplished in the 
treatment of this affection is to arrest or counteract the acidity of the se- 
cretions of the mouth. After each feeding the mouth must be thoroughly 
cleansed with borax and glycerine, or a weak solution of carbolic acid, and 
sulphate of soda. The diet should be restricted to milk with lime-water ; 
when there is emaciation, cod-liver oil and the lactophosphate of lime will 
be of service. The bowels must be regulated as in follicular stomatitis. 

GLOSSITIS. 

Glossitis is an inflammation of the parenchyma of the tongue. It may 
be acute or chronic, and when chronic, is generally circumscribed. 

Morbid Anatomy. — There is first intense hyperaemia, causing slight swell- 
ing and intense redness of the tongue. This is soon followed by so great 
an enlargement of the organ that it entirely fills the mouth and protrudes 
beyond the teeth. Its surface is covered by a thick secretion, and its sub- 
stance assumes a pale or grayish color. The oedematous condition may 
rapidly subside and leave the tongue in its normal state, or the innamma- 



GLOSSITIS. 



243 



tion may be so intense that small abscesses form which leave deep cica- 
tricial depressions, giving the tongue an uneven and lobulated appearance. 
In some instances the tongue may remain enlarged and hardened for life. 
There is a rare variety of glossitis which does not invade the deeper struct- 
ure of the tongue, but is confined to its mucous and sub-mucous tissue, 
causing thickening and sloughing of its surface, with depressions similar to 
the cicatricial depressions of the parenchymatous variety. 

Chronic glossitis occurs chiefly in patches along the edges of the tongue ; 
the thickening, induration, and cicatricial depressions occur in circum- 
scribed spots. When chronic glossitis is general, the tongue is uniformly 
enlarged and its color is much redder than normal, some spots being 
darker than others ; its movements are interfered with, and its surface pre- 
sents the appearance of eczema of the skin. 

Etiology. — Acute glossitis may develop under the influence of mercurial 
poison, or as a consequence of direct injury. Croton oil and other acrid 
matters taken into the mouth may cause it ; burns, blows, and the poison 
of insects have caused it. Chronic glossitis occurs in the old without any 
apparent cause. It may be produced by disease of the teeth, or of the maxil- 
lary bones, and may, in some instances, result from the action of the mate- 
rials of which false teeth are made. 

Symptoms. — With the enlargement of the tongue in acute glossitis, there 
is great restlessness and anxiety, accompanied by an increase of the pulse- 
rate, and an elevation of the temperature. In some cases, there is profuse 
salivation, and the swollen tongue protrudes between the lips. There is a 
sensation of heat in the mouth, and the swelling often causes severe pain. 
The glands at the angle of the jaw are enlarged and tender, and all move- 
ments of the tongue in talking, chewing or swallowing become exceedingly 
painful and frequently impossible. Dyspnoea and inability to lie down are 
sometimes caused by the obstruction to the free entrance of the air into the 
lungs. When the veins in the neck are compressed, c} 7 anosis of the face is 
marked. The patient is anxious, and very much depressed, and may show 
signs of asphyxia ; indeed death has occurred from suffocation in extreme 
cases. When it terminates in suppuration, the constitutional symptoms be- 
come severe, and all the oral symptoms are intensified.-. When clefts remain 
in the tongue after glossitis, the ulcers in them are painful, but otherwise 
there is no inconvenience. In superficial glossitis, which is apt to be pro- 
tracted, any movement of the tongue is painful, and there is constant sali- 
vation. In chronic glossitis patients sometimes complain of a dull aching 
in the tongue, and in some cases movements of the tongue induce pain of 
a burning character. 

Differential Diagnosis. — Chronic circumscribed glossitis may be mistaken 
for cancer. Cancer develops rapidly, and chronic circumscribed glossitis al- 
most imperceptibly. Cancer tends to speedy ulceration, and hemorrhage is 
frequent, while glossitis passes on to induration and there is no hemorrhage. 
Fetor of the breath is present early in cancer, while it is slight or altogether 
absent in glossitis. In cancer the pain is sharp and lancinating, running 
along the branches of the fifth nerve, while there is only a dull pain in 



244 



DISEASES OF THE DIGESTIVE SYSTEM. 



glossitis. In cancer the adjacent lymphatics are early involved, in glossitis 
they are uninvolved. In cancer, emaciation and cachexia are marked ; 
these are absent in glossitis. A microscopical examination of a portion of 
the diseased tissue will establish the diagnosis. 

Prognosis. — In acute glossitis, the prognosis is uncertain, for suffocation 
may occur unexpectedly; generally it subsides in from three to seven days. 
Of the modes of termination, that of thickening and induration is the most 
common, and is rarely entirely recovered from. 

Treatment. — In acute glossitis, ice should be freely applied to the tongue 
and a mild cathartic administered. If the patient is not able to swallow 
castor oil, a turpentine enema may be given. If the swelling interferes with 
respiration, free and deep incisions on the upper surface must be at once 
made, and if abscesses form they should be promptly opened and washed 
out with some disinfectant fluid. The ulcerations occurring in glossitis 
should be treated in the same way as those of ulcerative stomatitis. In the 
chronic form, if possible, remove the cause. In superficial glossitis, the 
local application of carbolic acid will be found the best remedy. If suffo- 
cation becomes imminent in either variety, tracheotomy should be per- 
formed. 

CANCER OF THE TONGUE. 

The most common variety of cancer of the tongue is epithelioma. 

Morbid Anatomy. — At some point that has been subjected to constant 
irritation, or in some ulcerative cleft in the tongue, there appears a small 
unhealthy ulcer or a small deeply seated nodule. When appearing on an 
otherwise healthy tongue, its locality is usually on its edge. In whatever 
way it may begin, an ulcer quickly forms, circular in shape with ragged 
everted edges, and a wide indurated base. The surface of the tumor has a 
dirty white or grayish-red appearance, is papillated and friable, and com- 
monly of a firm consistency. As the disease advances, it may involve the 
whole tongue, which is then larger than normal, unevenly lobulated, and 
covered with small ulcerations. The mucous membrane on the floor and 
sides of the mouth may be secondarily invaded. As the deeper tissues are 
encroached upon, hemorrhages occur. The sub-maxillary and sub-lingual 
glands early take part in the cancerous development, and the oral cavity 
may be filled with the cancerous mass. On scraping the surface of an epi- 
thelial cancer, a grayish granular mass is found beneath, a portion of which 
under the microscope will show the characteristics of an epithelioma. 

Etiology. — Cancer of the tongue is met with most frequently in middle 
life, between the ages of thirty-five and sixty, and occurs in men more often 
than in women. Its chief exciting cause is some local irritation, as from a 
projecting or carious tooth. It may develop in syphilitic fissures. Oc- 
casionally it appears on a- tongue whose mucous membrane has, for a long 
time, been thickened and indurated. Usually there is an hereditary pre- 
disposition to cancerous development. It may develop without any discov- 
erable cause. 

Symptoms. — In most cases, from the onset there is a sharp pain at the seal 



PAROTITIS. 



245 



of the disease. This pain is aggravated by any movement of the tongue, 
and generally runs along the branches of the fifth nerve. Salivation is pro- 
fuse, and swelling of the lymphatics in the neighborhood is present early. 
Hemorrhages not infrequently occur, which increase the anaemia that at- 
tends the cancerous cachexia. The disease runs a very rapid course, the 
pain becomes agonizing, and a fatal termination may at anytime occur from 
hemorrhage from the lingual artery, or suffocation may result from me- 
chanical interference with respiration. 

Differential Diagnosis.— This disease may be mistaken for syphilitic ulcer- 
ation. A syphilitic ulcer is long and oval or irregular in shape, while can- 
cer is circular. A syphilitic ulcer is developed slowly and with little or 
no localized pain, but cancer spreads rapidly and is accompanied by severe 
pain. The constitutional symptoms of syphilis are usually well marked, 
and the ulcer improves under anti-syphilitic treatment, while the evidences 
of syphilis are absent in cancer. A microscopical examination of a small 
portion of the ulcerating surface removes all doubt in diagnosis. 

Prognosis. — The disease advances rapidly ; its average duration is about 
fourteen months. I have known cases to last two years. Death results 
from the cancer, marasmus, exhaustion from hemorrhage, or from starva- 
tion, as the intense pain in eating causes the patient to refuse food. The 
constant and long-continued pain hastens the fatal termination. If, after 
removal, it does not reappear, death may result from cancerous develop- 
ments in other parts of the body. 

Treatment. — The relief of pain and the maintenance of the vital powers 
are the principal indications. The hypodermic use of morphia is the best 
means of relieving pain. Antiseptic gargles are grateful, and counteract 
the offensive odor of the breath and the unpleasant taste. The checking 
of hemorrhage, removal of the growth, removal of the tongue, ligation of 
the lingual artery and division of the gustatory nerve, belong to the surgical 
rather than to the medical treatment of the affection. 

PAROTITIS. 

Parotitis, or " mumps," is a catarrhal inflammation of one or both pa- 
rotid glands ; rarely are the other salivary glands involved. It is of two 
varieties, specific and non-specific. The latter is also called symptomatic. 

Morbid Anatomy. — The left parotid is usually first affected. The disease 
commences in the gland-ducts, not, as was formerly supposed, in the 
intercellular substance. Both varieties begin as a catarrh, the intense 
initial hyperasmia of the parotid being followed by a serous exudation and 
a soft swelling of the gland. From the few cases that have been examined 
at this stage, we learn that there is oedema of the acini, and that the gland 
is reddened and injected, presenting a fleshy appearance. The connective- 
tiss'ie about the parotid and often the parts beyond it are involved. The 
gland which is so enormously swollen may decrease to its normal size by 
the absorption of the exudation; or, when the process is very severe, the 
idiopathic variety may end in abscess ; this termination is much less fre- 



246 



DISEASES OF THE DIGESTIVE SYSTEM. 



quent than in metastatic parotitis. Occasionally, the gland remains per- 
manently enlarged. It may atrophy. 

Metastatic parotitis begins with a catarrh of the ducts ; there is first 
hyperemia., followed by an exudation into the ducts, which is semi-transpa- 
rent or yellow. The acini are wholly or partly filled with pus, and there 
result numerous little spots of suppuration, but if the process is severe and 
rapid the interstitial tissue becomes involved, and the whole gland may be 
converted into an abscess. The suppurating process may extend to the 
neighboring bones, muscles, connective-tissue, or, rarely, to the cranial 
bones and meninges. As in "cancrum oris," if the adjacent veins are in- 
volved, pyaemia and multiple abscesses are the result. The Eustachian 
tube may be involved, and sometimes pus burrows under the muscles at 
the back of the neck. 

Etiology. — Specific parotitis seldom occurs except as the result of conta- 
gion. It is contagious, but not infectious, and seems to be favored in its 
development by dampness. Consequently, it is common in autumn and 
early spring, and among those who live in cold, damp cellars. It prevails 
most in crowded localities, such as asylums and foundling hospitals. It 
resembles the exanthemata, in that it attacks the same gland but once. 
The exact cause of metastatic parotitis is obscure. The reason of its devel- 
opment in small-pox, typhus, typhoid, measles, pysemia, septicaemia, chol- 
era, and rarely in pneumonia, cannot always be given. The period of 
incubation in specific parotitis varies from seven to fourteen days. 

Symptoms. — In specific parotitis for a short time preceding the glandular 
enlargement there is chilliness followed by flashes of heat, frequently by 
dull pains in the limbs, general lassitude and loss of appetite. In nervous 
children headache, delirium, and often convulsions are its premonitory 
symptoms. In from thirty-six to forty-eight hours after these phenomena, 
there is a sensation of stiffness about the angle of the jaw, followed by pain 
and swelling in the parotid region. The pain is increased by speaking, 
swallowing, and by pressure. Both glands may be simultaneously affected 
but usually only one is involved at a time. The tumor is firmer over the 
centre than at its circumference, the outer rim being slightly cedematous 
and pitting on pressure. Moderate salivation occurs in a few instances. 
The disease reaches its height in from three to five days, and the swell- 
ing of the gland begins to subside on the seventh or eighth day. 

In the non-specific variety, if abscess form, constitutional symptoms in- 
dicative of the formation of pus are developed, and the adjoining lymphat- 
ics become enlarged. These abscesses may open externally, into the mouth, 
pharynx, or external ear. During or after the decline of specific parotitis, 
metastasis to the testicles, mammae, or ovaries may occur. Metastasis to the 
meninges of the brain (a rare occurrence) is indicated by delirium and active 
cerebral symptoms, which terminate in coma and death. Non-specific paro- 
titis, developing during some severe constitutional disease, produces few 
symptoms of its own, excepting the physical evidences of the tumor, which 
shows a tendency to suppurate from its beginning ; very soon a lobulated red 
swelling exhibiting fluctuation at various points is developed, which soon 



TONSILLITIS. 



247 



discharges laudable pus. In this variety, but one gland is usually in- 
volved. 

Differential Diagnosis. — There is little difficulty in recognizing this disease 
by the situation of the swelling. 

Prognosis. — In the specific variety the prognosis is favorable, the gland 
usually returning to its normal si e and consistence in from ten days to two 
weeks. If an abscess forms and implicates the ear or Eustachian tube, per- 
manent deafness may result ; when orchitis, mammitis, meningitis and 
other metastases complicate the parotitis, the prognosis is more or less un- 
favorable. Death may result from meningitis with active brain symptoms. 
Non-specific parotitis, occurring in the course of any acute general disease, 
must be regarded as a very unfavorable symptom. 

Treatment. — Specific parotitis is a self-limiting disease ; during its active 
period the patient must be kept in an even temperature, and a mild saline 
cathartic may be administered. The diet should be non-stimulating. If 
the parts are painful, warm fomentations may be applied. If the patient 
suffers severe pain or is restless, the bromide of potassium or hydrate of 
chloral may be given. Inunctions of oil, when the swelling is disappear- 
ing, are said to aid in reducing it. When orchitis or meningitis occurs it is 
to be treated as a complication. During convalescence tonics are indicated. 
The non-specific variety requires no treatment except the use of means 
which hasten suppuration and support the patient. 

DISEASES OF THE PHARYNX. 

I Tonsillitis:— {a) Acute or Quinsy ; and (b.) Chronic. — II. Inflam- 
mations: — (a.) Catarrhal which is either Acute or Chronic; and, (b.) 
Membranous, which is either Croupous or Diphtheritic. — III. Retro- 
pharyngeal Abscess. 

TONSILLITIS. 

<e Quinsy sore throat," sometimes called phlegmonous pharyngitis, is an 
inflammation of the parenchyma of one or both tonsils, and may be acute or 
chronic. 

Morbid Anatomy. — It must be remembered that beneath the external cov- 
ering of the tonsils fibrous trabecular enclose numerous groups of lymph-fol- 
licles, and that this interstitial stroma is very vascular. In acute tonsillitis 
there is first hypersemia and swelling of the gland and of the parts adjacent 
to it. The angry, red, lobulated surface of the enlarged gland and the 
back part of the tongue are covered with a tough, gelatinous or creamy 
secretion, and the uvula and anterior pillars of the fauces become swollen 
and cedematous. When suppuration is to occur a point on the surface of 
the inflamed tonsil becomes prominent, soft and fluctuating. The loose 
cellular tissue surrounding the tonsils may be involved in the suppurating 
processes. If chronic tonsillitis follows, subsidence of the acute hypertrophy 
of the stroma occurs, accompanied by enlargement of the supplying ves- 
sels. Chronic enlargement of the tonsils may also be developed slowly 



248 



DISEASES OF THE DIGESTIVE SYSTEM. 



without being preceded by the acute, and then the glands may become so 
large that they touch each other and are much firmer and harder than the 
normal gland. Their surface presents a pitted appearance, the mucous 
membrane usually being paler than natural. 

Etiology. — Quinsy is rare in those under twelve years of age, but it is more 
common in youth than in adult life. Certain atmospheric influences pre- 
dispose to it. There is a strong hereditary predisposition to it in certain 
persons. It "runs in families." Certain diseases, as scrofula and syphilis, 
favor its development. Exposure of the surface to cold almost always pre- 
cedes an attack. After a first attack it is liable to occur at stated intervals 
each year. Tonsillitis frequently occurs with scarlatina, measles, typhoid 
fever, and with inflammatory conditions of the mouth or tongue. Chronic 
tonsillitis, which is not a sequela of the acute, is almost always hereditary. 

Symptoms. — Acute tonsillitis is usually ushered in by a distinct chill fol- 
lowed by a rapid elevation of temperature ranging from 103° F. to 105° F., 
with a corresponding increase in the frequency of the pulse. In from 
twelve to thirty-six hours after the initial fever there is heat, pain and 
swelling in the region of the tonsils, and dryness of the tongue and throat. 
The attempts which the patient makes to swallow an imaginary substance 
in the fauces increase the pain. Fluids are often regurgitated through the 
nostrils. The respirations become difficult on account of the obstruction to 
the ingress and egress of air. The tumor produced by the swollen tonsil 
can be readily felt externally. Thick mucus is expectorated, and the 
tongue becomes swollen and covered with a thick pasty coating. The 
breath is offensive, the jaws are often immovable, any attempts to move 
them causing darting pains along the Eustachian tube to. the ear. There 
is a peculiar "nasal" tone to the voice, and if the throat can be examined, 
the passage to the pharynx is found obstructed by the swollen glands, the 
cedematous uvula, and the oedematous anterior pillars of the soft palate. 

These symptoms steadily increase in severity. The patient is unable to 
sleep, and suffers constantly from a sense of impending suffocation. He is 
sometimes delirious. The constitutional and local symptoms increase for 
several days, and then gradually subside, or something is felt to give way in 
the throat, and suddenly the patient is entirely relieved by the discharge of 
fetid yellow pus. Convalescence is rapid. When a chronic enlargement is 
the result of quinsy, violent paroxysms of coughing and loud snoring dur- 
ing sleep are caused by the enlarged tonsils and elongated uvula, which latter, 
in some cases, produces an inclination to vomit. The Eustachian tube being 
pressed upon, partial or permanent deafness results, and the voice has a thick 
and often husky tone. Chronic catarrhal stomatitis frequently accompanies 
this form of tonsillitis ; acute attacks may be engrafted upon the chronic 
condition. Slight dysphagia and impediment to full and deep inspirations, 
as well as a permanent change in the voice, are caused by chronic tonsillitis. 

Differential Diagnosis. — It is hardly possible to mistake quinsy for any 
other disease, if a proper examination of the throat is made. 

Prognosis. — The prognosis in acute tonsillitis is always good. The only 
thing to be feared is that chronic enlargement of the tonsils may result. 



CATARRHAL PHARYNGITIS. 249 

The duration of the urgent symptoms is from four to five days — the entire 
duration is eight days. It may be complicated by inflammatory conditions 
of the tongue and mouth, by inflammation of the Eustachian tubes, by 
pharyngitis and oedema glottidis. Death in rare instances may result from 
suffocation, exhaustion, or oedema glottidis. 

Treatment. — When seen early, astringent gargles and the carbolized spray 
will afford relief, and in some instances seem to arrest its progress. Paint- 
ing the surfaces with solution of cocaine will often relieve the dysphagia. 
After the chill, suppuration can rarely be prevented. Warm poultices of 
linseed meal, the wet pack, or external applications of turpentine, are then 
found most efficacious and agreeable. I have been able in a large number 
of cases to abort a quinsy by a twenty-grain dose of quinine administered at 
the time of the chill, followed by a large dose of bromide of potassium. 
Mild cathartics should be administered at the commencement of the at- 
tack ; a combination of belladonna, quinine and aconite has been thought 
by some to have a controlling influence over this disease. Acetate of am- 
monia, chlorate of potash, or some effervescing draught is generally grate- 
ful to the patient ; the diet should be highly nutritious; moderate stimula- 
tion is often required. As soon as an abscess forms it should be opened. 
Warm poultices may be applied over the region of the glands for some time 
thereafter. If suffocation threaten at an early stage of the disease, free 
scarification of the swollen and cedematous parts, or excision of the tonsils 
must at once be made. In chronic tonsillitis, tannin and glycerine, or a 
strong solution of alum or iodine, should be carefully and regularly ap- 
plied ; at the same time iodide of potash or iron may be given. It may 
be necessary to excise a part or all of the gland, and part of the uvula, af- 
ter other remedies have been tried and found unavailing. 

CATARRHAL PHARYNGITIS. 

This is an inflammation of the mucous membrane of the tonsils, uvula, 
soft palate and pharynx. It may be acute or chronic, and may affect all or 
only portions of the pharynx. 

Morbid Anatomy. — The morbid changes in the mucous membrane are the 
same as in catarrhal laryngitis and stomatitis. The uvula is enlarged, and 
the calibre of the pharynx is lessened. In chronic catarrhal pharyngitis 
the mucous membrane is either generally thickened and indurated, or the 
thickening occurs in irregular patches. The uvula is relaxed, and the af- 
fected parts are covered with a viscid mucus of a slightly offensive odor. 
The lymphatics are enlarged, especially at the back part of the pharynx, 
and small round nodules (often aggregated into masses of considerable size) 
present the appearance called ' 'follicular pharyngitis." The escape of secre- 
tions from the glands being prevented, the latter dilate and form cysts 
whose contents undergo cheesy degeneration, or, after forming vesicles, ul- 
cerate. The cheesy masses in the cysts may, after -a time, become calca- 
reous, or undergo purulent change. Follicular pharyngitis may extend 
upward and involve the posterior nares, or downward and involve the larynx. 



250 



DISEASES OF THE DIGESTIVE SYSTEM. 



Etiology. — The acute form occurs most frequently in children and in 
young adults. There seems to be a predisposition in some persons to this 
affection. One attack predisposes to others. The causes which predispose 
to quinsy induce acute pharyngitis. Chronic follicular pharyngitis may be 
produced by prolonged use of the voice in public speaking or singing, or 
by the excessive use of tobacco or of spirituous liquors. Weak, scrofulous 
persons, and those with chronic thoracic disease are frequently affected with 
it. Its chief cause is repeated acute attacks. 

Symptoms. — Slight fever may usher in an attack of acute pharyngitis, or 
precede the development of its local symptoms. The throat first becomes 
dry and redder than normal, and movement of the parts produces pain in 
the direction of the Eustachian tubes, so that swallowing and speaking be : 
come painful. The elongated uvula may induce violent fits of coughing. 
The local symptoms are very severe ; there will be more or less regurgita- 
tion of food through the nose. If particles of food do not readily pass into 
the oesophagus they may enter the larynx and cause severe fits of coughing. 
In these severe cases there is a nasal twang to the voice, and any movement 
of the throat, tongue, or mouth is carefully avoided on account of the pain 
it produces. If the inflammation invades the Eustachian tube, deafness 
may result, and not infrequently the tympanum is perforated by the pus 
which collects in the middle ear. The extension is more often forward, so 
that the mucous membrane of the tongue and mouth presents the same 
condition as that of the pharynx. These symptoms may gradually subside, 
after a few days, and the viscid secretion disappear from the tongue, 
mouth and pharynx. If it becomes chronic, the voice becomes hoarse, 
and there is a stridulous cough accompanied by a thick, tough mucous 
expectoration, often containing small firm, yellow masses. There is 
constant irritation of the throat, which is variously described as dry, tick- 
ling or tingling, and the secretion may be so much diminished tha,t slight 
hemorrhage may occur from the membrane when pressed upon. All these 
symptoms are most marked in the morning. The symptoms in a long 
standing case may lead to anxiety on account of the suppo'sed existence of 
pulmonary phthisis. These are all aggravated by " catching cold," atmos- 
pheric changes, and the prolonged use of the voice. 

Differential Diagnosis. — Follicular pharyngitis may be mistaken for pul- 
monary disease, and the early stage of mild chronic catarrh often excites 
suspicion of syphilis. In the former case an exploration of the chest and 
an examination of the throat will at once decide, while the presence or ab- 
sence of the constitutional signs of syphilitic infection will establish the 
diagnosis in the latter instance. 

Prognosis. — Acute catarrhal pharyngitis is a very mild disease, subsiding 
completely in most cases within one week from its onset, while chronic phar- 
ingitis is the most persistent of all catarrhal affections. 

Treatment. — In acute pharyngitis, ice-cold carbonated water affords the 
greatest relief during the first twenty four hours. The throat and mouth 
should be frequently sprayed with a solution of alum, tannin, or sulphate 
of zinc, and at the same time the wet pack should be applied to the throat 



MEMBRANOUS PHARYNGITIS. — RETRO-PHARYNGEAL ABSCESS. 251 



either hot or cold, but they should not be alternated. In chronic pharyn- 
gitis, the first thing to be done is to remove the cause and live an out- 
door life. Spraying the parts two or three times a day with the astringent 
just named, or a mild solution of nitrate of silver, will generally afford 
temporary relief. In some cases capsicum or guiacum may be advan- 
tageously combined with the astringents, and in obstinate cases the local 
use of iodine or a twenty per cent, solution of carbolic acid may be resorted 
to. In chronic (follicular) pharyngitis a nutritious diet is especially im- 
portant. German physicians recommend very highly the use of mineral 
waters, but alkaline gargles are as effective as a residence at some "spring." 

MEMBRANOUS pharyngitis. 
Under this head are included both croupous and diphtheritic inflamma- 
tions of the pharynx. Croupous inflammation may be primary, but diph- 
theritic inflammation is always secondary. This form of pharyngitis is 
considered in the history of membranous laryngitis and diphtheria. 

RETROPHARYNGEAL ABSCESS. 

Suppuration behind the pharynx, in the areolar tissue between it and 
the vertebras, is known as retro-pharyngeal abscess. 

Morbid Anatomy. — This is a cellulitis, and its moibid anatomy is the 
same as that of cellulitis terminating in an abscess elsewhere. It belongs 
properly to the province of surgery. 

Etiology. — Retro-pharyngeal abscess occurs more frequently in children 
than in adults. It is developed during the progress of caries of the cervical 
vertebras. It is rarely if ever due to the extension of inflammation from 
the pharynx. A strumous diathesis predisposes to it. Sometimes it appears 
late in pyaemia, septicaemia, typhoid, typhus, scarlet fever and measles. 
Now and then it occurs without any obvious cause. 

Symptoms. — The first symptom is dysphagia. With this there is stiffness 
of the neck, slight difficulty in articulation, and a change in the tone of 
voice, which becomes nasal in character. On examining the pharynx its 
calibre will be found diminished by a bulging from behind and perhaps a 
little to one side ; the pharyngeal mucous membrane is redder than normal, 
and there may be a slight swelling about the angle of the jaw. The head 
is thrown backward, and any attempt at flexion causes dyspnoea ; the jaws 
seem to be partially locked. There is regurgitation of food through the 
nose. In young children there may be snuffling, choking, coughing and 
great dyspnoea, with a certain hoarse tone to the voice. The mouth is 
filled with a mucous secretion. 

As the abscess increases in size the tumor may be seen nearly filling 
the space behind the soft palate. This swelling is soft, elastic and 
fluctuating, sometimes rupturing when pressed upon, and discharging 
an offensive pus. If it opens spontaneously the pus is vomited, swal- 
lowed, discharged through the nose, or is inspired into the trachea and 
may cause suffocation. Again, the abscess filling the pharynx may press 
on the rima glottidis and epiglottis and cause oedema glottidis. In rare 



252 



DISEASES OF THE DIGESTIVE SYSTEM. 



instances the pus makes its way around to the opposite wall of the 
pharynx, and then breaks into the oesophagus or trachea, or. burrows into 
the pleural cavity or even the pericardium. It may burrow between the 
tracheal muscles and appear at the anterior part of the neck. 

Differential Diagnosis. — When fully developed, a careful examination of 
the pharynx will detect at once the existence of a retro-pharyngeal abscess. 

Prognosis. — The prognosis is bad whenever caries of the spine has caused 
the abscess. The complications which may cause death are oedema glot- 
tidis, pleurisy, pneumonia, and pericarditis. Death may result from suffo- 
cation from pressure. 

Treatment. — Open the abscess early, and never wait for its spontaneous 
rupture. The position of the child when the bistoury is used should be 
such that the escape of pus through the mouth is facilitated. 

DISEASES OF THE (ESOPHAGUS. 
The following diseases of the oesophagus will be considered : 

I. Inflammation, either catarrhal or membranous, including Stricture 
of the (Esophagus ; and, II. (Esophageal Cancer. 

OESOPHAGITIS. 

Oesophagitis, or inflammatory dysphagia, is a catarrhal inflammation of 
the mucous membrane of the whole or a part of the oesophagus. It is an 
exceedingly rare disease. 

Morbid Anatomy. — In the acute variety the mucous membrane is red, 
swollen, softened and covered with a layer of mucus containing epithelium 
and pus. In the chronic variety the mucous surface is of a dull pink or 
slaty blue color. The sub-mucous tissue is thickened, and a thick viscid 
mucus or pus covers its surface. It may cause dilatation of the oesopha- 
gus, which may affect the whole tube uniformly or form a pouch at its lower 
portion, or it may give rise to a hernial protrusion of the mucous mem- 
brane through the muscular coat. In all cases of oesophageal dilatation due 
to chronic catarrh, there is more or less thickening of the oesophageal walls. 
In some cases the thickening may diminish the calibre of the tube. Ulcer- 
ation of the mucous membrane at the seat of the catarrh sometimes occurs. 
The ulcer may be superficial, or extend through the walls of the tube. 

Membranous Inflammation of the oesophagus may b % e either croupous or 
diphtheritic. In either case the morbid changes are the same as in croup- 
ous or diphtheritic inflammation of other mucous surfaces. 

Etiology. — Acute .oesophagitis has its most common cause in the irritation 
produced by acrid fluids or solids in their passage to the stomach. Irritat- 
ing drugs and corrosive poisons may excite it. Too frequent introduction 
of instruments into the stomach may cause it, and it may arise from the 
excessive use of alcohol. Extension of inflammation from the parts above 
or below it often induces acute oesophagitis. Chronic oesophageal catarrh 
may occur as part of a similar process affecting the whole alimentary tract. 
It may develop as the result of a strumous or phthisical diathesis, or follow 



(ESOPHAGITIS. 



253 



an acute attack. Membranous oesophagitis is always secondary and results 
from, or occurs with similar processes in the respiratory or other portions 
of the digestive tract. It also may appear after some of the eruptive fevers, 
cholera, pyaemia and septicaemia. 

Symptoms. — Varying with the intensity of the inflammation, an aching 
or severe burning pain is felt at the back, between the shoulders, or deep 
behind the sternum. Even the ingestion of fluids causes dysphagia, the 
pain being greatest as the fluids pass through the upper portion of the 
oesophagus. More or less febrile excitement and great depression and anxi- 
ety accompany the disease, and throughout its course the thirst is torment- 
ing. In severe cases there are paroxysms of coughing, and perhaps slight 
dyspnoea with hoarseness. Vomiting sometimes follows attempts at swal- 
lowing. All these symptoms gradually increase in severity. If extensive 
ulceration is present, sudden rupture of the oesophagus may occur during the 
act of deglutition. In chronic oesophagitis there is dysphagia and pain only 
on swallowing solids. If ulcers exist, there may be vomiting of viscid mucus 
tinged with blood, accompanied by the symptoms of oesophageal stricture. 

Stricture of the oesophagus is accompanied by gradually increasing 
dysphagia, emaciation and debility, which finally terminate in death from 
inanition. The most frequent seat of stricture of the oesophagus is at its 
cardiac extremity. It may be caused by structural changes in its wall, as 
in oesophagitis with or without ulceration, and cancer, or by compression 
from mediastinal and other tumors. As oesophageal strictures develop 
slowly, for a long time the only symptom 
is slight difficulty in swallowing solids, the 
patient usually referring the difficulty to a point 
behind the manubrium sterni. As the constric- 
tion increases there is difficulty in swallowing 
liquids. Food and drink collect in the oesopha- 
gus, and after a longer or shorter delay are re- 
gurgitated with the saliva through the mouth and 
nose. With oesophageal stricture there are usually 
painful eructations. Sometimes the pain is lan- Fig. 53. 

cinating in character, shooting from the region of ^E^S^^S^ 
the oesophagus back to the spinal column. The *ty. 

Lester curvature of" Stomach. 
Pylorus. 
D. Point of the stricture. 

Uniform dilatation cannot be recognized dur- 
ing life. "When dilatation is partial, or when pouches exist, there may be 
vomiting of undigested offensive food some hours after eating. In all cases 
of alteration in the calibre of the oesophagus, the oesophageal bougie will 
determine the amount of narrowing and the locality of the pouches. 
Membranous inflammations of the oesophagus cannot readily be determined 
during life. A portion of membrane may be vomited, but it cannot be 
determined whether it comes from the oesophagus, or has been swallowed 
and regurgitated. 

1 The treatment of stricture of the oesophagus belongs to surgery. 




introduction of a bougie will determine the seat, £ 
extent, and form of the stricture. 1 



254 



DISEASES OF THE DIGESTIVE SYSTEM. 



Differential Diagnosis. — This disease may be mistaken for cancer of the 
oesophagus ; the diagnostic points will be considered in the history of 
oesophageal cancer. At the onset it may also be mistaken for hydrojihobia, 
but the diagnosis is soon established by the development of the character- 
istic nervous phenomena of the latter disease. 

Prognosis. — The immediate prognosis in acute oesophagitis caused by 
chemicals or mechanical irritants depends more on the changes which have 
occurred around the larynx and in the stomach, than upon the oesophagitis. 
The prognosis in croupous and diphtheritic inflammations of the oesophagus 
is also determined by the conditions of the primary disease. In chronic 
oesophageal catarrh without stricture the prognosis is good. 

Treatment. — In acute oesophagitis, if the inflammation has been excited 
by foreign bodies lodged in the oesophagus, they must at once be removed ; 
if corrosive chemicals have been swallowed, the proper antidote must be ad- 
ministered. In severe cases, all movement of the parts must be prevented. 
Ice in the mouth is grateful and does no harm. Nutrient enemata may be 
given, and, if the pain is severe, hypodermics of morphine must be given 
in sufficient quantities to afford relief. Hot anodyne fomentations applied 
locally are usually of service. In chronic oesophageal catarrh, if ulcers ex- 
ist, spray the parts with astringent fluids, such as a solution of nitrate of 
silver. Surgery directs that if starvation seems imminent a gastric fistula 
should be made. In oesophageal stricture, bougies must be daily intro- 
duced for a long time, with the hope of dilating the stricture. No treat- 
ment is required in oesophageal dilatation. 

CANCER OF THE (ESOPHAGUS. 

The most frequent variety of oesophageal cancer is epithelioma, but 
scirrhus and medullary cancer are not unknown. It occupies the upper and 
middle third of the oesophagus more often than the cardiac portion ; in the 
former, it is associated with pharyngeal and laryngeal cancer, and in the 
latter with cancer of the cardiac extremity of the stomach. 

Morbid Anatomy. — Epithelioma begins in the mucous tissue, and pursues 
the same course as cancer of the tongue. The ulceration may be limited 
to a circular patch an inch in diameter, or may involve the whole circum- 
ference of the oesophagus. The growth after a time invades all the tissues 
of the oesophagus, and causes stricture of its calibre. Above the stricture 
there is either uniform dilatation or a pouch, sometimes as large as an 
orange. If the cancerous mass involves the entire oesophageal wall, it may 
press upon and destroy one or both pneumogastrics, and lead to the devel- 
opment of pneumonia or pulmonary gangrene. If the oesophagus is rupt- 
ured, openings may be made into the trachea, through the diaphragm into 
the peritoneal cavity, or into the posterior mediastinum. Cancer has some- 
times ulcerated into the aorta, pulmonary artery, and even into the right 
subclavian artery. 

Etiology. — Two-thirds of the cases of cancer of the oesophagus occur in 
males between the ages of forty and sixty. It is generally primary ; it 



CANCER OF THE (ESOPHAGUS. 



255 



may be secondary to cancer of the mouth, pharynx, mediastinum, or 
stomach. 

Symptoms. — The first thing noticed in cancer of the oesophagus is difficult 
deglutition ; soon well-marked dysphagia occurs. Pain is present early, 
and may be dull, burning, or lancinating in character ; it is located about 
the centre of the sternum, in the throat, or in the interscapular space. It 
varies greatly in kind and degree, but it is greatly aggravated when food 
reaches that portion of the oesophagus which is the seat of the cancer. As 
the stricture grows narrower, flatulence, regurgitation of food and vomiting, 
with steadily increasing emaciation, become prominent symptoms, and a 
well-marked cachexia is developed. Cough, dyspnoea, and hoarseness some- 
times result from pressure of the cancerous tumor. As the disease advances, 
the pain becomes more constant, the cachexia is better marked, and hem- 
orrhages are frequent ; the bloody fluid vomited often contains shreddy 
masses which contain cancer elements and show the character of the dis- 
ease. The neighboring lymphatic glands may also be implicated, and, by 
pressure on a main bronchus, cause feeble respiration in the lung to which 
the bronchus is distributed. If rupture occurs, it is followed by a sudden 
sharp pain in the chest, fainting, and coldness of the extremities, followed 
almost immediately by death. 

Differential Diagnosis. — (Esophageal cancer may be mistaken for stricture 
of the oesophagus from chronic catarrhal inflammation. In cancer, pain is 
constant and greatly aggravated by taking food, while in non-cancerous 
oesophageal stricture pain is absent, or is only present on swallowing. The 
glands about the neck are early involved in cancer, but are normal with 
chronic catarrh. Chronic pulmonary disease is rarely absent when oeso- 
phageal cancer is present, but is never induced by non-malignant stricture. 
Hemorrhage is frequent in cancer, and does not often occur with stricture 
from chronic catarrh. The bougie may bring up shreddy masses, with evi- 
dences of cancer in the one case, but merely meets with obstruction in the 
other. 

Prognosis. — This is always a fatal disease. Its average duration is one 
year, but death may occur in a few weeks. The prognosis as to time varies 
with the presence or absence of complications. Death may result from any 
of the complications, from hemorrhage or septicaemia. 

Treatment. — Early in cancer let the food be finely chopped and taken in a 
semi-fluid state ; later, it should be entirely fluid, and when the patient 
cannot swallow, nutrient enemata must be given. The diet in all cases 
must be nourishing in the highest possible degree, and stimulants can usu- 
ally be given with benefit. When the pain is intense morphia per rectum 
or hypodermically should be administered in doses sufficient to relieve it. 
Bougies should be used with great care ; early, they should only be used to 
locate and diagnosticate the disease ; later, tubes must only be used for the 
purpose of introducing food into the stomach, as fatal hemorrhage or rupt- 
ure has followed their use. The subject of gastrotomy comes within the 
domain of surgery. 



256 



DISEASES OF THE DIGESTIVE SYSTEM. 



DISEASES OE THE STOMACH. 

I, Inflammations of its mucous membrane and its submucous or areola? 
tissue. 

a. Acute or Toxic Gastritis. 

b. Sub-acute Gastritis, or Acute Gastric Catarrh, 

c. Chronic Gastritis, or Chronic Gastric Catarrh, 

d. Phlegmonous Gastritis, 

II. Dyspepsia. IV. Neuroses or Gastralgia, 

III. Cancer and Ulcer, V. Hwmatemesis. 

VI. Dilatation, 



ACUTE GASTEITIS. 

Acute or toxic gastritis is a general inflammation of the mucous and sub- 
mucous tissue of the stomach. It is of rare occurrence, unless the result of 
the introduction into the stomach of irritating poisons. 

Morbid Anatomy. — On opening a stomach which is the seat of toxic gas- 
tritis a thick layer of tough, viscid mucus will be found spread over its 
mucous surface.. Beneath this there will be found an intense redness of the 
membrane, which is most marked along the edge of the rugae, near the car- 
diac orifice. The mucous and submucous tissues will be soft and cedema- 
tous. In some rare instances the whole or a portion of the mucous mem- 
brane will be found to present the appearance of a detached brown or black 
slough ; it may be entirely eroded. Fibro-plastic exudation may cause com- 
plete occlusion of its cardiac or pyloric orifices. When the muscular tissue 
is involved it becomes soft, easily torn, often gelatinous. In severe cases 
perforations may exist. 

Etiology. — Acute gastritis is almost always caused by the entrance into 
the stomach of irritant poisons, such as sulphuric, nitric, and oxalic 
acids, arsenic, the chloride of zinc, and large quantities of concentrated 
alcohol. Mechanical irritation, such as results from the introduction into 
the stomach of knives, pins, false teeth, etc., may produce a local acute gas- 
tritis. Introduction into the stomach of boiling water, hot lead, or steam 
may cause a most intense gastric inflammation, with extensive sloughing of 
its mucous surface. 

Symptoms. — Soon after the introduction of corrosive substances into the 
stomach, there will be a dull, uneasy feeling, sometimes one of warmth, 
over the epigastrium. This is rapidly followed by an intense burning pain 
shooting through to the back. The epigastric region becomes extremely ten- 
der. With, or preceding these symptoms, there is nausea, and vomiting of 
tenacious mucus ; the vomiting is very distressing ; the ejected mucus often 
contains blood, and, at first, portions or traces of the substance which has 
caused the gastritis. As the pain becomes more severe the vomiting is more 
distressing ; there is intense thirst, and frequent spasms of the abdominal 
muscles. The temperature rapidly rises, sometimes to 105° F.; the pulse 



SUB-ACUTE GASTRITIS. 



257 



feaches 120 or 140 per minute and is feeble and irregular. If the oesophagus 
is implicated, there is dysphagia. The urine becomes scanty and high 
colored, and is sometimes suppressed. These violent symptoms soon give- 
place to a condition of general prostration, in which there is almost con- 
stant hiccough. The surface becomes cold and clammy, the radial pulse 
grows feeble and finally imperceptible, while the respirations are hurried, 
short and irregular, the mind remaining clear to the last. There are cases 
on record of poisoning by chloride of zinc and sulphuric acid, in which 
there was no pain in the epigastrium during the whole course of the disease. 

Differential Diagnosis. — The diagnosis is not difficult. The history of 
its cause and the character of the vomiting establish it. 

Prognosis. — The prognosis depends upon the cause. The more intense 
the pain, the more extensive the gastric inflammation. Death may occur 
in a few hours, or it may be delayed two or three weeks. Acute gastritis 
may be complicated by analogous conditions of the mouth, pharynx, or 
oesophagus, by enteritis, laryngitis, or oedema glottidis, and as sequelae there 
may remain constrictions at the cardiac or pyloric orifices. Death may 
result directly from the shock of the gastritis, from the constitutional effects 
of the poison which produces it, or from resulting peritonitis. 

Treatment. — The first thing is to administer the proper antidote to the 
poison which has caused the gastritis, and thoroughly wash out the stom- 
ach, after which the gastritis should be treated as a local inflammation. Four 
or five leeches may be applied over the epigastrium, followed by warm poul- 
tices or fomentations. Some prefer the application of ice to the epigas- 
trium. Unless contra-indicated by the chemical constitution of the poison, 
the intense pain should be relieved by hypodermic injections of morphia. 
During the whole period the patient should be kept absolutely at rest in 
the horizontal position. 

SUB- ACUTE GASTRITIS. 

Sul-acvte gastritis, or acute gastric catarrh, is always a secondary affec- 
tion. 

Morbid Anatomy. — The parts principally involved in this form of gas- 
tritis are the ridges between the depressions, the vessels which lie in imme- 
diate proximity to them, and the apertures of the tubules. The mucous 
membrane is mottled by red spots scattered over it in irregular patches ; 
sometimes there are extensive ecchymoses and blood extravasations. The 
gastric juice is much diminished in quantity, and being mixed with much 
mucus loses its acidity and to a great extent its digestive power. The sur- 
face of the mucous membrane is covered with abundant, tenacious mu- 
cus ; there is also a moderate production of pus cells on the surface of the 
mucous membrane. The gastric tubules become filled with granular mat- 
ter. Late in the disease the solitary and lenticular glands, especially 
about the pylorus, increase in size and stud the surface as small white 
specks. The inflammatory processes are superficial and do not involve 
the deeper tissue of the mucous membrane. Superficial sloughs are some- 
17 



258 



DISEASES OF THE DIGESTIVE SYSTEM. 



times formed varying in size from a pea to that of a three-cent piece ; they 
rarely involve the submucous tissue. Its most prominent lesion is the 

coating of the gastric mucous 

F 



surface with tenacious mucus. 

Etiology. — No period of life is 
exempt from this form of gastri- 
tis. It occurs most frequently 
under two conditions : — first, with 
acute alcoholismus ; secondly, 
with those diseases in which there 
is extensive blood-poisoning, as in 
scarlet fever, small-pox, measles, 
typhoid and typhus fevers, diph- 
theria, pneumonia, pyaemia and 
septicaemia. It sometimes com- 
plicates pulmonary phthisis, and 
may follow the disappearance of 
gout, rheumatism, or affections 
of the joints. 

Symptoms. — Vomiting is its 
first and most prominent symp- 
tom. The matter vomited con- 
sists of the substances which have 
been taken into the stomach, 
and sometimes streaks of blood. 




A Vertical Section of the Stomach walls in Sub-acute 
Gastritis. 



Muscular fibres in longitudinal section. 

The same cut transversely . 

Submucous tissue, in which are seen at 

D. Blood-vessels enlarged and filled with blood. 

Mucous coat. The gastric follicles are shown filled 

with granular detritus and covered with pus— G. 
Small vessels between the follicles, x 40. 



mingled with a grayish, stringy mucus, 
When the vomiting is severe and prolonged, bright green, bitter fluid 
is often ejected. The fermentation which takes place in the fluid con- 
tained in the stomach sometimes develops gases which cause distention 
of the stomach and a prominence of the epigastrium. The patient has no 
desire for food, but constantly craves ice and cooling drinks. The thirst is 
intense. The smallest quantity of food taken into the stomach causes nausea 
and vomiting, which may be so severe as to induce extreme exhaustion or 
collapse. Accompanying the nausea and vomiting there is more or less 
pain at the epigastrium. This pain is sometimes intense, and shoots back- 
ward between the shoulders, but usually it is not severe unless firm pressure 
is made over the stomach. The tongue is coated with a yellow or ash-col- 
ored material, and becomes dry and red at the tip. The papillae are prom- 
inent. The breath has an offensive odor. Late in the disease, herpetic 
eruptions make -their appearance about the lips and in the mouth. Often 
during its course there will be flashes of heat, with a burning sensation in 
the palms of the hands and the soles of the feet. The thermometer may 
indicate an axillary temperature of 103°, or even 105° F. The patient be- 
comes restless and irritable and often has attacks of syncope. In alcoholic 
cases the anorexia is absolute, and vomiting occurs mostly in the morning. 
Delirium tremens is often a complication. Its symptoms are always more 
or less varied by the diseases with which it occurs. In rare instances I have 
seen an icteric and sometimes a bronzed hue of the skin come on during a 



CHROMIC GASTRITIS. 



259 



prolonged attack of acute gastric catarrh. Diarrhoea is usually present, the 
stools having a very offensive odor. Obstinate constipation is rare. The 
urine is scanty and high colored, and in severe cases presents slight traces 
of albumen. Nitric acid gives a deep red color to it, or there is a copious 
deposit of lithates. 

Differential Diagnosis. — The diagnosis is easily made, and it is not likely 
to be confounded with any other affection, if its etiology and symptoms are 
carefully analyzed. 

Prognosis. — The prognosis is decided by the disease which it complicates. 
Unless associated with acute alcoholismus, it rarely becomes chronic. Its 
duration is from ten days to two or three weeks. It may be complicated by 
catarrhal conditions of the oral and pharyngeal mucous membranes, and in 
very rare instances by implication of the intestines (gastro-enteritis). It only 
causes death when it is extensive and complicates some grave acute general 
disease, as septicaemia, pyaemia, typhoid or puerperal fever. 

Treatment. — The most important thing in the treatment of this affection 
is rest to the stomach. In mild cases, entire abstinence from food for twenty- 
four hours, and then peptonized milk, or milk with lime-water, in small quan- 
tities at stated intervals, is all that is required. In severe cases, and in all 
eases occurring in children, nourishment must be given per rectum as long 
as the gastric symptoms are urgent. One or two leeches applied over the 
epigastrium, followed by warm fomentations, usually afford marked relief. 
In adults, if the pain is so severe as to prevent sleep, or if there is great 
restlessness, small hypodermics of morphia may be administered. After the 
patient has passed twenty-four hours without vomiting, peptonized milk 
may be given in small quantities. In those cases in which vomiting is per- 
sistent, and there are symptoms of collapse, stimulants must be freely admin- 
istered by the rectum. None of the remedies which are so often employed 
for the relief of vomiting are serviceable in the treatment of this affection. 
During convalescence, if the stomach is in an atonic condition, mineral acids 
and the vegetable bitters will be found of service ; great care must be exer- 
cised in the diet during the whole period of convalescence. The improve- 
ment of the diet must be gradual, and those who have been spirit drinkers 
should be warned of their danger, and the use of stimulants prohibited. 

CHROMIC GASTRITIS. 

Chronic gastritis is known under the names of simple gastritis, chronic 
catarrh of the stomach, morbid sensibility of the stomach, and chronic in- 
flammatory dyspepsia. 

Morbid Anatomy. — The morbid appearances in chronic gastritis vary 
with, its character and duration, and are usually best marked around the py- 
loric extremity of the stomach. Over all, or part of the mucous surface, 
there is a layer of gray mucus, varying in thickness and tenacity with the 
duration and character of the disease. On its removal the mucous mem- 
brane is seen studded with ecchvmotic and pigmented spots, the result of 
small extravasations. In some cases the mucous tissue is oedematous and 



260 



DISEASES OF THE DIGESTIVE SYSTEM. 



presents a well-marked granular appearance. The walls of the stomach are 
usually thickened and more or less indurated, especially about the pyloric 
orifice, which gives rise to more or less constriction, or "pyloric stenosis." 
The thickened membrane is often "leathery" to the feel, and the indura- 
tion may be so great that it tear,] with difficulty and can be stripped 
off the submucous tissue. The submucous tissue may also be thickened 
and congested, the color varying from an inflammatory blush to a livid, al- 
most purple red. When the submucous tissue is involved, there is an infil- 
tration of cells into it ; and upon their organization into new connective- 
tissue, and the subsequent contraction of this tissue, there will be more or 
less interference with the peristaltic motion of the stomach. Besides this 
there will be hypertrophy and distention of the gastric tubules, for their 
secretion is retained by the tissue-increase in the intertubular structure, 
which will cause them to stand out as small granulations in the atrophied 
tissue, presenting an appearance denominated " mammillation " This condi- 
tion may also be the result of hypertrophy of the glandular layer, which thus 
becoming too large for the basement muscular layer is corrugated and gives 
rise to another form of mammillation. It is only in rare instances that 
there is any mammillation about the cardia. 

In long-continued chronic catarrh of the stomach the muscular coat of 
the organ may become involved, and then the peristaltic movements 
will be still more impaired ; finally, the peritoneum may become thickened 
and adhesions take place between it and the adjacent parts. 

A microscopic examination of the gastric tubules in chronic gastritis will 
sometimes show that their epithelium has undergone granular degeneration, 
and in others there is a complete loss of epithelium, the tubules being filled 
with a granular detritus. Occasionally there will be found on the 

mucous membrane dirty white spots in 
irregular patches, which appear like de- 
pressions on the mucous surface. Under 
the microscope, there will be found in 
those spots some tubules completely filled 
with discrete fat spherules, and others 
whose epithelium has undergone fatty de- 
generation. If the tubules are constricted 
near their openings, cysts are formed from 
distention of the portion near the base by 
the secretion which cannot escape. In 
rare cases the fatty degeneration will in- 
volve the interstitial tissue as well. If 
hemorrhagic extravasation occurs into the 
gastric mucous membrane, the tubules 
will have their epithelium stained and 
their base blackened as a result of the 
sanguineous infiltration. Sometimes there 
is an increase in the intertubular lymphatic elements, with hyperplasia of 
the nuclei in the sheath of the vessels. 




A Vertical Section of Mucous Membrane of 
the Stomach, showing changes in the Tu- 
bules in Chronic Gastritis. 

A. Muscularis mucdm. 

B. Small blood-vessels around the follicles. 

C. Tubule with granular epithelium and filled 

■with granular detritus. 
I). Another tubule, iu which the epithelium is 
lost—filled with fat. globules. 

E. Granular matter filling the follicles. 

F. A small cyst, formed by dosing of the month 

of the follicle, with proliferation of the epi- 
thelial wall, x 250. 



CHEOXIC GASTRITIS. 



261 



In long-standing chronic gastritis there may be abrasions of the mu- 
cous surface and formation of ulcers (chiefly about the lesser curvature 
and the pylorus), circular in shape, varying in diameter from half an inch 
to an inch. These ulcers are very superficial, rarely extending beyond the 
mucous coat. They are pale in color, and their surface is covered with 
mucous cells, nuclei, and epithelium ; between the ulcers the rugae are con- 
gested. The intervening tissue is rarely normal. There may also be small 
follicular or punctate ulcerations, originating, it is supposed, in the enlarged 
solitary and lenticular glands. The base of these ulcers is infiltrated with 
lymph-cells and granular detritus ; they are never present except in the ad- 
vanced stage of chronic gastric catarrh. Chronic gastric catarrh may 
involve a large portion of the mucous surface of the stomach, and is gen- 
erally associated with a like condition of the intestinal mucous membrane. 
Waxy degeneration may be associated with these morbid changes, but in 
such cases other organs, as the liver and spleen, will have been primarily 
affected by the amyloid infiltration. The size of the stomach varies : some- 
times it is smaller than normal ; at others it is dilated. 

Etiology. — Chronic gastric catarrh is essentially a secondary affection ; it 
is rarely the sequela of sub-acute, much less of acute, gastritis, unless the 
former has been caused by an abuse of alcoholic stimulants. In many persons 
there is an hereditary tendency, after middle life, to chronic gastric catarrh. 
The principal general cause of this affection is anmmia. The most common 
local cause is the daily use of alcoholic stimulants. 

Mechanical obstruction to the capillary circulation of the stomach, indue- 
ing continued passive hyperemia (congestion) will cause it, and hence we find 
it associated with cirrhosis of the liver and other chronic hepatic affections 
where the blood is dammed back in the formative branches of the vena 
porta?. In the same way, valvular and other cardiac lesions, and pulmon- 
ary diseases, such as emphysema, chronic bronchitis, and phthisis, which, 
offer an obstacle to the venous return, will induce chronic gastric catarrh. 
Pressure on the walls of the stomach by tumors produces first congestion, 
and then chronic catarrh. Degeneration of the capillaries — " arterio- 
capillary fibrosis" — occurring in the cirrhotic form of Bright's disease, 
causes it, and it often accompanies ulcer and cancer of the stomach. 

Those causes which may be denominated recent are rapid ingestion of 
food, improper quality of food, or food which is known "to disagree 'with 
the stomach," and the sudden arrest of the digestive process after hearty 
meals. The prolonged use of arsenic, mercury, cubebs, and purgatives 
often causes it. Finally, scrofula, syphilis, and gout seem to predispose 
to it, and I am inclined to regard the chronic gastritis which is so often 
found associated with these diseases as the result of some degeneration of, 
or alteration in, the blood-vessels of the stomach. 

Symptoms. — The early symptoms of chronic gastric catarrh are chiefly 
those of indigestion. There is at first a sense of weight and fulness in the 
epigastrium, sometimes amounting to constriction, which comes on from 
half an hour to an hour after meals. Later there is actual pain and 
heat in the epigastrium (" heart-burn "). Pressure increases the pain and 



262 



DISEASES OF THE DIGESTIVE SYSTEM. 




causes it to shoot backward and upward toward the scapulas. Following, 
or with the advent of, these symptoms there is loss of appetite, first for 
solids such as meats ; later there is complete anorexia. Nausea and eruc- 
tations accompany the anorexia ; the stomach, and often the intestines 
become distended with gas, but vomiting is not usually present unless 
pyloric stenosis exists. The most important of the dyspeptic symptoms are 
the acid risings after meals, and the vomiting or regurgitation of acid 
mucus in the morning, which may be regarded as characteristic, and with- 
out which the diagnosis is uncertain. It is this acid material belched up into 
the oesophagus that causes " heart-burn." If there is actual vomiting of 
food, traces of butyric acid are present, with the sarcince ventriculi, cuboid 
cells averaging 1-2500 inch in diameter, each being divided into 
four equal parts containing nuclei, usually heaped into large 
cubes. 

As the disease progresses, the feeling of malaise and un- 
easiness following meals changes to one of languor or ex- 
fig. 56. haustion, and there is a sensation of heat in the epigastrium : 

Sarcmas, Ventri- 9 . L to . ' 

cult, x 750. thirst becomes a prominent symptom, one person craving 
cold, another hot drinks. The thirst is greatest in the evening, but 
the taking of fluids is usually followed by a sense of weight in the 
epigastrium, and by acidity and flatulence. The appearance of the tongue 
varies : it may be normal, paler than normal, florid and "beefy," or may 
be covered with a white or brown coating. The general symptoms which 
accompany the anaemic condition which attends this disease are headache, 
vertigo, cardiac palpitation, a gradual loss of strength and emaciation. 
Constipation and hemorrhoids are usually present, and the stools are often 
coated with mucus. In the chronic gastric catarrh of phthisis, diarrhoea is 
present. In cases of long standing, the hair becomes harsh and loses its 
lustre or turns gray ; the skin is dry, sallow, and shrivelled, sometimes 
covered with an eczematous eruption ; the nails are corrugated and exhibit 
a tendency to split, while in some there is premature caries of the teeth. 
Hypochondriasis, despondency, and irritability of temper are generally 
more or less marked. Ha3matemesis often occurs in that form of gastritis 
which accompanies cirrhosis of the liver, and the bleeding may for a time 
relieve the unpleasant gastric symptoms. Vomiting in the morning al- 
ways accompanies the gastritis of Bright's disease. 

The urine in chronic gastritis is cloudy, usually alkaline in reaction, 
depositing urates, phosphates and oxalates. Its specific gravity is highest 
at evening. The alkalinity is due either to imperfect gastric digestion or im- 
paired function of the liver and pancreas. The greater the mental depres- 
sion the more of earthy phosphates will be found in the urine. 

If hemorrhagic erosion exist in a stomach which is the seat of chronic 
catarrh, the pain in the epigastric region is constant, frequently shoot- 
ing back to the scapula?. Vomiting occurs not only in the morning, on 
rising and after meals, but also in the intervals. The vomited matter con- 
tains traces of blood, and bile mixed with mucus ; all of the gastric symp- 
toms are augmented in hemorrhagic erosion. Punctate or follicular ulcer- 



CHRONIC GASTRITIS. 



263 



mtion presents few, if any, symptoms differing from those of ordinary 
chronic catarrh. In most instances where a post-mortem has revealed 
this pathological state, there was vomiting of coffee-ground material 
during life. 

Differential Diagnosis. — Chronic catarrh of the stomach is to be differ- 
entiated from atonic dyspepsia, from cancer, and ulcer of the stomach. 

Atonic dyspepsia is associated, with anaemic conditions dependent upon 
habits of life and an unhealthy occupation ; while chronic catarrh is asso- 
ciated with the immoderate use of alcoholic stimulants, or is secondary to 
chronic thoracic, renal, or hepatic disease. In atonic dyspepsia there is 
little or no pain or tenderness in the epigastric region, which is always 
present in chronic gastritis. In atonic dyspepsia the tongue does not 
present the coated appearance so constant in chronic gastritis, but is 
broad, pale, and flabby. In atonic dyspepsia there is loss of appetite, but 
never the complete anorexia and constant thirst which are present in 
chronic gastritis. Spices and stimulating ingesta often relieve the gastric 
symptoms of atonic dyspepsia, while in chronic gastritis they aggravate the 
gastric symptoms. The constitutional symptoms in atonic dyspepsia are 
slight, while in chronic gastritis they are marked and severe. The urine is 
altered in atonic dyspepsia only during the attack ; while it is cloudy and 
alkaline, and persistently deposits urates, oxalates, and phosphates in 
chronic gastritis. Nausea and vomiting are more apt to occur in chronic 
gastritis than in dyspepsia. 

In its earlier stages cancer presents no symptoms other than those of a 
chronic gastritis ; later the vomiting and other evidences of obstruction 
will be persistent, and the vomited matters will more certainly be coffee- 
ground in character. Dilatation of the stomach is more frequent with 
cancer. The recognition of an abdominal tumor alone can render the 
diagnosis certain. 

The points in the differential diagnosis between chronic gastritis and 
ulcer of the stomach are given under the latter heading. 

Prognosis. — The duration of chronic gastric catarrh is variable ; it may 
'last for months or years, and may terminate in ulcer or stenosis of the 
pyloric orifice. It is amenable to treatment except when associated with 
advanced hepatic, renal, or pulmonary diseases, or where stricture at the 
pyloric orifice exists. A not infrequent complication is disease of the 
suprarenal capsules, and the connection between the two diseases has 
by some been supposed to be a "sympathetic" one, but no rational 
explanation has yet been offered. Sub-acute gastric catarrh sometimes 
complicates chronic gastric catarrh and renders the prognosis unfavor- 
able. Gastro-enteritis is a very rare complication. Death may result 
from haematemesis or from stricture of the pylorus. The general fee- 
bleness which results from long-standing gastritis predisposes to acute 
disease. 

Treatment. — The most important thing to be accomplished in the treat- 
ment of chronic gastritis is the removal of its cause. Each case requires a 
special treatment suited to its special indications and to its complicating 



264 



DISEASES OF THE DIGESTIVE SYSTEM. 



causes. When alcohol is the cause, all stimulants must at once be pro- 
hibited, and the patient placed on a diet in which there are few fats or 
carbo-hydrates. The food should be taken slowly in small quantities, at 
shorter intervals than in health, and thoroughly masticated. I have found 
i( underdone beef" and milk to be especially adapted to this class of 
cases. In catarrh induced by dram-drinking th^ best drug to allay 
morbid sensibility of the stomach and the morning sickness is opium, 
which also, by inducing sleep, relieves the nervous symptoms, which 
are always prominent. Strychnia and zinc in combination with min- 
eral acids have a wide reputation in this class of cases, acting favor- 
ably on both the nervous and digestive disturbances. The vegetable 
bitters as tonics are often serviceable when the craving for alcohol is 
excessive. 1 

Thorough washing of the stomach with an alkaline fluid used by the 
syphon tube is of great service in severe cases. In milder conditions the 
patient may drink a large glass of very hot alkaline water half an hour 
before eating. Such treatment is often combined with an exclusive meat 
diet. 

When there is marked anaemia, preparations of iron and pepsin may be 
given. When chronic catarrh is associated with cardiac disease, granules 
of digitaline, 1-50 of a grain each, may be given twice a day with advan- 
tage. When associated with pulmonary diseases, an out-of-door life in a 
suitable climate not infrequently effects a cure. In phthisical gastritis, a 
form that is very obstinate, hydrocyanic acid with the alkaline carbonates 
combined with bismuth is often of service. If hepatic disease exists, the 
portal congestion may be relieved by leeches about the anus and an 
occasional brisk mercurial purge ; a course of mineral waters will in a 
large proportion of cases give temporary relief. The daily use of cold- 
water enemata will in these cases preclude the necessity of resorting to 
cathartics. 

Scrofulous subjects should be treated with iodine and cod-liver oil. 
The Vichy waters in combination with colchicum are indicated in gouty 
patients. Free purgation and warm alkaline baths are also serviceable in 
this class of cases. There is, perhaps, no remedy which will for a time 
relieve the irritability, pain, and acidity after meals as certainly as bis- 
muth. When it fails in cases of long standing, zinc, alum, tannin, or 
nitrate of silver may be tried. The habitual constipation which often com- 
plicates these cases will be relieved by daily use of aloes and strychnia, or 
rhubarb and soda. When there is evident deficiency of gastric juice, five 
or six drops of hydrochloric acid in a wine-glass of water, and ten or fifteen 
grains of saccharated pepsin, will greatly assist the digestive process. If 
there is an excess of gastric juice, alkaline waters should be freely used 



I have found the following to allay this craving : 

fy Tr. cinchona comp 1 iv. 

Tr. capsici 3 s=s. 

Tr. nuc. vomicae 3 ij. 

M. A teaspoonful every two or three hours. 



PHLEGMONOUS GASTEITIS. 



265 



during, and after meals. When fermentation is very active, and flatulence 
is annoying, sulphite and salicylate of soda or creosote, given after meals, 
are serviceable. If the stomach rejects food as soon as it is taken, rest is 
essential, and the patient must be nourished for a time by the rectum and 
then placed on a milk diet. Minute doses of arsenic and of belladonna 
have been recommended as curative agents, but there is no evidence that 
they have any such power. Blisters, moxaa and issues over the stomach 
are sometimes of service in very chronic cases. 

PHLEGMONOUS GASTRITIS. 

Phlegmonous gastritis is a suppurative inflammation of the areolar (sub- 
mucous) tissue of the stomach ; it has also been called "suppurative 
lenitis." 

Morbid Anatomy. — The suppurative process may be circumscribed or 
diffused. On removal of the stomach its wall is found thicker than normal, 
And its substance cedematous and very friable. The submucous tissue is 
distended by, and infiltrated with fibrin and pus, which not infrequently 
accumulate in large quantities in the muscular tissue as well. The entire 
mucous coat is, in rare instances, yery much thinned and undermined by 
the purulent accumulation which perforates it at different points ; the 
email openings thus formed give exit to the pus from the spongy, irregular 
shaped cavities, or "abscesses/ 1 lying beneath. The raucous surface is 
/eddened in patches, or is of a deep purple color ; sometimes it is gangren- 
ous. If the peritoneal coat is involved it presents the usual appearance of 
acute peritonitis. The abscesses in the sub-mucous tissue tend to open 
into the cavity of the stomach, although they may perforate externally and 
be discharged into the peritoneal cavity. In circumscribed phlegmonous 
gastritis these pus cavities may be the starting-point of ulcers of the 
stomach. 

Etiology. — Phlegmonous gastritis is a very rare disease, usually occurring 
between the ages of twenty and forty years. It may occur idiopathically in 
previously healthy persons, without any assignable cause, or it may be 
secondary to pysemia, septicaemia, puerperal fever, typhus fever, and 
diphtheria. 

Symptoms. — Phlegmonous gastritis is ushered in by a distinct chill, fol- 
lowed or accompanied by intense pain and tenderness over the region of 
the stomach. Complete anorexia is an early symptom, and is accompanied 
by intense and constant thirst ; there is persistent vomiting, which increases 
in severity with the advance of the disease ; the ejected matters are some- 
times purulent, but usually consist of a dark colored, bitter fluid. The 
pain increases in severity until it becomes as severe as in peritonitis. The 
temperature may reach 104° or 106° F. When the disease has reached 
its climax there is great depression and exhaustion ; the patient is anxious 
and fretful, not infrequently passing into active delirium, but, whether 
the latter is present or not, typhoid symptoms with low muttering delirium, 
jaundice, stupor, and collapse are rapidly developed, and the patient passes 
into a state of coma and dies. 



266 



DISEASES OF THE DIGESTIVE SYSTEM. 



Differential Diagnosis. — The diagnosis of phlegmonous gastritis is only- 
made by exclusion ; it often passes unrecognized during life. 

Prognosis. — The prognosis is always unfavorable. The majority die dur- 
ing the first week. When it is circumscribed its duration may be pro- 
longed to two or three weeks. Its only complications are secondary 
abscesses in other organs (as the liver) and peritonitis. When primary, 
the disease reaches a fatal termination either from peritonitis or from 
exhaustion with typhoid symptoms. 

Treatment. — When phlegmonous gastritis is secondary the primary dis- 
ease will demand attention; in all cases the treatment is merely palliative ; 
stimulants are indicated very early, and the sufferings of the patient must 
be relieved by morphia hypodermically. 

GASTRIC DYSPEPSIA. 

Dyspepsia and indigestion are terms used to indicate a train of symp- 
toms caused by a functional derangement of the digestive processes. When 
these derangements are confined to the stomach they constitute gastric 
dyspepsia. 

Morbid Anatomy. — Strictly speaking, gastric dyspepsia has no morbid 
anatomy. If it has continued for a long time the walls of the stomach 
may be found thinned, the mucous membrane atrophied, and many of the 
gastric tubules shrunken and in a state of fatty degeneration. Not infre- 
quently the tubular structure of the stomach is replaced by a fibro-nucle- 
ated tissue. After death the power of self-digestion in such a stomach is 
markedly diminished or entirely lost. It is often met with as a part of 
senile decay. 

Etiology. — Dyspepsia is often an inherited condition and accompanies 
the changes of advancing age. There is no affection in which individual 
idiosyncrasies are so strongly marked. Its etiology can best be considered 
under the following heads : — 

First: — A class of cases in which there is a deficiency in the quantity of 
gastric juice secreted. Such deficiency often occurs in those disordered 
states of the blood which precede the onset of acute diseases. It occurs in 
enfeebled conditions, as the result of exhausting discharges, venereal 
excesses, masturbation, leucorrhcea and phthisis, and from the excessive 
use of narcotics, the tannin of tea, and the nicotine of tobacco. 

Second : — There is a class of cases in which there is an excess in the gas- 
tric secretion. This is most apt to occur in those suffering with chronic 
hepatic and cerebral diseases and in gouty subjects. It is sometimes 
changed in quality and in quantity in young persons who have grown 
rapidly, and in females at the menopause. 

Third: — There is a class of cases in which the gastric secretion is 
changed in quality. This occurs with ulcer and cancer of the stomach, 
gout, rheumatism, disease of the kidneys, uterus, and gall bladder. A 
lithic-acid diathesis is said to cause a change in the quality of the gas- 
tric juice. 



GASTRIC DYSPEPSIA. 



267 



Fourth : — There is a form of gastric dyspepsia due to impaired motion 
of the stomach, which may be the result of its adhesion to neighbor- 
ing parts, to an omental hernia dragging it out of its normal position, 
to cicatrices and new growths at its pyloric extremity, to thickening of its 
walls, or to a weak, flabby, enfeebled condition of its muscular coat, 
and to pressure on the stomach from tight lacing and from positions 
assumed by shoemakers, needlewomen, writers, etc. 

Fifth : — Mental emotion, prolonged mental labor, and anxiety rather 
than continuous and regular brain work, cause dyspepsia ; in such cases it 
is the sudden arrest of the digestive functions, especially after eating too 
much, which is the main etiological factor. Organic cerebral disease and 
pressure on, or disease of one or both pneumogastrics act in the same 
way. 

Sixth : — Deficient or excessive physical labor may be a cause of dyspepsia. 
"Walking immediately after a full meal, is a prolific cause of this variety, ex- 
amples of which are frequently met with in letter-carriers. 

Seventh : — Improper diet is a common cause of dyspepsia. It may arise from 
an excess of starchy materials, as potatoes ; or from deficiency of meats. Un- 
der improper diet may be included decomposing food, impure water, badly 
cooked food, too rapid eating, the food not being sufficiently masticated, or 
taken at too short intervals and irregularly. Articles of food that may be 
suited to one climate, season, or age may in another be wholly indigestible 
and cause dyspepsia. 

Symptoms. — The symptoms of dyspepsia are a series of phenomena which 
vary not only in different individuals, but in the same individual at differ- 
ent times ; the most constant is an abnormal appetite : it may be lost, in- 
creased, or perverted. There is a weight, dull pain, and a sense of burning 
in the epigastrium after ingestion of food, accompanied by flatulence, heart- 
burn, gastralgia, constipation or diarrhoea, a dull headache, languor, de- 
pression of spirits and irritability of temper. Indiscretion in eating or drink- 
ing, and exercise or exposure in dyspeptic subjects are apt to bring on an at- 
tack of sick headache. There is frequently a bitter taste in the mouth, 
bilious vomiting and sluggish bowels ; this is called a bilious attack. If 
these symptoms immediately follow the taking of food, it is called "inges- 
tive dyspepsia," or "morbid sensibility of the stomach.*' In some dyspep- 
tics the breath and faeces have a very offensive odor. 

Pyrosis, which is the chief symptom in another class of cases, is the 
regurgitation into the mouth of a large amount of thin, w r atery, saline fluid, 
preceded by a sense of constriction and pain in the epigastrium. This fluid 
consists mainly of saliva. Sometimes there is not only a feeling of oppres- 
sion in the thorax, but a severe pain is referred to the heart, accompanied 
by palpitation and dyspnoea. In such cases the patient is very apt to im- 
agine he has heart-disease. 

Accompanying some cases there is vertigo, ringing in the ears, spots 
before the eyes, and other sensations which together have been called 
"stomachic vertigo." These patients hear a buzzing sound and feel as if a 
vapor were enveloping them; they grow pale, and grasp for support through 



268 



DISEASES OF THE DIGESTIVE SYSTEM. 



fear of falling. When in any case the " indigestion " has lasted a long 
time, chronic gastric catarrh will almost always be developed, and evi- 
dences of mal-nutrition show themselves by anaemia, premature old age, 
corrugation of the nails, caries of the teeth, etc. At other times the patient 
will surfer from dyspnoea, with a short, dry cough, and occasional parox- 
ysms of an asthmatic character. The skin becomes sallow, dry, and rough, 
while various eruptions appear on it, and the abnormal contents of the 
urine show that the functions of the kidneys are disturbed. Often in long- 
standing dyspepsia in females there will be a feeble pulse, leucorrhoea, 
and irregularities in the menstrual functions. There is no characteristic 
change in the appearance of the tongue ; in one case it is white and heav- 
ily coated, in another it is clean, large, and indented. The urine often 
contains oxalate of lime (" oxaluria"). After the oxalates disappear, 
lithiates may appear for a time, soon to be followed by normal urine. 

Differential Diagnosis. — The phenomena of dyspepsia closely resemble those 
of chronic gastric catarrh. Repeated attacks of dyspepsia are apt to result 
in a sub-acute or chronic gastric catarrh. Their differential diagnosis has 
already been considered. Acidity from hypersecretion may be confounded 
with acidity from fermentation, and stomachal may be confounded with 
cerebral vertigo. 

The following are the principal points in their differential diagnosis : 
pain in acidity from hypersecretion either immediately follows the taking 
of food, and is accompanied by " heartburn, " or, quite as often, it is felt 
most when the stomach is empty, and is relieved by taking food ; but the 
pain from fermentation, due to obstruction to movements of, or to chronic 
inflammatory processes in, the stomach, comes on some time after eating, 
and is more a sense of weight or fulness in the epigastrium than pain. It 
is never present during the intervals between taking food. Vomiting is 
rare in acidity from fermentation, but if it does occur, the ejected materi- 
als will contain organic acids, torulae, and sarcinse ; while with hypersecre- 
tion vomiting is a common symptom, and very frequently there is an 
excess of hydrochloric acid in the matter vomited. The constitutional 
symptoms, mental depression and emaciation, the sallow skin, etc., are 
much more marked in dyspepsia with fermentation than in dyspepsia with 
hypersecretion. In case of acid stomach from fermentation, flatulence is 
very common, while it rarely occurs with acidity from hypersecretion. 
The urine is alkaline or neutral in acidity from fermentation, while it is 
always acid with hypersecretion. Lastly, acidity from fermentation has a 
history of some cause or causes which interfere with digestion, while hyper- 
secretion is usually a reflex symptom, or occurs with ulcer of the stomach, 
or in perfectly healthy persons. 

With vertigo or dizziness from stomachal causes, there is a history of indi- 
gestion, and it usually occurs in middle life, while in cerebral vertigo the 
individual is beyond middle life, and there will be no history of difficult or 
impaired digestion. Vertigo from stomachal causes occurs during an attack 
of indigestion, or after some particular kind of food has been taken. Cere- 
bral vertigo occurs wholly independent of the state of the stomach. Con- 



CANCER OF THE STOMACH. 



269 



sciousness is never lost, nor are the special senses — sight alone excepted — 
involved in stomachal vertigo, while ringing in the ears, temporary deaf- 
ness, and often complete loss of consciousness occur in an attack of cerebral 
vertigo. A person suffering with stomach vertigo knotus that the apparent 
motion of the surrounding objects is unreal — while a patient with cerebral 
vertigo believes the apparent movement of the objects to be real. 

Prognosis. — The prognosis varies with the etiology. Dyspepsia in most 
cases can be cured, but the cure depends for the most part on the will of 
the patient. The only danger is that the conditions induced by dyspepsia 
may predispose to organic diseases in other organs, as the lungs or kidneys, 
and that it may lead to a condition of melancholia. 

Treatment. — First, if possible, remove the cause. When the gastric juice 
is deficient in quantity, hydrochloric acid and pepsin are indicated. In 
these cases, also, the vegetable bitters are especially beneficial ; indeed, in 
most cases of dyspepsia they are valuable adjuvants to the other remedies. 
Tea and tobacco are always to be avoided ; alcoholic stimulants in moder- 
ate quantities may sometimes be combined with the vegetable bitters with 
advantage. When acid risings occur after ingestion of food, and are 
due to active fermentation, the sulphite of soda or salicylic acid imme- 
diately after meals may prevent such changes. When fermentation is 
present, these remedies, with alkalies, will relieve the heartburn and other 
gastric distress. A course of saline waters will be found, in such instances, 
to aid the other remedies. 

When there is great irritability of the stomach, bismuth acts almost as a 
specific, and should be given in twenty-grain doses before eating. Creosote, 
codeia, oxalate of cerium, and morphia may be employed to arrest vomit- 
ing. If there is pain in the epigastrium, the local application of heat by 
means of the hot- water bag will relieve. Dyspeptics should never wear 
corsets or belts about the abdomen ; they should retire and rise early, and 
eat slowly, masticating their food thoroughly. The meals should be small 
and taken at stated intervals. The diet must be determined for each case. 
Most patients do best on a diet free from hydrocarbons, but many cases of 
a lithaemic diathesis must be deprived of meats. No mental or physical 
work should be performed directly after or before eating. Horseback- 
riding and walking in the open air should be insisted upon. A change of 
scene and climate works rapid cures in many instances. Dyspeptics should 
take plenty of rest, have their sleeping-rooms well ventilated, and take a 
cold sponge-bath morning and evening. The general principles of treat- 
ment in gastric dyspepsia are similar to those given in chronic gastric 
catarrh. 

CANCER OF THE STOMACH. 

The stomach, next to the liver, is the most frequent seat of internal 
cancerous developments ; one thirl of all the cases of primary cancer have 
their seat in the stomach. The varieties of cancer of the stomach, in the 
order of their frequency, are as follows : 

First, scirrhus; second, medullary ; third, epithelial. Any one may 



270 



DISEASES OF THE DIGESTIVE SYSTEM. 



undergo colloid degeneration, and thus may appear as either villous or 
melanotic cancer. 

Morbid Anatomy. — Cancer has its seat at the pyloric extremity of the 
stomach in about three fifths of the cases. The next favorite seat is the 
cardia and the lesser curvature. When it is developed at the pylorus, it 
sometimes extends an inch or two into the duodenum ; cancer at the 
cardia usually involves the lower part of the sesophagus. 

Scirrhus of the stomach first appears as a small, grayish -white, opaque 
nodule in the submucous tissue, the normal structures of which aro en- 
closed by the new growth. These nodules are developed from off-shoots 
of the gastric tubules which have pushed their way through the mucous 
membrane into the loose submucous tissue. The primary change is thus 
epithelial in character. 1 The fibrous stroma is far in excess of the cell- 
element ; it develops rapidly at the exterior of the mass, causing indura- 
tion and contraction 
of the surrounding 
structures. The mass 
sometimes extends 
iuward toward the 
cavity of the stomach, 
causing flattened tu- 
mors which project 
into it. The contrac- 
tion of these nodules 
puckers the mucous 
surface, which be- 
comes immovably 
fixed upon them, and 
fibrous lines radiat- 
ing from the growth 
penetrate the mucous 
membrane, which 
first undergoes a 
slight increase in 
thickness, and then becomes pale from compression of its vessels. The 
solitary glands are enlarged, and the gastric tubules are matted together 
in an indistinguishable bundle. A dark slough sometimes forms upon its 
surface and exposes the cancerous growth, which then ulcerates. The 
ulceration may extend so deeply as to destroy the new growth and invade 
the wall of the stomach underneath it, causing irregular cavities, bounded 
by a raised and indurated band of connective-tissue, and sometimes open- 
ing into the stomach. These polypoid tumors are sometimes as large as a 
hen's egg aud develop upon the cancerous mass. The glands and villi are 
the longest to resist this encroachment of the cancerous development, the 
first change in them being an increase in the number of their epithelial 
cells. After a time the muscular coat becomes fused with the areolar, 




Fig. 57. 

Cancer of the Pyloric Extremity of the Stomach. 

A. Mucous membrane of the stomach beyond the seat of the cancerous in 

filtration. 

B. Pylorus. 

C. Commencement of the Duodenum. 

Z>, D. Vertical section of the cancerous mass. 

E % E. Internal surface of the cancerous infiltration encroaching on the py- 
loric orifice. 

F. Small opening in the cancerous growth at the pyloric extremity. 



J Waldeyer. 



CANCEK OF THE STOMACH. 



271 



so that at the seat of the neoplasm they cannot be distinguished from each 
other on section of the mass. At other times the parts affected arc hard 
and fibrous, the stomach walls being so thickened that the disease is only dif- 
ferentiated from hypertrophy of its coats, by the glistening, pearly look 
and cartilaginous texture of the mass. After involving the muscular coat, 
the growth may involve the peritoneal covering ; local peritonitis estab- 
lishes adhesions between it and the diaphragm, liver, pancreas, and spleen. 

The lesions which follow the development of scirrhus in the stomach 
are as follows : 

Dilatation of the stomach is a frequent result of the obstruction at the 
pylorus caused by the cancerous development. Less common than dilata- 
tion of the stomach is the gizzard appearance caused by the same contrac- 
tion that shrivelled the mucous membrane, inducing a shrinking of the 
whole stomach wall, which sometimes becomes an inch thick, the carclia 
and pylorus not infrequently being closely approximated, and the anterior 
and posterior stomach walls being almost in juxtaposition. 

Chronic gastritis is developed when the new growth attains sufficient 
size to cause pressure, and in such cases the mucous membrane presents 
the characteristic appearances of that affection. 

Perforation of the stomach sometimes occurs, causing a fatal peritoni- 
tis ; a secondary opening may penetrate into the duodenum, liver, jejunum, 
or ileum, or through the anterior wall of the abdomen, and thus form an 
external opening. In rare instances openings are made into the pleural 
cavity, lungs, bronchi, or pericardium. Large branches of the pneumo- 
gastric may be destroyed by the new growths. In five per cent, of the cases 
of cancer of the stomach, secondary cancer is developed in other organs. 
The organ which is the most frequent seat of this secondary development 
is the liver, and after the liver the lymphatic glands in the immediate 
vicinity of the peritoneum, and various segments of the intestine, espe- 
cially the rectum. The kidneys, bladder, sjrieen, pancreas, and ovaries may 
also be the seat of these secondary developments. The position of the 
stomach is sometimes changed, the weight of the tumor dragging it into 
the lower portion of the abdomen, and there it may be bound to the intes- 
tines, bladder, uterus or ovaries by firm adhesions. 

Medullary or acute cancer of the stomach commences in the same tis- 
sues as scirrhus, in the form of nodules much softer than those of scirrhus. 

On section, cancer-juice can be readily expressed from the cut surface 
of the cancerous mass ; the proportion of the stroma being much less, and 
the cells more abundant. The growth is more vascular, and not infre- 
quently contains small blood extravasations. It is much more rapid in its 
development than scirrhus, and while proliferation of the epithelial struc- 
ture occurs at the periphery, fatty degeneration breaks down the centre, 
and it sometimes becomes diffluent. The mucous tissue is rapidly invaded. 
Large, spongy, " fleshy " excrescences project into the cavity of the stomach. 
Around the growth, which varies in size from that of a pigeon's egg to that 
of an orange, is a ring of tissue infiltrated with cancer, beyond which the 
solitary glands are enlarged, and the stomach follicles degenerated. ". Vil- 



272 



DISEASES OF THE DIGESTIVE SYSTEM. 



lous " cancer of the stomacli is a modification or variety of medullary can- 
cer. If medullary cancer ulcerates, the slough is thrown off, and an ex- 
cavated ulcer is exposed, surrounded by an elevated rim, from which pro- 
jects the cauliflower-like growth, very friable and vascular. The surface 
exposed by such ulceration is often very large, even six or seven inches in 
diameter. Epithelial cancer is rare in the stomach. When present, it pre- 
sents the same characteristics as when developed on other mucous surfaces. 

Colloid or alveolar cancer has the same structure as colloid cancer occur- 
ring in other parts of the body. It appears oftener in the stomach than 
elsewhere, but even here it is rare. There are different opinions as to its 
starting-point ; some state that it begins in the subserous, others in the 
submucous tissue. Recently a glandular origin has been ascribed to it, 
similar to epithelioma of the skin. Wherever commencing, it rarely ap- 
pears as nodules, but commonly as an irregular mass of "gum-like" glis- 
tening material, contained in large and distinctly marked alveoli, in which 
are embedded polygonal nucleated cells. The walls of the stomach, the 
seat of colloid degeneration, are very much thicker than normal. Its ten- 
dency is to spread rapidly over a large surface. The contents of some of 
the alveoli are discharged into the stomach, thus giving to its inner sur- 
face an irregular, " honey-comb " appearance. 

Etiology. — Cancer of the stomach occurs most frequently between the 
ages of forty-five and sixty-five. It is more frequent in males than females. 

Hereditary predisposition is undoubtedly its most important etiological 
factor. Beyond this its etiology is obscure. 

Symptoms. — The earliest and most prominent symptom of cancer of the 
stomach is anorexia, accompanied by a sense of uneasiness or distention in 
the epigastrium, with nausea and vomiting. Pyrosis is often present quite 
early. Patients describe the pain as dull, gnawing, or as a tightness or 
"soreness" over the stomach; after a time it becomes lancinating, fixed, 
and constant ; the locality of the pain does not correspond to the seat of 
the cancer ; when the growth has its seat in the lesser curvature, the pain 
is referred to the interscapular region ; it is not usually increased by inges- 
tion of food, and if it is, it does not cease at the end of the digestive pro- 
cess ; it may become constant and severe. These symptoms usually exist 
before the appearance of a tumor. During the period of its growth, vomit- 
ing becomes frequent. There are three prominent causes of the vomiting : 
first, from obstruction. Vomiting from this cause comes on comparatively 
late ; when the obstruction is at the carclia it occurs immediately after 
eating. If it is situated at or about the pylorus, the food is retained for 
one or two hours. Secondly, from irritation. This occurs independent 
of taking food and the time of its digestion. Thirdly, from fermentation. 
This occurs after a large accumulation of food in the stomach ; and the 
matters vomited are dark and yeasty, not infrequently containing sarcince 
ventricnli. When free hydrochloric acid is persistently present in the 
gastric contents, cancerous obstruction may be quite certainly excluded. 
When this acid is persistently absent, the probabilities are in favor of can- 
cerous disease being present ; but no absolute deductions can be made. 



CANCER OF THE STOMACH. 



273 



Hiccough, flatulence, and constipation are often very annoying, some- 
times very distressing symptoms ; and emaciation, debility, and the hag- 
gard " cancer countenance," are often present. There is mental depres- 
sion, anxiety, and the patient is morose or apathetic. 

When ulceration of the free surface of the cancerous mass occurs, the most 
constant symptom is hemorrhage. This may be copious and bright red in 
color, but usually the blood is so altered by the gastric juice, and so mixed 
with food, that it is rusty, brown, or blackish in color ("coffee-ground" 
vomit). In the later and larger hemorrhages, the blood may in part es- 
cape by the bowels, and then diarrhoea occurs, caused by the decomposing 
blood ; the stools have a dark tarry appearance, with a very offensive odor 
(" melsena"). The yellowish green color of the skin, usually present, 
may change to a jaundiced hue, due to pressure of the cancerous mass 
upon the bile ducts. 

One may be deceived or puzzled, during the course of cancer of the stom- 
ach, by a remission of the anorexia, pain, hemorrhage, and vomiting, so 
that improvement seems to be taking place, and the patient believes he 
is recovering ; but in a short time all these symptoms will return with 
increased severity, and the disease will progress more rapidly than before. 

Again, there is sometimes a febrile reaction — not a definite hectic, but a 
symptomatic fever — which appears irregularly during the progress of the 
cancer, and often misleads on account of the belief that the temperature 
in malignant disease is normal or sub-normal. During the advanced stage 
in many cases the tongue becomes covered with aphthae, typhoid symptoms 
develop, and death is often preceded by delirium and coma. The urine is 
scanty, high colored, and of a high specific gravity. It is loaded with urates, 
and deposits a pink sediment regarded by some as a diagnostic symptom. 

Physical Signs. — By palpation a tumor may be discovered — sometimes 
large, hard, irregular, and nodulated ; sometimes small, deep-seated, and 
elastic. In the former case it is easy, in the latter very difficult of recog- 
nition. If the cancer is situated at the cardiac extremity of the stomach, 
no tumor will be felt. The tumor is usually movable, except when adhe- 
sions have formed between it and the adjacent tissues. If the cancer is at 
the pyloric extremity of the stomach, the tumor is usually situated in the 
median line ; it may, however, be felt at the lower part of the epigastric 
region, in the right hypochondrium, at or just above the line of the 
umbilicus, or it may be far over on the left side. It may receive and 
transmit the impulse of the aorta, that is, become a pulsating tumor. The 
epigastric region is prominent, hard, resisting, and tender. It is impor- 
tant, during the examination, to have the patient distend his stomach by 
drinking one or two tumblers of carbonated water. • 

Percussion over the tumor elicits circumscribed dulness with a tympa- 
nitic or a peculiar hollow quality ; light percussion may give absolute 
flatness, when forcible percussion gives a tympanitic resonance. 

Auscidtation gives negative results. 

Differential Diagnosis. — Cancer of the stomach may be mistaken for gas- 
tric ulcer, abdominal aneurism, cancer of the pancreas, cancer of the left 
18 



274 



DISEASES OF THE DIGESTIVE SYSTEM. 



lobe of the liver, and for chronic gastric catarrh with hcematemesis ; the two 
latter are considered under those heads. It is hardly possible, after a care- 
ful study of a case, to mistake cancer of the stomach for gastric dyspepsia, 
or to confound a cancerous tumor at the pylorus with an ovarian tumor. 

Ulcer of the stomach occurs most in young adults, especially females, 
while cancer is seldom met with in persons under forty. In cancer there 
is usually a history of hereditary cancer ; while ulcer of the stomach is 
usually associated with anaemia, chlorosis, prolonged lactation, or pro- 
longed compression of the stomach, as in the case of shoemakers and sew- 
ing-girls. The pain in cancer is continuous, and described as lancinating ; 
while in ulcer the pain is intermittent, greatly increased by taking food, 
often referred to the lower dorsal vertebras, and described as "gnawing" 
or burning. Hcematemesis, in cancer, has a sooty or "coffee-ground" 
appearance, is small in amount, and appears late in the disease ; while in 
ulcer it is bright red arterial blood, is profuse, and appears as an early 
symptom. Vomiting in cancer does not relieve the pain, is not very severe, 
and comes on late ; but in ulcer it is severe, comes on early, and affords 
temporary relief from the pain. The cancerous cachexia and debility are 
present early and steadily progress in cancer ; while in ulcer there may be 
pallor, but no characteristic cachexia. The presence of an epigastric tumor 
establishes the diagnosis of cancer. 

An aneurismal tumor is smooth and ovoid ; a cancerous tumor is hard 
and irregular. An expansive, dilating impulse is given to the hand on 
palpating an aneurismal tumor ; but in cancer this impulse is lifting in char- 
acter. In aneurism there is constant pain in the back corresponding to the 
position of the tumor, which is absent in cancer. There is a change in the 
femoral pulse in aneurism, which is not present in cancer. The gastric symp- 
toms, the cachexia, and the debility of cancer are not present in aneurism. 

In cancer of the pancreas, vomiting is less frequent, and when present is 
not coffee-ground, and the vomited matters contain free hydrochloric acid. 
There is no dilatation of the stomach, constipation is less severe, and the 
passages often contain fat. Jaundice is more frequent from implication 
of, or pressure on, the hepatic duct. 

The tumor in pancreatic cancer is always high up and fixed ; in gastric 
cancer it may be low in the abdomen or freely movable. 

Glycosuria is occasionally present with pancreatic cancer, and not with 
gastric cancer. 

Prognosis. — The prognosis in cancer is always unfavorable. Its shortest 
duration is seven weeks, and its longest three and one-half years, the aver- 
age duration being one year. Early vomiting, with haamatemesis, great 
and sudden emaciation, and complete anorexia, are especially unfavorable 
symptoms. The important complications of cancer of the stomach are the 
development of secondary cancer in other organs, peritonitis, — independent 
of or with perforation, — pleurisy and pneumonia, pericarditis, endocardi- 
tis and fatty heart, tuberculosis, coagula in the sinuses of the dura mater, 
phlegmasia dolens, non-cancerous ulcerations in the rectum and colon, 
ascites, and general anasarca. Death may occur from hemorrhage, peritoni- 
tis, exhaustion, marasmus, and from complications. 



ULCER OF THE STOMACH. 



275 



Treatment. — The treatment is altogether palliative. The indications are 
to make the patient comfortable by relieving pain and vomiting. The diet 
may be determined by the experience of each patient. In the majority of 
cases alcoholic stimulants in moderation are beneficial. When the pain be- 
comes severe, morphia may be administered hypodermically. If at any 
time the stomach becomes overloaded, its contents may be carefully re- 
moved by means of a stomach pump. The constipation, which is often ob- 
stinate, is best overcome by aloes ; the flatulence and painful eructations by 
sulphite of soda or oil of cajeput. During the whole course of cancer, 
subnitrate of bismuth may be administered, its combination with soda, 
conium, and stramonium being highly recommended by English physicians. 
Some assert that arsenic is effective in retarding the cancerous growth, and 
that its administration with iodine and carbolic acid may arrest its devel- 
opment. My experience does not confirm this statement. If the stomach 
entirely rejects food, rectal alimentation may be resorted to. 



ULCER OF THE STOMACH. 

Statistics show that gastric ulcers, or cicatrices caused by ulcers, are found 
in three out of every hundred cases of diseases of the stomach. They may 
be classed as follows : 

I. Superficial Ulcer, or Hemorrhagic V. The Typhoid Ulcer, 

Erosion. VI. The Variolous Ulcer. 

II. Follicular Ulcer. Vli. The Diphtheritic Ulcer. 

III. The Chronic, Round, ov Per for a- VIII. 'The Syphilitic Ulcer. 

ting Ulcer. IX. The Tubercular Ulcer. 

IV. The Typhus Ulcer. X. The Cancerous Ulcer. 

The first two have already been considered. 

The specific ulcers which receive their names from the diseases in which 
they occur as occasional pathological lesions, will be considered in connec- 
tion with the history of those diseases. 

The chronic, round, perforating ulcer is by far the most frequent form 
of gastric nicer, and is the one indicated when the unqualified term, ulcer 
of the stomach, is used. 

Morbid Anatomy. — Chronic perforating nlcers most frequently occupy 
the posterior wall of the stomach near its pyloric extremity. They vary 
in size from half an inch to two or three inches in diameter ; an ulcer 
one-half inch in diameter may exhibit all the clinical characteristics of 
one of large size. These ulcers are at first circular or elliptical in form ; 
occasionally they become irregular when two or more are fused together. 
When oblong they have their axis either parallel with, or transverse to 
the axis of the stomach ; sometimes they form a zone about the pyloric 
end of the stomach. The large ulcers are formed by the fusion of several 
small ones. They begin in the mucous membrane of the stomach ; their 
boundary is nearly vertical, smooth and sharp, so that now and then at a 



276 



DISEASES OF THE DIGESTIVE SYSTEM. 




Fig. 58. 

Perforating Ulcer of the Stomach, 

A- Mucous surface. 

i>\ Perforation, tvi/h clean cut edges, 
tirely through the gastric walls. 



post-mortem the mucous membrane will present an appearance as if a cir~ 
cular piece had been "punched out" with a sharp instrument. There is 

no evidence of an inflammatory process. 
The loss of substance may involve only the 
mucous layer, or it may extend to the sub- 
mucous tissue, or penetrate deeper and in- 
volve the muscular and peritoneal coats ; 
as it extends, smaller and less regular cir- 
cles are formed, gradually diminishing in 
diameter, a small opening in the muscular 
coat, or a mere point upon the peritoneum, 
being the apex of the conical or "funnel- 
shaped" excavation. As the ulcer spreads 
transversely in the course of the vessels, this 
" step-like/' bevelled appearance becomes 
more and more marked. The tissues around 
the ulcer are sometimes normal, especially 
when the mucous membrane alone is in- 
volved ; at other times the mucous layer encircling the base of the ulcer is 
thickened and indurated. The mucous membrane in the vicinity of an 
ulcer is sometimes the seat of a circumscribed chronic catarrh ; but more 
often chronic catarrh involves the whole gastric mucous membrane. 

The variations from these usual pathological appearances consist, first, in a 
mass of black blood adhering to the base of the alcer ; secondly, in petechial 
extravasations around the injected margin of the ulcer ; thirdly, in the villous 
or "polypoid" vegetations springing up from the mucous membrane sur- 
rounding the base of the ulcer ; and fourthly, in suppuration in the coats of 
the stomach with subsequent suppurative pylephlebitis. The progressive in- 
crease in the depth of the ulcer, which is part of its natural history, would 
always lead to perforation and discharge of the contents of the stomach into 
the peritoneal cavity, were it not for the establishment of a local peritonitis 
which causes the corresponding portion of the stomach to become adherent 
to the adjacent parts. These adhesions may join it to the pancreas, liver, me* 
sentery or spleen. 

The number of ulcers which may be found in a stomach varies from one 
to six ; as a rule there is but one. Gastric ulcers, if not large or deep, 
may heal without producing deformity of the stomach. If they are large 
or deep, the resulting cicatrix, by its contraction, causes deformity of the 
stomach. When the mucous and submucous tissues are alone involved, 
the loss of substance is replaced by new connective-tissue, which does not 
contract ; the resulting cicatrix is merely a white spot, with little or no 
puckering. The usual process of repair in deep ulcers is that of a local in- 
flammation with lymph exudation. The connective-tissue formed at the 
base and around the ulcer contracts, and there remains a central, hard 
mass from which radiate bands of connective-tissue into the adjacent 
mucous membrane. The contraction of this cicatricial tissue may cause a 
stricture at the pylorus, or, if the ulcer extends around the central portion 



ULCER OF THE STOMACH. 



27? 



of the stomach, may give it an " hour-glass " shape. When there is steno- 
sis at the pyloric orifice, the stomach is dilated and the walls are thickened 
in one subject and thinned in another. 

Ulcers may extend by degeneration of the newly-formed tissue. "With 
the extension of the ulcers, some of the larger vessels (as the superior py- 
loric) may become involved, and extensive hemorrhage result; usually, a 
"protective thrombosis " prevents this accident. Hemorrhages, the result 
of intense passive hyperemia, or of erosion of small vessels, are of little con- 
sequence compared with those which result from the opening of vessels of 
large size or of the organs with which the stomach becomes adherent. In 
this way the portal vein, and the splenic, pancreatic and hepatic arteries 
have been pierced. Perforation of the stomach in gastric ulcer occurs 
only in about one-eighth of all the cases. Though the posterior surface 
of the stomach is the more frequent seat of these ulcers, the liability to 
perforation is greatest when the ulcers are situated in its anterior wall. 
If perforation and escape of the contents of the stomach take place into 
the peritoneal cavity a general, rapidly fatal peritonitis immediately fol- 
lows ; when adhesions prevent the contents of the stomach from escaping 
into the peritoneal cavity, a local peritonitis is developed and an abscess 
may be formed in the neighborhood of the ulcer, which abscess may com- 
municate with the pleural cavity, duodenum, colon, or gall-bladder. 1 

Etiology. — Ulcer of the stomach occurs in females oftener than in males, 
the proportion being more than two to one. The liability to it is greatest 
between the ages of fourteen and thirty, although no age is exempt ; it has 
been found in the new-born babe and in the octogenarian. Anaemia an(f 
chlorosis are the two great predisposing causes. Chronic and phlegmonous 
gastritis, cirrhosis of the liver, and obstruction of the gall-ducts may lead 
to ulcer of the stomach by inducing obstruction in the vessels of the walls 
of the stomach. Ulcer may result from an habitual stooping position, as in 
milliners, seamstresses, and shoemakers, or may come from the constant 
striking of the shuttle of the weaver against the epigastrium. Miliary 
aneurisms in the gastric walls may cause gastric ulcers. Such ulcers are 
most frequently met ivith in connection with a cirrhotic kidney. It may 
occur without any recognized cause. 

Symptoms. — The symptoms of gastric ulcer are sometimes obscure, at 
others well marked. 

Pain is one of its constant symptoms : at first it is dull and heavy ; 
then it becomes burning and gnawing, causing a sickening sensation quite 
distinct from nausea. It usually comes on soon after the ingestion of 
food, and lasts during the entire period of stomach digestion ; occasionally 
it is not present until an hour or so after eating. It is circumscribed to a 

1 Many theories have been advanced in regard to the pathogenesis of gastric ulcers ; the following are 
the principal ones : perforating ulcers may be the result of an inflammatory process, a sequel, oftentimes, 
of chronic gastritis. Rokitansky attributes them to congestion, extravasation, and subsequent necrosis of 
the tissue. Virchow maintains that embolism or a venous stasis deprives a portion of the stomach of its 
vascular supply, and that the stomach-tissue thus deprived of its nutrition, is acted upon by the gastric 
juice as dead tissue ; as a result, there is a loss of substance and the formation of ulcers. He compares the 
funnel or cone-shaped appearance of the ulcer to embolic infarctions elsewhere, the capillaries always ram- 
ifying outwards from the main trunk. 



278 



DISEASES OF THE DIGESTIVE SYSTEM. 



spot rarely larger than a silver dollar, is accompanied by tenderness on 
deep pressure, and its intensity is usually greatest just above the umbili- 
cus. The "dorsal" pain of gastric ulcer was first recognized by Cruveil- 
hier. It comes on some weeks or months after the pain in the epigas- 
trium ; it is located at the eighth or ninth dorsal vertebra, and is constant, 
although it may sometimes alternate with the epigastric pain. In a few 
cases the pain is paroxysmal ; there are intervals of freedom from pain, fol- 
lowed by severe attacks, resembling those of neuralgia. Eelief from the 
pain of gastric ulcer is frequently obtained by a recumbent posture ; this 
happens when the ulcer has its seat on the anterior wall of the stomach. 

Nausea, vomiting or regurgitation of food may accompany the pain ; 
in some instances there is pyrosis, or " water brash ; v usually the vomit- 
ing occurs when the pain is most severe. The matter vomited consists, 
first, of the food taken into the stomach, which has a strong acid re- 
action ; later it is mingled with bile. The vomiting temporarily relieves 
the pain. After a time these dyspeptic symptoms are complicated by 
haematemesis, which may be regarded as essential to its diagnosis. In a 
few cases there is no vomiting. Some will vomit several times in the 
twenty-four hours, others once a day, and others every two or three days. 
As small bleedings do not cause vomiting, and as attention is rarely 
paid to the stools at this period, the exact date of the first hemorrhage 
is usually unknown. The symptoms which attend the haematemesis are 
a sense of unusual fulness in the stomach, accompanied by a feeling of 
faintness ; the face is blanched, nausea exists for a varying period, and this 
is followed by vomiting of partially coagulated blood, which is so bright 
as to leave no doubt of its arterial origin. In rare instances the first hem- 
orrhage causes distention of the stomach, syncope and painless collapse, 
followed by death. Sometimes the blood vomited has a dark, grumous 
appearance, looking like coffee-grounds. In young females the hemor- 
rhage is usually preceded by a diminution or stoppage of the menses. 

Preceding and accompanying the haematemesis there are usually dyspeptic 
symptoms similar to those of gastric dyspepsia. Cachexia is a late symp- 
tom, the appetite is rarely impaired, sometimes it is even increased ; great 
debility and extreme anaemia result from the recurring hemorrhages. The 
face assumes an earthy pallor ; when the pain is intense it is " drawn " 
and haggard, which by some is regarded as characteristic of ulcer of the 
stomach. Perforation of the stomach is attended by the symptoms of 
rapidly developed and extensive peritonitis. Pain in the right shoulder is 
a prominent symptom if an ulcer of the stomach involves the under sur- 
face of the liver. If cicatrization of a gastric ulcer takes place without 
adhesions or stricture all the above symptoms remit and complete recovery 
follows ; if adhesions or stricture remain dyspepsia and cardialgia may con- 
tinue for the remainder of the patient's life. Obstinate constipation is the 
rule in ulcer of the stomach, but hemorrhage may cause diarrhoea. 
The blood gives to the dejections a dark color and a "tarry" consist- 
ence, a condition called " melaena." The only physical sign of gastric 
ulcer is extreme tenderness on firm pressure over the epigastric and 
dorsal regions. 



TJLCEE OF THE STOMACH. 



279 



Differential Diagnosis. — The diagnosis in a typical case of ulcer of the 
stomach is not difficult ; in the more obscure cases it may be mistaken 
for cancer of the stomach, hepatic colic, the second stage of cirrhosis, 
cardialgia, and chronic gastric catarrh with hwmatemesis. The diag- 
nosis of cancer of the stomach, hepatic colic, and the second stage of 
cirrhosis are considered under these headings (q. v.). 

In neuroses causing cardialgia, there will be a history of neuralgia in 
other parts of the body or a well-marked history of hysteria. The 
pain of cardialgia is not excited or increased by the introduction of 
food into the stomach, but often comes on when the stomach is empty ; 
while in ulcer the pain is associated with ingestion of food. In cardialgia 
pressure over the epigastrium and the ingestion of food relieve the 
pain ; the reverse is the case in ulcer. Again, cardialgia is relieved by 
the constant current and Faradization, which increase rather than 
relieve the pain of gastric ulcer. Dyspeptic and gastric disturbances 
are constantly present in ulcer ; while these are absent in the intervals 
between the paroxysms of neurotic cardialgia. Hsematemesis never occurs 
in cardialgia. 

In chronic gastritis with hemorrhage there is the history of disease 
of the liver, heart, lungs or kidneys ; while in gastric ulcer there is 
usually no such history. The pain in gastritis is not so intense or 
of the same character as in ulcer of the stomach. A coated tongue, 
great thirst, malaise, and pyrexia are prominent in cases of chronic 
gastritis, and absent in ulcer. The vomiting in chronic gastritis comes 
on in the morning, and the matter vomited is stringy mucus, some- 
times streaked with blood ; while in ulcer the attacks of vomiting usually 
follow the taking of fluids or solids, and the blood is vomited in consider- 
able quantities. 

Prognosis. — More than one half of the cases of ulcer of the stomach re- 
cover. The average duration cannot be determined. Some terminate 
fatally in a few weeks, others continue for a long period. In the protracted 
cases, the symptoms are probably due to the existence of more than one 
ulcer. Most of the cases that recover continue for more than a year. The 
prognosis is bad where ulcer occurs in the aged and in feeble women. 

The complications of gastric ulcer are chlorosis and hysteria ; thoracic 
complications, such as pneumonia, bronchitis, pulmonary tubercle, acute 
pleurisy, and empyema ; abdominal, such as suppurative pylephlebitis. and 
peritonitis. Death occurs from hemorrhage four times as often in the 
male as in the female. Exhaustion, either from pain or from vomiting 
or from starvation, causes death in 5 per cent, of the cases. Perforation, 
with peritonitis or without it, occurs in about 13 per cent, of all the cases. 
The liability to perforation is greatest in the female between the ages of 
fifteen and thirty ; while in the male the liability is greatest about the 
fortieth year. Cicatrization of an ulcer at the pyloric extremity of the 
stomach is usually followed by dilatation of the stomach. When the cicatrix 
surrounds the pylorus and the obstruction is extreme, persistent vomiting 
and all the evidences of inanition may simulate cancerous obstruction. 



280 



DISEASES OF THE DIGESTIVE SYSTEM. 



Treatment. — The most important thing to be accomplished in the treat- 
ment of gastric nicer is to give rest to the stomach. To this end the patient 
must be kept in bed, and the diet restricted to peptonized milk. From a 
tablespoonful to a teacupfnl may be given at intervals of two honrs during 
the day and night. This makes it possible to keep the gastric contents per- 
sistently alkaline, and thusavoid the possibly destructive action of excessively 
acid gastric juice. When milk is refused, digested beef -juice maybe given 
in its stead ; all vegetables, tea, coffee, starchy food and fruits must be pro- 
hibited. If all kinds of food are rejected, rectal alimentation must be prac- 
tised, four ounces of defibrinized blood (containing four grains of chloral to 
prevent its decomposition) may be thrown into the rectum every six hours. 

The remedial agents which have been found most useful in gastric 
ulcers are the sub-nitrate of bismuth, in twenty-grain doses, four times 
a day, sulphite of soda, oxalate of cerium, and hydrocyanic acid. 
Half a grain of nitrate of silver, three times a day, seems to exert a bene- 
ficial effect on gastric ulcers of long standing, as well as on the accompany- 
ing gastric catarrh. Several observers claim that arsenic retards the spread 
of gastric ulcers ; my experience does not confirm this observation. If the 
pain is severe, and there is no hemorrhage, warm poultices may be applied 
to the epigastrium ; but morphia hypodermically is far more reliable for 
the relief of pain, and may be used at regular intervals with benefit. Hypo- 
dermic injections of ergotin, and ice-bags to the epigastrium, will usually 
check the hemorrhages. The flatulence, which is often very distress- 
ing, may be mitigated by sulphite of soda, carbolic acid, or the alka- 
lies. Constipation when present is relieved by ox-gall enemata, or saline 
mineral waters, the latter being especially useful when there are acid eruc- 
tations. When the patient will bear it, castor-oil is a safe and efficient 
laxative. Stimulants must never be given by the stomach. They may be 
given by enemata in emergencies. 

Rest in bed and a restricted diet should be enforced for at least three 
months. Then, if the symptoms indicate that cicatrization is well es- 
tablished, maccaroni, potatoes, stale bread and cocoa may be allowed ; still 
later oysters, soft eggs, and sago. The patient must not return to an 
ordinary mixed diet for at least six months. The anaemia which follows 
gastric ulcer must be overcome by fresh air, moderate exercise, iron, and 
quinine. It must be remembered that the higher the nutrition is carried, 
the more rapid and complete will be the repair of the ulcer. This end 
must be had constantly in view in the management of these cases. The 
establishment of nitric acid issues, and the employment of moxce over 
the abdomen or epigastrium, as recommended by some, are of doubtful 
service, either for the relief of pain, or to hasten the healing of the ulcer. 



LEUKOSES OF THE STOMACH. 



281 



NEUROSES OF THE STOMACH. 

These are comparatively rare independent of a well-marked neuralgic 
diathesis. They are known as nervous gastralgia, or cardialgia, and as 
erythism of the stomach. They have no distinct pathological lesions. 

Etiology. — Neuroses of the stomach are met with most frequently in 
females, and occur especially in those with an hereditary neurotic predis- 
position. Exhaustion, anaemia, and chlorosis, especially when accompanied 
by depressing influences, as grief, fear, anxiety, or great intellectual effort, 
play a most important part in its etiology. In the same way exhaustion 
from hemorrhage, insufficient food, venereal excess and masturbation will 
induce it. Central nervous diseases and disease of the pneumogastrics or 
sympathetic will sometimes cause it. The excessive use of tea or coffee has 
been cited as a cause, but those cases where some particular article of diet, 
as milk, brings on attacks of pain in the stomach, are not true neuroses. 
Reflex irritation caused by painful affections of the teeth, ear, kidneys, 
testicles, ovaries and disturbances in the alimentary canal, as hemorrhoids, 
constipation, worms and hernia, has been regarded as a cause of gastralgia. 
Diseases and displacement of the uterus, accompanied by disturbance of its 
functions, will very frequently give rise to attacks of cardialgia. 

Hysteria and hypochondriasis are its two most frequent causes ; statistics 
show that of 360 cases of these two diseases only 30 were free from gas- 
tralgia. Malarial gastralgia is accompanied by other forms of malarial 
neuralgia?. 

Symptoms. — Gastralgia usually begins with a sense of distention and 
tightness in the epigastrium, followed by a severe and agonizing pain, 
which will be described differently by different patients. In many in- 
stances the pain shoots through to the back. During an attack the abdomen 
is sometimes distended and rigid, sometimes flattened and retracted. The 
pain is often so severe that the heart's action becomes irregular, the ex- 
tremities cold, the face pinched, and there is a tendency to syncope ; in 
rare instances convulsions occur. The pain is relieved by firm pressure 
over the epigastrium, by the constant current, and by Faradization ; the 
duration of these attacks is not at all regular, sometimes lasting only a few 
minutes, at other times an hour or two, generally terminating with gaseous 
eructations, or the ejection of an acid or an alkaline fluid. Sometimes be- 
fore the first attack there will be complete anorexia. Vomiting, preceded 
by nausea, may be a part of an attack, and, though very severe, it does not 
depress the patient. Between the attacks, which occur at intervals of days 
or weeks, regularly or irregularly, the digestive functions are normal. 

Differential Diagnosis. — Neurotic cardialgia may be mistaken for ulcer of 
the stomach, which has already been considered. 

Prognosis. — This depends upon the cause ; cardialgia may continue for 
years and not endanger or shorten life. 



282 



DISEASES OF THE DIGESTIVE SYSTEM. 



Treatment. — In the treatment of this affection, tonics are always indi- 
cated. Iron, arsenic, nitrate of silver, and oxide of zinc maybe tried alter- 
nately. For relief when pain is intense, morphia may be given hypoder- 
matically. Great care must be exercised not to repeat the hypodermatic too 
frequently, for this class of patients readily become addicted to the use of 
opium. Obstinate and protracted cases sometimes yield quickly to the 
constant current or to Faradization. 

HJSMATEMESIS. 

Haematemesis, or blood vomiting, is a symptom in a variety of diseases ; 
it varies in amount and frequency with the morbid conditions which in- 
duce it. Rupture of a blood-vessel is one of its essential conditions. 

Etiology. — I. Injury to the mucous tissue of the stomach by traumatism 
or poisons. 

II. Diseases of the wall of the stomach, associated with diseased condi- 
tions of the blood-vessels. 

III. Obstruction to the portal circulation, as in cirrhosis, acute yellow 
atrophy, aneurism of the hepatic artery and tumors compressing the vena 
portae ; gastric hemorrhage may remotely be produced by obstruction in 
the portal tissue, the result of cardiac and pulmonary diseases ("nut- 
meg liver "). 

IV. Blood poisoning may cause haematemesis, as scurvy, yellow, typhus, 
and relapsing fevers, snake-bites, and cholera. It also occurs in patients 
with the "hemorrhagic diathesis," and in " bleeders," or those affected 
with licemopliila. 

V. Cancer and ulcer of the stomach cause it. 

VI. Passive hyperemia, stoppage of menses in the female, and the sud- 
den arrest of hemorrhoidal discharges, are supposed to cause haematemesis 
by suddenly raising the blood-pressure in the portal system. 

VII. Finally, this symptom appears nearly three times as often in females 
as in males, and usually between the ages of twenty and forty years. 

Symptoms. — In haematemesis, if the hemorrhage is profuse, the patient 
experiences a sense of heat and distention in the epigastrium, with nausea 
and vomiting ; he becomes pallid, and the surface cold and clammy, as 
the blood rushes up in a full stream through the mouth and nose, or is 
thrown up by successive acts of vomiting. When the blood comes up with 
a sudden gush, some portion of it may enter the larynx and excite cough- 
ing, and then it may appear to be coughed up. The appearance of the 
blood differs according to the length of time it has been acted upon by 
the gastric juice. If it is vomited in large quantities immediately after the 
bleeding has occurred, it will be partly fluid and partly coagulated ; but 
if it has been retained in the stomach for a considerable time, it will be 
fluid and have a black, or brownish-black appearance, with an acid reac- 
tion. 

Differential Diagnosis. — Haematemesis may be confounded with Jimmopty- 
sis or "blood-spitting." 



DILATATION OF THE STOMACH. 



283 



Hcemoptysis is preceded by bronchial or pulmonary symptoms, and 
haematemesis by gastric symptoms. Haemoptysis is preceded or accom- 
panied by a sense of constriction across the chest, by dyspnoea and cough ; 
while before hsematemesis, there is nausea, with oppression and distention 
felt in the epigastrium. If cough is associated, it follows the expulsion 
of blood. Blood is coughed up in mouthfuls, bright red, frothy, alkaline 
and mingled with sputa in haemoptysis ; while it is vomited more or less 
profusely, is dark colored, mixed with, food, coagulated, and often acid in 
haematemesis. In haemoptysis there is a sense of " trickling " behind the 
sternum, and for a few days after the hemorrhage, small blood-spittings ; 
and a physical examination of the chest readily determines the origin of 
the hemorrhage and establishes a diagnosis. 

Prognosis. — Haematemesis, though a grave symptom, does not often 
directly cause death ; the prognosis is. determined by the diseased condi- 
tions with which it occurs. Haematemesis from cirrhosis of the liver or 
ulcers is always more dangerous than from any other conditions. 

Treatment. — During the hemorrhage the patient must be kept absolutely 
quiet, in a horizontal position. Ice should be taken freely, and ice-bags 
applied to the epigastrium. Morphine and ergotin may be hypodermically 
administered, and the patient sustained by rectal alimentation. Astrin- 
gents given by the stomach usually do more harm than good, and should 
not be employed. In severe cases the head must be kept low and brandy 
may be given by the rectum. If there is evidence of heart-failure, brandy 
and digitaline may be given hypodermically. After the hemorrhage ceases 
great care must be exercised in the diet of the patient ; milk is the only 
nutritive article that should be allowed for the first week. The conditions 
which cause the hemorrhage must receive their appropriate treatment. 



DILATATION OE THE STOMACH. 

Morbid Anatomy. — The amount of dilatation is very variable ; in one in- 
stance the stomach was found capable of containing ninety pounds of fluid ; 
it may be either uniformly dilated, or there may be dilated, circumscribed 
pouches corresponding to ulceration or erosion of its walls. When stenosis 
at the pylorus exists, the walls of the stomach are first hypertrophied, and 
then a muscular paralysis is followed by atrophy, thinning of its walls, 
and dilatation of its cavity, which is usually to the left and upwards. 
The muscular coat may be so stretched and thinned as sometimes to be 
scarcely traceable ; this is more frequently the case when the dilatation is 
independent of stenosis. In some few instances fatty degeneration of 
the muscular coat has been found, and with it the rugae of the mucous 
coat have disappeared, and the mucous membrane has become pale and 
thin. 

Etiology. — Dilatation results first from pyloric stenosis, and this may be 
caused by cancerous or non-malignant ulceration, by the effects of cor- 



284 



DISEASES OF THE DIGESTIVE SYSTEM. 



rosiye poisons (acute gastritis), by thickening from chronic and phlegmo- 
nous gastritis, and from fibroid indurations of the pylorus. Whether spasm 
of the pylorus is sufficient to cause dilatation or not, is as yet undecided. 
Secondly, dilatation of the stomach may be caused by obstruction of the 
pylorus by tumors external to the stomach and duodenum, as cancer of 
the liver, pancreas, gall -bladder, and lymphatics of the lesser omentum. 
Thirdly, paralysis and consequent impaired peristalsis will cause dilatation 
of the stomach. It may be the result of parenchymatous degeneration 
occurring in fevers and severe constitutional diseases. Suppurations about 
the stomach, as empyema and purulent pericarditis, may induce dilatation 

by diminishing its nerve supply. 
Fourthly, habitual over-disten- 
tion of the stomach results from 
drinking inordinately and eating 
immoderately, especially of food 
which will ferment, and, by pro- 
duction of gases, will still more 
distend an overloaded stomach. 
Fifthly, hernia, by dragging down 
the stomach, and fibrous bands 
binding it to other organs, may 
lead to dilatation. 

Symptoms. — Dilatation of the 
stomach may be acute or chronic. 
Acute dilatation usually occurs 
after exhausting diseases, though 
in some instances there is no dis- 
coverable cause. It begins with sharp pain in the epigastric region, with 
tympanitic distension and sometimes with tenderness on pressure. These 
symptoms rapidly subside, and the subsequent dilatation is revealed by a 
physical examination of the abdomen. 

In chronic or slow dilatation, vomiting is the first important symptom. 
This sometimes occurs only after eating, but usually every two or three 
days there is ejected the accumulation of a portion of the previous day's 
food : the quantity vomited varies in amount from one to three gallons, 
and has a fetid odor, a black, yeasty" appearance, and an intensely acid 
reaction. On a microscopic examination of the matter vomited, sarcinse 
and torulse are found in abundance. The eructations are offensive, con- 
sisting of sulphuretted and phosphurettecl hydrogen, the results of the fer- 
mentation and putrefaction accompanying this condition ; pyrosis is a very 
annoying and often painful symptom. There is progressive emaciation, 
with pain, and a sense of weight and distension in the epigastrium. 
Muscular cramp in the calves of the legs is often a painful attendant. 
The pulse is compressible : the appetite remains good, often amounting 
to "bulimia." In some cases where there is complete paresis, there is no 
vomiting, but rapid emaciation, and anorexia from the commencement. 
The bowels are constipated, and the faecal discharges hard and dry. 




Fig. 59. 



Diagram Illustrating Dilatation of the Stomach. 

A. Greater curvature. 

B. Lesser curvature. 

C. Pylorus, the clotted line indicates the point of sten- 

osis. 

D. Line shelving the usual direction of the dilatation, to 

the left arid upward. 



DILATATION" OF THE STOMACH. 



285 



Physical Signs. — Inspection reveals a prominent rounding just above the 
umbilical region. In some cases there is a peculiar depression just at the 
epigastrium. "When the patient takes an effervescing draught, the stomach 
is visibly enlarged and the epigastrium becomes prominent. 

Palpation shows slight resistance at or below the epigastrium, the walls 
of the stomach being tense and elastic ; sometimes the motions of the 
stomach and a prominence at the pylorus can be detected. 

Percussion. — If the stomach is empty, percussion reveals an increased 
tympanitic area, by which the position and shape of the stomach can be 
quite accurately mapped out ; or, on tilling the stomach with fluid, an 
abnormal area of dulness indicates the enlarged stomach area. 

On auscultation, a splash or " succussion sound" is heard on shaking 
the patient ; and when fluid is swallowed, it can be heard dropping into 
the enlarged cavity. 

Differential Diagnosis. — This condition may be mistaken for ascites, dis- 
tended urinary Madder, or for hydatids of the liver. In ascites the fluid 
distends the lower and not the upper portion of the abdomen ; the area of 
the abdomen broadens and flattens when the patient assumes the supine 
posture, and there is fluctuation on palpation. 

An hydatid tumor does not change its shape or position when fluids are 
taken into the stomach ; it is fixed in its position and is not accompanied 
by gastric symptoms. 

The special diagnosis is of the cause. It is important to determine if this 
be pyloric obstruction, and the nature of such obstruction. In all cases 
careful examination should be made for external tumors causing pressure, 
or the presence of any pyloric growth. The two important ones are cancer 
and a cicatricial growth following gastric ulcer. The diagnosis by the his- 
tory has been given ; when the tumors have developed, cancer is more 
irregular, distinct in outline, and tender on pressure. With cicatricial con- 
traction the vomited matters will contain free hydrochloric acid and be 
free from blood. With the history these points are usually sufficient for a 
diagnosis. 

Prognosis. — The j)rognosis is determined by the conditions which cause 
the dilatation. Most cases are incurable. Surgical measures may afford 
relief in cases of cicatricial obstruction. 

Treatment. — The most important thing to be remembered in the treat- 
ment of this affection is to adapt the diet to the condition of the patient ; 
food must be taken in small quantities ; as small a quantity of fluid as pos- 
sible should be allowed. When the stomach is overloaded, its contents may 
be withdrawn by the stomach-pump, and thoroughly washed out with 
warm water. The daily use of the siphon in washing out the viscus in 
these cases has not proved to be as useful a therapeutic measure as was 
claimed for it when it was first employed. To overcome the paresis of the 
muscular coat, strychnine has been very extensively employed. Benefit 
may be obtained in some cases by the use of galvanism. To prevent fer- 
mentation, the sulphites or salicylic acid may be used. All saccharine 



286 



DISEASES OF THE DIGESTIVE SYSTEM. 



and starchy foods must be abstained from, and a diet suited to each case 
must be persisted in. Resection of the pylorus for cancer has not given 
such results as to justify the operation. Loreta's operation of digital 
divulsion has been followed by quite invariably favorable results. It 
should be employed in all cases of undoubted cicatricial nature, and in 
many doubtful cases an exploratory laparotomy may be justified. 



ENTERITIS OR INTESTINAL CATAREH. 



287 



DISEASES OF THE INTESTINES. 



I shall consider Intestinal Diseases under the following heads : — 

I. Enteritis or Intestinal Catarrh. IX. Intestinal Obstruction. 
II. Diarrhosa. X. Waxy Degeneration of the 



Diarrhoea. 

III. Cholera Morbus. 

IV. Cholera Infantum. XI. 
V. Dysentery. XII. 

"VI. Typhlitis and Perityphlitis, XIII. 

VII. Intestinal Ulcers. XIV. 

VIII. Intestinal Hemorrhage. XV. 



Waxy Degeneration 

Intestine. 
Cancer of the Intestine. 
Rectitis or Proctitis. 
Intestinal Parasites. 
Intestinal Colic. 
Constipation. 



ENTERITIS OR INTESTINAL CATARRH. 



Enteritis is a general term applied to a catarrhal inflammation of the in- 
testinal mucous membrane. It may be. acute or chronic, circumscribed or 
ditfused. The name "muco-enteritis" has been applied to it, when the 
mucous coat of the intestine only is involved ; when the inflammation in- 
volves the muscular and peritoneal coats, it is termed "phlegmonous en- 
teritis." When situated in the colon, it has been called "inflammatory 
diarrhoea. " 

Morbid Anatomy. — At its onset acute enteritis is characterized by conges- 
tion, tumefaction and dryness of the mucous surface of the intestines ; this 
is soon followed by an abundant secretion 
of mucous and pus, which covers the in- 
flamed surface. Peyer's patches and the 
solitary glands are congested and swollen, 
and stand out over the inflamed surface, 
causing it to present an appearance as if 
it were sprinkled with sand. After a 
time a thin serous fluid is copiously exud- 
ed into the intestinal canal. The layer of 
mucus and pus which covers the mucous 
membrane is either loosely attached or 
firmly adherent ; in the latter case it re- 
sembles in appearance a diphtheritic exu- 
dation ; when portions of the muco-puru- 
lent layer are removed, the mucous surface 
underneath is found eroded. This is the 
severest form of muco-enteritis. 

Simple or erythematous i n testinal catarrh 
begins in the small intestine, and may rap- 
idly spread over the entire alimentary tract. 
The membranous variety is usually confined to the large intestine andrectum, 
the portion near the ileo-ccecal valve being most extensively implicated. In 




Acute Enteritis. Small Intestine, near mid- 
dle of Ileum, showing hyperemia. 

A, A. Enlarged solitary glands. 

B, B. Congested Peyer's patches, presenting 

ike "shaven beard " appearance. 



288 



DISEASES OF THE DIGESTIVE SYSTEM. 




severe cases the mucous membrane is often dotted with ecchymotic spots. 
These changes in the intestinal mucous membrane are not infrequently ac- 
companied by changes in its lymphatic structures. The lymph follicles be- 
come greatly enlarged, and are surrounded by an inflammatory areola. Their 
contents soften, undergo necrosis, and a small, round, funnel-shaped ulcer is 
formed, called a " follicular ulcer." This ulcerative process may extend be- 
yond the follicles and involve the sub- 
mucous and muscular tissues. A dull 
pink flocculent substance, of a "por- 
ridge-like" consistence, is often found 
in the intestine at the seat of numer- 
ous follicular ulcers. In nearly every 
case of acute intestinal catarrh, the 
mesenteric glands are congested. 

In phlegmonous enteritis all the coats 
of the intestine are involved. It is usually 
limited to a small portion of the intestine, 
varying in length from two or three 
inches to one or two feet. The affected 
portion is excessively dilated ; the mu- 
cous and submucous tissues correspond- 
ing to its seat are thickened, softened 
and congested, and are either of a dark 
color from blood extravasations, or pale 
from purulent infiltration. The muscular 
Upon the peritoneal coat are irregular 
patches of submucous extravasations, and the free peritoneal surface is 
covered with a thin plastic exudation. The intestine below the seat of the 
phlegmonous inflammation is contracted, empty, and its mucous membrane 
healthy, while above its seat the intestine is dilated and filled with faecal 
matter, its mucous membrane remaining normal ; sometimes at the seat of 
the inflammation numerous ulcers appear, extending in rings transversely 
about the intestine. It may be confined to the caecum and ascending colon. 

In chronic intestinal catarrh the mucous membrane has a slaty, blue or gray 
color ; sometimes black pigment deposits are found in the villi, and between 
the follicles. The membrane is thicker than normal, and, as a result, the 
peristaltic motion of'the intestine is impeded. Hyperplasia of the connective- 
tissue immediately beneath the epithelium, and perhaps of the solitary 
and agminated glands, occurs. The epithelium itself, in most cases, un- 
dergoes fatty or granular degeneration. The lymphatics are enlarged, and 
project from the mucous surface, as numerous distinct white nodules, cov- 
ered with viscid gray mucus, which is sometimes purulent. The veins un- 
derneath the mucous membrane are enlarged and tortuous. If acute intes- 
tinal catarrh passes into chronic, the intestinal coats become thinned and 
pale, or hypertrophied, causing stricture of the intestinal canal ; such ste- 
nosis occurs most frequently at the sigmoid flexure and in the rectum. 
Follicular ulcerations occur more frequently in chronic than in acute 



Acute Follicular Enteritis. Transverse Colon laid 
open, showing enlarged follicles, which have 
ulcerated at their apices. 



coat is thick, soft and oedematous. 



ENTERITIS OR INTESTINAL CATARRH. 



289 



intestinal catarrh. In prolonged cases, there may be 'developed polypoid 
cysts ; similar changes in the stomach may accompany intestinal catarrh. 
Acute and chronic catarrh of the duodenum are attended by changes similar 
to those which take place in other portions of the tract ; but in duodenal 
catarrh, the secondary catarrh of the ductus communis, by obstructing its 
opening into the duodenum, leads to catarrh of the hepatic ducts. 

Etiology. — Intestinal catarrh is ordinarily caused by direct irritation of 
the mucous membrane by improper or decomposing food, impure water, 
or irritating medicines, or by exposure to wet or cold. Extensive burns 
will also cause it. Certain atmospheric conditions produce it in children 
during dentition, or during convalescence from one of the exanthemata. 

Chronic intestinal catarrh is often a 'complication of chronic malarial in- 
fection and chronic Bright's disease. It may also be an accompaniment of 
hernia. Obstructed venous return, from hepatic, cardiac or pulmonary dis- 
ease, as cirrhosis of the liver, chronic valvular lesions, and pulmonary em- 
physema, is a predisposing cause. It occurs at all ages ; one-third of the 
diseases of children have intestinal catarrh as their primary or principal 
lesion. Its two great predisposing causes in children are dentition and bad 
hygiene, especially during the hot months, when there are the greatest vari- 
ations of temperature. It may be epidemic or endemic. 

The membranous and phlegmonous varieties occur as complications of 
t]ie exanthemata, pyaemia, septicaemia, puerperal fever, and, in rare in- 
stances, acute tuberculosis, and acute Bright's disease. 

Symptoms. — As the symptoms of acute enteritis vary with the portion 
of intestine involved, as well as with its severity, the symptoms will be 
considered without attempting a history of its course. 

Diarrhoea is its earliest and most constant symptom. It is called mucous, 
bilious, or serous, according to the varying character of the discharges. In 
mucous diarrhoea watery mucus is mixed with ordinary faeces. In cases 
where the stools consist almost exclusively of mucus, rectitis and "colitis" 
may be suspected. In colitis, cylindrical casts of varying lengths and pus 
are often present in the discharges. In the so-called bilions diarrhoea, pain 
and cramps in the calves of the legs are not infrequent. There is vomiting, 
headache, sallowness of the surface, furred tongue, weight and fulness in 
the right hypochondrium, and more or less prostration. The color of the 
stools is more distinctly green than in any other variety. Serous diarrhoea 
is the most common, and when the unqualified word diarrhoea is employed 
this form is indicated. At first the dejections contain undigested food ; 
after twenty-four or forty-eight hours the faecal odor of the discharges is 
lost. At the onset of duodenitis, jejunitis, or ileitis, diarrhoea may be 
absent if the large intestine is not simultaneously involved. Diarrhoea may 
occur independent of intestinal catarrh. 

Pain is another symptom which, although not always present, is so con- 
stant that its absence is the exception to the rule ; sometimes it is colicky 
and griping in character, at others it is severe and paroxysmal, or dull and 
unremitting. In all cases it is rendered more severe by the ingestion of 
food. "With the pain, there is a sense of fulness and distention of the 
19 



290 



DISEASES OF THE DIGESTIVE SYSTEM. 



abdomen, and tendeimess on firm pressure ; yet moderate pressure sometimes 
relieves the pain. In local intestinal catarrh the pain is confined to the 
portion of the intestine involved. 

Flatulence, gurgling, and tympanitic distention of the abdomen are 
usually present, and offensive borborygmi occur with the passages and with 
eructations which may give a sense of relief. When gurgling or borborygmi 
are prominent the small intestine alone is involved. When the passages 
contain unchanged ingesta, the large intestine is usually the seat of the 
catarrh. Nausea and vomiting indicate that gastric catarrh is associated 
with the intestinal, the combination being called g astro -enteritis. If 
severe intestinal catarrh has continued for a long time, there may be 
nausea, but rarely vomiting. 

The local symptoms of enteritis are usually preceded and accompanied 
by a mild remittent type of fever. The skin is dry when the temperature 
is much elevated, and sweating often occurs at night. The change in the 
pulse corresponds to the elevation of temperature. Headache, thirst and 
loss of appetite accompany the fever, and are more marked the nearer the 
inflammation is to the stomach ; in one case there may be great restlessness, 
m another extreme lassitude and prostration. The tongue is usually dry 
and heavily coated; in children it is often glazed and "beefy;" in 
either case the breath is offensive. The urine is scanty and dark, almost 
black in the bilious variety. 

lYhen it occurs in children, it has been called gastric or (( infantile 
remittent fever;" in the evening the temperature may rise to 101° 
or 104° P., and be normal the next morning. The diarrhoea is severe 
in this class of cases, and the abdomen is usually very much dis- 
tended. There is great restlessness, thirst is excessive, and the little pa- 
tients are constantly calling for cooling drinks. The features become 
pinched, the lips pale and drawn, and the eyes deeply sunken. Vom- 
iting is frequent and is " retching " in character. The papilla? of the tongue 
are elevated and covered with a yellowish coating ; all the other symp- 
toms of acute enteritis attend it. 

Duodenitis rarely occurs independently of gastric catarrh, in fact "gas- 
tro-duoclenal catarrh " is much more common than simple duodenitis. 
The prominent symptom of duodenitis, independent of the symptoms of the 
accompanying gastric catarrh, is jaundice, which results from the secondary 
inflammation of the ductus communis, causing obstruction to the passage 
of the bile into the duodenum. A very acute duodenitis is liable to com- 
plicate extensive burns of the surface ; in obscure cases the urine should 
be analyzed for bile pigment, which may be found before the jaundiced hue 
of the skin is apparent. Some regard dyspeptic symptoms coming on three 
or four hours after meals as indicative of duodenal catarrh, but this symp- 
tom is only valuable in connection with the others. 

Membranous enteritis has few distinctive symptoms, all the symptoms 
of acute simple catarrh are much exaggerated. The stools often contain 
bloody mucus and pus. If shreds of false membrane, or cylindrical 
casts of segments of the lower bowel, are voided in the diarrhoeal dis- 



ENTERITIS OR INTESTINAL CATARRH. 



291 



charges, the diagnosis is readily made, but without these it cannot be 
recognized. 

Phlegmonous enteritis is a very grave disease. Pain and tormina are in- 
tense and come on in paroxysms. The abdomen is distended, tympanitic, 
and extremely tender, and the position of the patient is similar to that as- 
sumed in peritonitis. Vomiting is frequent, and severe ; late in the dis- 
ease it becomes fetid and even fa?cal, although in some cases there is a mere 
regurgitation. The temperature rises to 103° or 105° F., the pulse keeps 
pace with the temperature, and is small and compressible. During a par- 
oxysm of severe pain, the otherwise dry skin becomes covered with a pro- 
fuse perspiration, and the distended intestine may rupture and gas escape 
into the peritoneal cavity. Constipation generally attends these cases, and 
the appearance of diarrhoea generally indicates the commencement of con- 
valescence, during which the weakness increases for a time. With this 
convalescing diarrhoea the tongue is red, dry and glazed. But if a fatal 
termination is to be reached, the face becomes shrivelled, prostration be- 
comes extreme, distressing hiccough occurs, the extremities become cold, 
and collapse closes the scene, the mind remaining clear to the last. The 
urine is very scanty, and frequently suppressed, a precursor of a fatal 
termination. 

In chronic enteritis casts of mucus, already described, are passed with 
the stools, and are sometimes thought by the patient to be the mucous 
membrane of the intestine or a large intestinal worm. If the disease is 
long continued there is progressive emaciation, until the wasting is greater 
than in any other disease. The skin has a pale or dirty muddy hue, and 
the accompanying hypochondria may lead to a condition of melancholia. 
The tenacious layer of mucus which coats the intestine acts in the same 
way as in chronic gastritis, the contents of the intestine undergo decompo- 
sition, and gases are set free which distend the abdomen, interfere with res- 
piration, and secondarily induce a passive hyperemia in other organs. The 
passage of this flatus, and an occasional diarrhoeal attack afford great 
relief to the patient. Chronic enteritis in children is marked by a diar- 
rhoea which, though at first mucous in character, soon becomes serous 
and afterward dysenteric. The mouth shows evidences of "thrush," 
and emaciation is steadily progressive. 

Differential Diagnosis. — Acute intestinal catarrh may be mistaken for 
dysentery, hernia, acute and chronic poisoning, peritonitis, or for typhoid 
fever. The diagnosis between intestinal catarrh and dysentery will be 
considered under the head of dysentery. 

In hernia, the sudden onset of the symptoms with a history of previous 
good health, the localized pain, constipation, vomiting often following 
some sudden exertion or extreme muscular effort, and the existence of a 
hernial tumor establish the diagnosis. 

Acute poisoning from certain articles of diet (as eating toadstools for 
mushrooms) can often only be' differentiated in the first twenty-four hours 
by the history of the case. Poisoning from arsenic or any other chemical 
irritant causes severer gastric symptoms than are ever present in intestinal 



292 



DISEASES OF THE DIGESTIVE SYSTEM. 



catarrh. The vomiting in arsenical poisoning is never stercoraceous, while 
phlegmonous enteritis of the same severity is usually attended by stercora- 
ceous vomiting. A chemical analysis of the ejected matters will establish 
the diagnosis. 

Peritonitis comes on rapidly, and at its onset the abdomen becomes ex- 
ceedingly tympanitic and tender to pressure, while the advent of enteritis 
is comparatively slow, and excessive tympanitis is very rare. Vomiting 
rarely occurs in peritonitis until the peritoneum over the stomach is in- 
volved, and then it is "spinach-green;" in enteritis so severe as to be 
confounded with peritonitis, vomiting would be an early symptom and 
would not have a spinach-green character. There is constipation in peri- 
tonitis, while diarrhoea is the rule in enteritis. The pulse is tense and 
wiry in peritonitis, rapid and feeble in enteritis. The temperature is 
usually higher in enteritis than in peritonitis. As peritonitis becomes 
general, there are symptoms of collapse, and the anxious face, thoracic respi- 
ration, the immobility and the position of the patient are all characteristic. 

Enteritis, particularly gastro-enteritis, is sometimes mistaken for typhoid 
fever, but in typhoid fever nausea, vomiting, and diarrhoea follow the fe- 
brile movement, whereas they precede it in gastro-enteritis. The tempera- 
ture rarely rises to 103° F. in gastro-enteritis, while it may reach 104° 
or 105° in typhoid fever. The typical range of temperature during the 
first week of typhoid fever is characteristic, and is never met with in 
gastro-enteritis. In children the diagnosis is difficult without a complete 
thermometrical record. 

Prognosis. — The prognosis in simple intestinal catarrh is generally good, 
particularly in children during dentition. The prognosis in membranous 
or phlegmonous enteritis is always bad, especially when it occurs with 
pyaemia, or Bright's disease. The duration in mild acute intestinal 
catarrh is ordinarily from three to five days. Chronic intestinal catarrh 
will persist as long as the cause which produces it is in operation. 
The signs which indicate recovery are subsidence of pain, the appear- 
ance of normal fsecal discharges, the clearing of the tongue, and a hope- 
ful countenance. But when emaciation is progressive, the pulse irreg- 
ular, or continuously rapid, constipation alternating with a serous 
diarrhoea, and profuse sweatings occurring at night the prognosis is 
unfavorable. Death may result from exhaustion, peritonitis, or from some 
of the more serious complications. 

Treatment. — First, compel the patient to remain in bed until all active 
symptoms subside. If there is reason to believe that irritating sub- 
stances in the intestine excite and keep up the catarrh, give a dose of 
castor-oil or calomel. It is safe to begin the treatment in every case of 
acute intestinal catarrh by the administration of castor-oil. The diet 
should consist of skimmed milk, or milk with lime-water, prepared 
meats, and light broths containing but little starchy matter. The yolk of 
eggs may be given with the milk. No fats should be allowed, or bread or 
any form of starchy food. Young infants should be immediately placed 
on a healthy wet-nurse. "When prostration is marked stimulants may be 



DIARRHOEA. 



293 



carefully administered. The abdomen should be covered with flannel, and 
if pain is excessive warm fomentations of belladonna or opium may be 
employed. Opium is the most efficient agent in the treatment of all 
varieties. It must be given in sufficient doses to secure rest to the intes- 
tine, and to relieve the pain, half a grain every two or three hours is 
usually sufficient for an adult ; its use must be continued until the diar- 
rhoea ceases. 

Rectitis is the only variety where astringents may be used. Here an 
anodyne and astringent plan may be combined, the best results having 
been obtained by enemata. When the catarrh is of malarial origin, 
quinine must be given in large doses. If it has been the result 
of exposure to wet and cold diaphoretics are indicated. In an intense 
form of enteritis three or four leeches may be applied to the abdomen, 
around the anus, or at the points of tenderness. Membranous or phleg- 
monous enteritis is to be treated the same as dysentery. 

Chronic intestinal catarrh may be treated by astringents : the best are 
the nitrate of silver, the acetate of lead, and the sulphate of copper. A 
course of mineral waters will in many cases have a beneficial effect, and 
sea-bathing, cold sitz-baths, or sponging the abdomen with cold salt water 
may be of service in mild cases. 

DIAEEHOEA. 

Diarrhoea is the frequent discharge of fluid or semi-fluid faeces (without 
tenesmus) ; it may be acute or chronic. It is a symptom of a variety of 
morbid conditions which will be considered under their appropriate heads. 

The following are the principal varieties of acute diarrhoea : 

Irritative diarrhoea includes those fluxes attended by pain and griping so 
often met with in children during the summer months in our large cities ; 
those "brought up by hand" and those who have just been weaned are 
most liable to it. In adults, this form of diarrhoea may be caused by excess 
of food, improper and unseasonable food, improperly masticated food, foul 
water, tainted meats, etc. Personal idiosyncrasies play an important part 
in its causation. The diarrhoea produced by drugs causing hyper-purgation 
is "irritative." So also the pseudo-diarrhcea induced by hardened faeces, 
the result of long-standing constipation. The presence of worms, excessive 
discharges from the liver and intestinal surface, especially if they are in- 
flammatory in character, are causes of irritative diarrhoea. 

Symptomatic diarrhoea is part of the natural history of typhoid fever, 
waxy intestines, intestinal ulcerations, inflammation of the large and some- 
times of the small intestine, Bright's disease, pyaemia, the exanthemata, 
Hodgkin's and Addison's diseases, leukaemia, and all forms of cholera. 
The diarrhoea of enteritis and proctitis is symptomatic. 

Mechanical diarrhoea is that form in which the faeces are made fluid by a 
large amount of serum poured into the intestinal canal, the serous flow !)eing 
induced by the action of salines, as Epsom or Rocheile salts. Hepatic, 
pulmonary^ and cardiac diseases which retard the returning blood current 



294 



DISEASES OF THE DIGESTIVE SYSTEM. 



from the superior and inferior mesenteric veins, will cause a transudation 
of serum into the intestine, which will dilute the faeces and wash out the 
intestine, causing diarrhoeal discharges. 

Nervous diarrhoea may be caused by fright, grief, great anxiety and 
severe pain. It is marked by profuse watery faecal discharges, which, when 
once established, are apt to persist. It often comes on so soon after taking 
food that the food is passed undigested, and it is then called Uenteric diar- 
rhoea. The discharges usually are largely serous. 

Choleraic diarrhoea precedes an attack of cholera, and is a prominent 
symptom in cholera morbus. 

Vicarious diarrhoea is usually compensatory. When the functions of the 
skin, kidneys, or lungs are suppressed a flux from the bowels affords relief. 
Some regard a gouty diarrhoea as vicarious. Chilling the body .suddenly 
produces a vicarious diarrhoea, provided enteritis is not established. In the 
latter case the diarrhoea would be symptomatic. Intense heat brings on a 
vicarious flux. Many fevers and acute diseases attended by an ushering-in 
chill cause diarrhoea, as much from chilling the surface (inducing a vicari- 
ous flux) as from the action of their specific poison (in which the flux would 
be symptomatic). Thus malarial, puerperal, and septic fevers are often 
attended by diarrhoea. 

Some authors make different varieties of diarrhoea according to certain 
prominent symptoms, and speak of simple, faecal, or stercoraceous diar- 
rhoea (usually irritative), bilious diarrhoea, — when the dejections con- 
tain a large quantity of greenish -yellow fluid, — serous, mucous, and 
dysenteric diarrhoea. The discharges in the last variety contain mucus and 
blood. 

Fatty diarrhoea is the result of faulty pancreatic digestion. 

The term crapulous was formerly given to that variety caused by over- 
indulgence at table, or the ingestion of unwholesome food. 

A diarrhoea is critical when it attends the crisis of a disease, not having 
existed before that time and ceasing directly after it. 

A colliquative diarrhoea is a copious watery flux, occurring in wasting 
diseases towards their close, e. g., phthisis, cancer, Bright's disease, 
etc. 

The diarrhoea accompanying pyaemia and certain septic blood conditions 
is by some called eliminative. It is a question whether the flux carries away 
the poison or the poison induces the flux. 

Symptoms. — The symptoms of diarrhoea are too well known to need repe- 
tition ; but cases vary greatly, not only in the kind of fluid dejections, but 
in their amount and frequency. A diarrhoea from over-eating may be 
harmless or even beneficial in relieving an overtaxed digestive system. 
Again, a profuse diarrhoea may be exhausting enough to cause anaemia, and 
in some chronic diseases hastens the fatal issue. Colicky pains and cramps 
in the limbs almost always accompany diarrhoea attended by profuse watery 
discharges. Thirst, anorexia, and febrile movement indicate that the diar- 
rhoea has an inflammatory origin. In copious fluxes (serous diarrhoeas) the 
urine becomes scanty, acid and albuminous. In fatty diarrhoea, free fat 



DIARRHOEA. 



295 



is found mixed with the faecal masses. 1 Jaundice and melaena accompany 
some cases of fatty diarrhoea. 

Chronic diarrhoea is always associated with some form of chronic organic 
disease, e. g., chronic enteritis, intestinal ulcers, syphilis, malaria, scurvy, 
phthisis, etc. In India, chronic diarrhoea is called the white flux. Ansemia 
and exhaustion are its most constant symptoms. After (apparent) recovery 
there is a strong tendency to its return. 

Differential Diagnosis. — Diarrhoea may be mistaken for cholera, dysentery, 
or a condition produced by the prolonged retention of faces. 

In cholera, the history of the epidemic, the watery stools resembling rice- 
water, the persistent vomiting, the cramps, suppression of urine, and the 
tormina will be sufficient to exclude a simple diarrhoea. 

In dysentery there will be fever, rapid pulse, early and great exhaustion, 
tormina and tenesmus, scanty bloody stools having a dysenteric odor, and 
more or less tenderness along the line of the large intestine. 

A diarrhoea dependent upon prolonged retention of faces is recognized 
by the history of previous constipation and the presence of thin muco- 
feculent faeces accompanied by straining, a sense of soreness in the sacral 
region, and the detection of a faecal mass by a rectal exploration. It is im- 
portant to recognize this condition early. 

Prognosis. — The prognosis in symptomatic and inflammatory diarrhoea 
depends upon the primary causative disease with which it occurs. The 
prognosis in simple diarrhoea is good, yet the disease is dangerous in the 
very young and very old. Nervous diarrhoea is apt to become chronic and 
often proves very obstinate. In fatty diarrhoea 50 per cent. die. 

Treatment. — The treatment of diarrhoea will be determined by the causes 
which produce it, and the symptoms which attend it ; if it depends on un- 
digested food, the first indication is to remove the substances which are 
causing the intestinal irritation by a full dose of castor-oil, or rhubarb and 
soda. The diet should be restricted to milk and lime-water, and rest in 
bed should be enjoined. In the feeble a teaspoonful of brandy may be 
given every two or three hours. If the discharge continue, camphor, kino, 
bismuth or dilute sulphuric acid may be administered after each passage. 
If the discharges are accompanied by colicky pains and griping, opium may 
be combined with bismuth and camphor, or a simple diarrhoea mixture 
will be found efficacious. 2 In malarial diarrhoea, quinine must be given in 
combination with opium and capsicum. In bilious diarrhoea hydrargyrum 
cum creta may be combined with opium. In the summer diarrhoea of 
children, the treatment described under cholera infantum is indicated. It 
is often rapidly cured by enemata of chloral hydrate (gK. ij) in two or 
three drachms of starch water. In nervous diarrhoea I have found oxide 



1 Dr. Bright stated that fatty diarrhoea probably indicated disorder of the pancreatic functions before 
Bernard discovered what these functions were. 



2 I£ Spts. lavand. com 



I ij. 
3 ij. 
3 ss. 

gtt. X. 



Tr. opii 

Tr. rhei 

Oh sassafras 



M.— Sig. Teaspoonful after each movement. 



296 



DISEASES OF THE DIGESTIVE SYSTEM. 



of zinc the most beneficial. Scorbutic diarrhoea is not influenced by drugs ; 
lemonades, anti-scorbutics and fresh vegetables will usually check it readily. 
A vicarious flux frequently needs to be encouraged rather than checked, 
unless the patient is anaemic. As regards the treatment of fatty diarrhoea 
we have but few observations ; large quantities of olive oil in one case, 
large quantities of whiskey in another, and a change from an indoor to an 
outdoor life in still another case, resulted in recovery. 

In lienteric diarrhoea, arsenic is beneficial ; it may be combined with bis- 
muth or the alkalies. Hydrochloric acid is sometimes useful ; astringents 
are not indicated. 

In the treatment of chronic diarrhoea, bismuth is the most reliable 
drug. There should be great care in diet, and the body should be cov- 
ered with flannel, even in warm weather. Sea voyages and change of 
climate are often of service. Tonics are indicated, and copper and silver 
salts are the best astringents. Hope's mixture — a well-known combina- 
tion — will often control it when all other means have failed. In chronic 
nervous diarrhoea, arsenic and the bromides are indicated. 

CHOLERA MORBUS. 

Cholera Morbus, called also cholera nostras, English cholera, and sporadic 
cholera, is in reality a simple entero-catharsis. 

Morbid Anatomy. — If any anatomical lesion exists, it consists in an acute 
gastro-enteritis ; but the disease may occur without any discoverable lesions, 
thus simulating a functional disorder. It is so rarely fatal, that there 
has been little opportunity to study its morbid changes. In the few cases 
where post-mortems have been made, no adequate lesions have been dis- 
covered. Death may occur, and the intestinal tract may exhibit no mor- 
bid changes. Sometimes there is cerebral anaemia with serous effusion into 
the sub-arachnoid spaces. 

Etiology. — Cholera morbus almost always occurs during the summer 
months. In this country it is most prevalent in July and August. Sud- 
den checking of the perspiration, or suddenly chilling the surface of the 
body by external cold, or iced drinks, and sudden changes in the tempera- 
ture after a heated term will produce it. Its most frequent cause is undi- 
gested food, as shell-fish, unripe fruit, cucumbers, etc. Sudden arrest of 
the digestive process from mental emotion is said to induce it. Some claim 
that malaria will cause it, especially in those greatly exhausted. Overdoses 
of tartar emetic and elaterium bring on attacks of vomiting and purging 
very similar to cholera morbus. Its prevalence during certain seasons seems 
to indicate a specific cause, perhaps some peculiar atmospheric condition. 
It is infrequent in old age. It attacks males oftener than females. In many 
cases its only discoverable cause is intense nervous disturbance, on account 
of which the peristaltic action of the intestines is greatly exaggerated. 

Symptoms. — The symptoms of cholera morbus are familiar. An attack 
usually begins at night by vomiting and purging. The matters vomited 
are first, undigested food, gastric mucus and bile ; afterward large quan- 



CHOLERA MORBUS. 



297 



titles of acid or bilious fluid. The vomiting is projectile in character, and 
there is temporary relief after each attack. The bitter fluid ejected 
leaves a burning sensation in the mouth and throat. Although the thirst 
is intense, fluids as well as solids are immediately rejected. In some in- 
stances, instead of an abrupt onset, the attack is preceded for several hours 
or a day by nausea, general malaise, or sense of weight and uneasiness in 
the epigastrium and lower part of the abdomen, occasionally accompanied 
by colicky pains. Evacuations from the bowels follow each other in 
quick succession, the dejections becoming watery and profuse, and having 
a mouse-like odor. In some cases purging alone is present. After an at- 
tack has continued for some hours the discharges become watery and odor- 
less, but they always contain bile. Pain generally accompanies or precedes 
every act of vomiting or purging, which either occur together or rapidly 
succeed each other. The larger the evacuations the lighter their color, and 
greater the thirst. 

In all severe cases there are cramps in the lower extremities, es- 
pecially in the calves of the legs and feet. Both vomiting and purging 
occur suddenly and without premonition. The skin is cool and covered 
with a profuse perspiration. The pulse grows weak and rapid as the 
vomiting and purging become more severe. The abdomen, at first dis- 
tended, becomes retracted ; sometimes the abdominal muscles are knotted 
by cramps. The urinary secretion, after the excessive watery discharges 
from the alimentary track, is greatly diminished, and traces of albumen 
and desquamated epithelium may be found in it. These severe symptoms, 
although seeming to threaten the life of the patient, usually continue only 
for a few hours, and the patient rapidly convalesces. If the attack is 
protracted, the pulse becomes flickering and imperceptible at the wrist, the 
countenance pale and shrunken, the voice feeble and the surface icy cold. 
This condition is called the algid stage of cholera morbus, and the patient 
may pass into a state of collapse, which may be followed by death. In all 
cases the mind is perfectly clear, and recovery or death occurs within twenty- 
four or forty-eight hours from the beginning of the attack. A fatal issue 
in adults is exceedingly rare. Sometimes a fever, attended by typhoid 
symptoms, follows the stage of collapse, called " the reaction fever." Gen- 
erally, the stools become normal in character the day after the commence- 
ment of the attack, and the patient is simply weak. There are rarely any 
febrile symptoms during its active period. 

Differential Diagnosis. — During a cholera epidemic, it is difficult to differ- 
entiate cholera morbus from either cholerine or true Asiatic cholera. When 
not prevailing as an epidemic, Asiatic cholera is differentiated by the ab- 
sence of faecal odor, by the color of the stools and by the duration of the 
attack. Cholera morbus rarely continues longer than twelve or eighteen 
hours. In cholera, collapse comes on early and the discharges have the dis- 
tinctive rice-water appearance from its commencement. 

Cholera morbus may be mistaken for the effects of irr itant poisons. In 
cases of poisoning, the mouth and pharynx are usually intensely hy- 
peraemic, and the pain is more intense and constant than in cholera morbus. 



298 



DISEASES OF THE DIGESTIVE SYSTEM. 



If there is diarrhoea, the discharges are blood-stained, and this never occurs 
in cholera morbus. In poisoning, the pain over the stomach is more severe, 
and an analysis of the vomited matters quickly decides the question. 

Cholera morbus is differentiated from typhlitis and perityphlitis, by the 
absence of a tumor, the short duration of the attack, and by the intens- 
ity and character of the gastric symptoms. Typhlitis is, in the majority 
of cases, accompanied by constipation ; cholera morbus by diarrhoea. 

Prognosis. — Cholera morbus is rarely a fatal disease. Its duration va- 
ries from two hours to two days. In the aged, and in the feeble, the prog- 
nosis is more unfavorable than in healthy adults. It is also more unfa- 
vorable when cholera and dysentery prevail epidemically, or when there is 
co-existing renal disease. When a patient passes into the algid stage or 
stage of collapse there is always danger. 

Treatment. — In mild cases of cholera morbus, ice may be given to check 
the vomiting, and sinapisms applied to the epigastrium. In the severer 
cases, a quarter of a grain of morphine hypodermically will generally re- 
lieve the distressing symptoms. In all cases sinapisms should be applied 
over the abdomen, and if there is great coldness of the surface, dry heat 
should be applied to the extremities. If there is great prostration, with 
coldness of the extremities, alcoholic stimulants must be given with mor- 
phine, and if there is hepatic tenderness, one-half grain of calomel every 
hour for six hours will be of service. Small doses of the mineral acids are 
often beneficial after the vomiting is relieved. 

If the diarrhoea is protracted, vegetable astringents may be given. All 
remedies should be given in small doses. After the subsidence of the 
attack, care should be exercised in the diet for several days, and the patient 
should be kept in bed. 

CHOLERA INFANTUM. 

Cholera infantum, or summer complaint in children, is a very common 
disease in cities and large towns during the heat of summer. 

Morbid Anatomy. — Its principal lesions are found in the colon next to 
the ileum, but sometimes the whole intestinal tract is involved. Patches 
of arborescent injection are scattered over the intestinal mucous surface, 
which sometimes assumes a bright red color and becomes more or less tume- 
fied. The most constant change is enlargement and softening of the fol- 
licles. Peyer's patches present the shaven-beard appearance, and in pro- 
tracted cases the mucous membrane is studded with follicular ulcers. Over 
the inflamed patches the peritoneum may be reddened and covered with 
lymph. The intestines usually contain a thin rice-water fluid, more rarely 
fluid faeces. The mesenteric glands are sometimes enlarged and the liver 
congested. Death may occur and the intestinal tract exhibit no morbid 
change. 

Etiology. — The prevalence of cholera infantum in summer is indirect 
proportion to the height of the temperature. Teething children are es- 
pecially liable to it. Those over three years are less liable to it. Over- 



CHOLERA INFANTUM. 



299 



crowded and anti-hygienic surroundings predispose to it. It prevails 
extensively among the children of tenement-house districts and in asylums. 
The greatest mortality occurs during hot, still, sultry days. Gases from 
cesspools and malarial influences are powerful predisposing causes. 
The improper feeding of children which prevails in the densely packed 
tenement-house districts of New York City, where the death-rate from 
this disease is twice that of any other city in the world, has as much to 
do with its prevalence as the high temperature. Artificially fed children 
are more subject to it than those who nurse. 

Symptoms. — It begins either with vomiting or diarrhoea, or both. There 
may be prodromata, but they are vague and inconstant. The child rejects 
all food, and becomes peevish or languid and apathetic. Purging is always 
present, and the passages are watery and greenish in color, rarely colorless, 
and contain curdy masses mixed with mucus. There is a peculiar odor to 
the discharges which is characteristic of the' affection. Sometimes the stools 
contain particles of undigested food that have passed through the intestinal 
tract unchanged. The discharges are more or less slimy, sometimes frothy, 
and at first have a distinctly sourish odor. The child is constantly thirsty, 
although all liquids, even its mother's milk, are instantly rejected. Prostra- 
tion and emaciation begin almost with the first discharges, and two or three 
days suffice to bring the healthiest child into an extremely exhausted con- 
dition. The reaction of the vomited matter varies ; it may be acid or alka- 
line. 

The patient becomes stupid, with a marked tendency to coma. Con- 
vulsions are not infrequent. The temperature is rarely above the normal, ex- 
cept during the first few hours, and then it is remittent in character. The 
urinary secretion is diminished, and ursemic symptoms often precede a fa- 
tal termination. The number of passages varies from six to seventy-five in 
the twenty-four hours ; the abdomen at first may be distended and tympa- 
nitic ; later, it is retracted, and always tender. The pulse varies from 120 to 
160, and there is often marked dyspnoea. These little patients die from 
inanition, or rapidly recover after having seemingly been on the verge of 
death. Not infrequently they gradually pass into a condition where months 
will elapse before normal intestinal digestion is re-established. The disease 
usually lasts a week, at the end of which death or recovery takes place. 
Deceptive remissions may occur, only to be followed by graver and often 
fatal symptoms. Tenderness on pressure is generally marked along the 
whole line of the colon, and the diffuse erythema about the anus causes in- 
tense pain whenever a passage occurs. 

Differential Diagnosis. — Cholera infantum may be mistaken for Asiatic 
cholera. The points already given for the differential diagnosis of cholera 
and cholera morbus will suffice to establish the diagnosis. 

A spurious hydrocephalus sometimes follows cholera infantum, the symp- 
toms of which, and the termination in coma, resemble very closely those of 
acute hydrocephalus. In spurious hydrocephalus there is diarrhoea and a 
history of previous vomiting and purging. In acute hydrocephalus, there 
is constipation. In spurious hydrocephalus, the pupils are dilated bun reg- 



300 



DISEASES OF THE DIGESTIVE SYSTEM. 



alar, while in tubercular meningitis they are contracted and irregular. In 
spurious hydrocephalus the pulse is accelerated but regular, while in acute 
hydrocephalus it is slower than normal, irregular and intermittent. In 
acute hydrocephalus the abdomen is retracted ; in spurious hydrocephalus 
it is distended and tympanitic. The hydrocephalic cry and convulsions, 
on the one hand, and the age of the patient and the mode of the attack on 
the other, will further aid in the diagnosis. 

Prognosis. — The prognosis in a severe attack of cholera infantum is always 
unfavorable. Its duration depends upon the vigor of the child and the se- 
verity of the attack. It may continue a week, or death may occur in twenty- 
four hours. Children who are artificially fed are less likely to recover than 
those who receive the breast. The rate of mortality is greater in those liv- 
ing in badly ventilated tenements than in those with better hygienic sur- 
roundings. Continued vomiting, excessive purging, stupor, or great rest- 
lessness and convulsions, are unfavorable symptoms. The prognosis is 
favorable when the vomiting and purging are not excessive. Death may 
occur from exhaustion, or cerebral effusion causing convulsions and coma. 
(Edema of the lungs may result from heart- failure, and this, with hypo- 
static congestion, may cause death. In all cases the prognosis must be 
guarded. 

Treatment. — The treatment of cholera infantum is mainly prophylactic ; 
the diet and hygienic surroundings are the most important. Occurring as it 
does in large cities in the summer it is best treated by removing the children 
of the poor to the sea-shore. When this is impossible, the child must spend 
the morning and evening in the fresh air. The first indication, then, 
is change of air and location. The establishment of various seaside sani- 
tariums for children during the summer months in the neighborhood of 
large cities is the most important advance that has been made in the 
management of this disease. At the same time great care must be exer- 
cised in the diet ; fresh cow's milk with barley and lime-water added, is 
the best artificial diet ; a good wet-nurse is always to be preferred. The 
amount of food taken should be regulated by the capacity of each case to 
retain it. At the onset of the attack a few drops of brandy in a teaspoon- 
ful of barley-water is all that should be allowed, and absolute rest in the 
horizontal position should be maintained as long as the vomiting con- 
tinues. To relieve the intense thirst the child may suck pounded ice in a 
linen bag. The only drug that I have found efficacious in controlling the 
vomiting is calomel, which should be given dry on the tongue in minute 
doses, 1-12 of a grain every half-hour. Some claim excellent results from 
the administration of bismuth and carbolic acid ; salicylic acid is also of 
value in arresting fermentation. Both bismuth and calomel are efficacious 
when the stools contain large quantities of mucus. If the intestinal 
symptoms persist after the vomiting is relieved, camphor and opium may 
be given — five or ten drops of the tr. opii cam ph. every two hours. 

In malarial districts, quinine should be given as soon as the stomach will 
retain it. When vomiting is slight and purging is excessive with great 
prostration, benefit will be obtained from camphor and brandy. The vege- 



IXTESTI;N"AL DYSPEPSIA. 



301 



table astringents, such as hsematoxylon, kino, and catechu, are of service 
in controlling the diarrhoea which so often follows a severe attack of cholera 
infantum. During convalescence, wine- whey may be given in connection 
with cod-liver oil, and the phosphates and oils may be applied to the sur- 
face as a means of sustaining the strength of the child. Seaside resorts 
and salt water baths are especially beneficial to this class of patients after 
the severity of the attack has passed. Spiced poultices wet with brandy 
and worn over the epigastrium are of service. 

Flannel should be worn next the surface during convalescence, and great 
care should be exercised to avoid exposing the surface to changes of tem- 
perature, for capillary bronchitis carries off a large number of convales- 
cents. 

INTESTINAL DYSPEPSIA. 

Closely connected with diarrhoea is a functional disturbance of the intes- 
tines which may be designated intestinal dyspepsia. It depends upon a 
derangement of the functions of the small intestine independent of any 
organic lesion. 

Etiology. — Intestinal dyspepsia may be a primary disease, or it may be 
secondary to gastric dyspepsia, diseases of the liver, pancreas, or large intes- 
tine. Its causes are similar to those of gastric dyspepsia, such as structural 
changes in the mucous membrane, altered conditions cf the secretions of 
the small intestine, the presence of undigested food, or the ingestion of 
improper food ; an altered condition of the muscular coat of the intestine 
often accompanies general malnutrition. 

Symptoms. — Pain, which is generally a constant symptom, is of a dull, 
aching character and not circumscribed, but radiates over the upper por- 
tion of the abdomen. It is rarely acute, like that of peritonitis, nor as 
sudden in its advent as the pain of colic, nor does it bear any relation to 
the ingestion of food. Nausea and vomiting, when present, depend more 
upon the accompanying stomach derangement than upon any intestinal 
disturbance. Constipation and gaseous distention of the large intestine 
are prominent symptoms. It is only after repeated attacks that the 
patient's health becomes impaired, so that he loses flesh and strength, and 
begins to worry about himself, fearing some serious organic lesion. It is a 
peculiar fact that the appetite is seldom if ever impaired. 

Treatment. — The immediate condition can usually be relieved by five- 
grain doses of pancreatin taken two hours after eating. This also prevents 
fermentation and thus decreases intestinal irritation. Hygienic measures 
are the most important and should first be tried. If possible the patient 
should travel ; if this cannot be done, out-of-door exercise, such as horse- 
back riding and walking, will be most beneficial. This class of patients 
should abstain from all fats and starches, eat principally meat, and vege- 
tables containing but little starch ; of the drugs which yield the best 
results, ipecacuanha and cubebs in the form of a powder stand first, 
although some prefer bismuth combined with iron and quinine. 



302 



DISEASES OF THE DIGESTIVE SYSTEM. 



DYSENTERY. 



Dysentery is a specific febrile disease, with a characteristic local lesion. 
Its local lesion is an inflammation of the mucous membrane, and of the 
solitary and tubular glands of the large intestine, which may be catarrhal 
or croupous in character. It has points of resemblance to acute infectious 
diseases, being attended by feyer, and having a characteristic local lesion. 
It may be acute or chronic, epidemic, endemic, or sporadic. 

Morbid Anatomy. — The difference between sporadic or simple dysentery 
and epidemic, often malignant, dysentery, is that in the former the ana- 
tomical changes do not pass to extensive ulceration, and it attacks com- 
paratively few individuals in the same locality. In mild cases, the lesions 
are confined to the lower portion of the large intestine, while in severe 
cases the whole length of the large intestine is involved. 

The first change, in the mild as well as in the severe types, is a more or 
less intense hyperemia of the intestinal mucous membrane. Its color varies 
from a slight inflammatory blush to a purplish red ; this change in color is 
never uniform throughout the affected portion. With the change in color,- 
the mucous membrane becomes swollen and softened, from oedema of the 
mucous and submucous tissue ; the latter being infiltrated with inflamma- 
tory products which give it a " cloudy" appearance. The thickening and 
softening are more marked at some points than at others. They are usually 
most distinct at the summit of the folds of the mucous membrane. In mild 
cases, only a small number of prominences indicate the localities which 

are involved, whereas in severe cases these 
prominences are so numerous that they 
give the membrane a lobulated appear- 
ance. In the first stage, the solitary fol- 
licles become distinct, enlarged, promi- 
nent, and vary in size from a millet-seed 
to a small pea. Each is surrounded by a 
zone of turgid and enlarged vessels. These 
glands enlarge, become distended with a 
whitish, albuminous exudation, having a 
dark central spot surrounded by a vascular 
ring. The next change, in most instances, 
is rupture of some of the distended capil- 
laries in the wall, thereby filling the fol- 
licular cavity with blood. Molecular dis- 
integration of the gelatinoid contents now 
Mucous surface o/iower portion of Large occurs, and ulcers are formed after the 

Intestine iu the First Stage of Acute Dysen- contents of the follicles are discharged. 

A % a. EYdarged follicles. These ulcers are at first round; later 

b. small ulcers. fhey gradua]]y enlarge ^ and two or more 

may coalesce, their edges becoming everted and flattened, and assume an 




DYSENTERY. 



303 



irregular, serpentine, or rodent shape. The long axis of the ulcer usually 
corresponds to the fold of mucous membrane circumscribing the intestinal 
canal. The condition of the different ulcers in the same case varies ; one 
is pale and superficial, another deep, angry, and irritable ; again they may 
be covered by a more or less dense layer of lymph, or a thin film of 
serous fluid. The adjoining tubular glands are involved. Sometimes 
ulceration destroys every solitary follicle of the involved part. The floor 
of the ulcer may be on the muscular or on the peritoneal layer of the intes- 
tine. Between the ulcers is often found a polypoid growth, which is simply 
a flaccid, vascular tuft of mucous membrane. 

As the mucous membrane of the large 
intestine has the poorest blood supply of 
any mucous membrane, a very acute dys- 
enteric process may cause the whole length of 
the intestine to become a black, shaggy, gan- 
grenous, pus-infiltrated slough. In high 
grades of dysentery, large tracts of the mu- 
cous membrane are converted into dark brown 
or black, ecchymotic, and nodular carbonified 
masses (sphacelus) more or less friable, and 
underneath them the submucous tissue is 
sometimes infiltrated with pus. When this 
occurs around the ileo-caecal valve, invagina- 
tion and obstruction may result. This puru- 
lent infiltration must be regarded as part of a 
"reactive inflammation," following the re- 
moval of the charred-looking mass. Some 
observers, however, are of the opinion that in 
rapidly sloughing dysentery the process begins 
by a submucous purulent cellulitis, which detaches the mucous mem- 
brane, this membrane then becoming gangrenous. Many pathologists 
regard coagulation-necrosis as the basis of all dysenteric processes in the fol- 
licles and tubular glands. 

In some of the severe forms, the submucous cellular tissue becomes infil- 
trated with a sero-sanguinolent fluid, and its vessels become filled with black 
masses of altered blood. The muscular coat of the intestine is sometimes 
condensed, friable, and of a pale ashy-gray color. In severe epidemics, a 
thin dark-colored exudation covers the peritoneal investment of the affected 
portion of the intestine. In many cases the intestine becomes dilated, and 
is filled with dark blood and disintegrating inflammatory products. When 
the intestine contains a putrid, coffee-ground, fluid, the case must be re- 
garded as malignant. I have sometimes found the intestine collapsed and 
empty at the post-mortem of one who had suffered from severe dysenteric 
symptoms. In the mildest form of dysentery, cicatrization is accompanied 
by an exudation of lymph, which rapidly organizes. This lymph exuda- 
tion first appears upon the floor of the ulcer ; the edges become rounded, 
and are then drawn down towards the base, and so cicatrization is com- 




Stage of 



Fig. 

Mucous Surface of lower portion of 
Large Intestine in Second 
Acute Dysentery. 

Ulcers are seen of varying size, from 
that of the single follicle to larger ones 
formed by their coalescence. 



304 



DISEASES OP THE DIGESTIVE SYSTEM. 



pleted When a large extent of the mucous membrane is removed, the 
edges of the nicer are not approximated. The cicatrices which remain 
after the deep structures have been destroyed often cause " valve-like" or 
(s annular" folds, which constrict the colon. 

Perforation and peritonitis may result from an ulcer perforating the in- 
testinal walls. If the caecum is perforated, faecal abscesses may form in the 
right iliac fossa. The liver is frequently congested, and it may be the seat 
of multiple abscesses. The mesenteric glands are enlarged, softened, and of 
a dark blue color. The lower part of the small intestine, in rare instances, 
may be involved in the dysenteric process. In the croupous variety, the 
mucous membrane of the large intestine undergoes changes similar to those 
which occur in croupous inflammation of other mucous membranes. It 
usually occurs in patches ; the size of the patches will correspond to the 
severity of the inflammation. If the inflammation is mild in character, 
the membranous exudation will disappear after a few days, and the mucous 
membrane return to its normal condition. If it is severe, and the sub- 
mucous tissues become infiltrated, there will be destruction of the mucous 
membrane and the formation of ulcers. These ulcers may involve the 
muscular and peritoneal coats of the intestine. They behave the same as 
those already described. 

In chronic dysentery, the mucous membrane of the large intestine is 
studded either with slaty-blue cicatrices or pigmented ulcers. In the ma- 
jority of cases, complete cicatrization of the ulcers does not occur. The 
edges of these ulcers are always made up of unhealthy tissue. These 
ulcerations are especially marked at the sigmoid flexure and in the rectum, 
while the mucous membrane in the remainder of the large intestine is 
thickened, tough, and pigmented. In some cases the intestinal walls 
atrophy and are thinner than normal, but generally, on account of the 
changes in the submucous connective-tissue, they are thickened and indu- 
rated ; consequently there is more or less rigidity of the whole intestine, 
with narrowing of its calibre. Sometimes sinuses exist between the layers 
of the intestine ; these are most often found about the rectum. In chronic 
dysentery, more frequently than in acute, are annular and valve-like con- 
strictions formed, which cause subsequent constipation. Multiple ab- 
scesses in the liver are often met with in chronic dysentery. Small polypoid 
tumors sometimes form and project into the intestine. 

Etiology. — Dysentery is especially liable to prevail in malarial districts. 
There are localities in which it is endemic, and others in which it is epi- 
demic. It seems probable that there is a specific dysenteric miasm, and that 
the discharges from a dysenteric patient, when they have undergone certain 
changes, are capable of causing the disease. This may account for the oc- 
currence of the disease in hot climates and in early fall in our own climate, 
under conditions similar to those which favor the development of typhoid 
fever. Impure air and water are recognized causes of its development ; 
thus, seamen and those who live in crowded barracks are especially liable 
to it. In districts where it prevails, exposure to cold or chilling the sur- 
face is often an exciting cause. Bad or insufficient food, or a diet wanting 



DYSENTERY. 



305 



in vegetables, alcoholismus, mental anxiety, and excessive fatigue are among 
its predisposing causes. 

Symptoms. — Dysentery is preceded by loss of appetite, a furred tongue, 
constipation, or constipation alternating with diarrhoea, a dry skin, and a 
feeling of general malaise. The severer forms of acute dysentery commence 
with a chill or distinct rigor, followed by a slight rise in temperature, ac- 
companied by anorexia and nausea. The temperature usually ranges from 
101° to 103° ; it may reach 105° F. The pulse is increased in fre- 
quency, small and compressible. 
With, or following these constitu- 
tional symptoms, there is a constant 
desire to go to stool, with tormina, 
both during and after a passage 
from the bowels. The evacuations 
are at first semifeculent mucus, 
watery looking, and contain lumps 
of hard faeces, "scybalae." After 
and during stool, there occurs that 
painful straining with bearing down, 
called "tenesmus." The tenesmus 
is due to the abnormal sensibility 
of the lower bowel, and the invol- 
untary action of the muscular fibres 
of the rectum. At the very onset 
of the attack, the nervous depres- 
sion is very marked, the strength is 
diminished, and the face assumes a 

pale, anxious expression. The discharges soon become scanty and more fre- 
quent, containing blood and mucus (the " bloody flux "), and have the pecu- 
liar dysenteric odor. Twenty or thirty discharges from the bowels may occur 
in twenty-four hours, although they usually do not exceed eight or twelve. 

If the disease has its seat at the upper part of the large intestine, altered 
biliary secretions will be intimately mingled with the blood and mucus. If 
the dysenteric process is confined to the lower portion of the intestine, the 
blood will be separated from the mass and occur in streaks. As the disease 
progresses, the patient becomes more nervous and anxious, irritable and 
restless, and his countenance will be expressive of intense suffering. There 
is seldom much abdominal pain or tenderness on pressure during the first 
few days, but the slightest amount of solid food taken into the stomach 
causes tormina. The tongue is moist and covered with a thick whitish fur. 

As the disease advances, in the severe type, the stools change in character ; 
they contain sloughy shreds of exudative matter, looking like "washed raw 
meat," mixed with blood and purulent matter, or they are of a greenish 
color resembling spinach. The thickened intestine may now be felt through 
the abdominal parietes. The abdomen becomes tympanitic and tender ; 
the tenderness is usually most marked at some point along the line of the 
20 



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Fig. 64. 

Temperature Record in a case of Acute 
Dysentery. 



306 



DISEASES OF THE DIGESTIVE SYSTEM. 



large intestine. In some cases the stools become brownish, serous in char- 
acter, and are often so copious as to cause extreme exhaustion. The pulse 
increases in frequency, and is extremely small and feeble ; the tympanitis 
increases, the tongue becomes dry, its centre brown or black, and its edges 
red. The restlessness increases, with a mild delirium at night, which some- 
times becomes violent. The urine is dark and scanty. There may be great 
difficulty in passing it, only a few drops at a time being voided, —stran- 
gury. If the case tends to a fatal termination, irregular febrile exacerba- 
tions and remissions occur, the stools have a cadaverous or gangrenous odor ; 
hiccough, subsultus tendinum, cold perspiration, a flickering pulse, deeply 
sunken eyes, and cyanosis of the extremities usher in the fatal termination. 
If recovery is to take place, the discharges during the second week become 
less frequent and acquire a faecal odor. The temperature falls, the pulse 
diminishes in frequency and gains in force. The tympanitis subsides and 
gases are discharged from the bowels with the faecal discharges. As recov- 
ery is reached, the face loses the anxious, despondent expression which it 
had during the active period of the disease. Convalescence is slow. 

Microscopically examined, the stools voided at the height of dysentery 
are found to contain fat spherules, blood globules, pus corpuscles, vibri- 
ones, triple phosphates, and traces of ingesta, all crowded into a molecular 
mass ; while, if examined in a test tube, the amount of albumen present 
causes the entire contents of the tube to coagulate on the application of 
heat. 

Acute dysentery in children is often accompanied by vomiting and convul- 
sions. In some cases tenesmus is so great that prolapsus ani occurs. 

A malarial dysentery is recognized by the periodicity of its febrile 
symptoms. The temperature is higher than in non-malarial dysentery, and 
exacerbations and remissions of all its symptoms occur at regular inter- 
vals ; the hepatic, renal and splenic changes are the same as in malarial 
fevers. The stomach is very irritable, and the stools are likely to be 
serous from the onset, showing but slight traces of blood. 

In malignant dysentery the typhoid state is present with the first dysenteric 
stool ; the passages soon assume a gangrenous odor and contain gan- 
grenous shreds of membrane, with abundant serum and blood. The coun- 
tenance is not anxious, but listless and apathetic, the pulse is rapid and 
weak, the voice feeble, the stomach irritable, the skin cold and covered 
with a cold perspiration — indeed, a state of collapse is very quickly reached. 
The urine may be entirely suppressed, but, if passed, scalds, and has a 
fetid odor. Xot infrequently, just before death, large amounts of blood 
are discharged from the bowels and also from the mouth and nose. 

When all the causes of "scurvy" are added to those of dysentery, the 
symptoms of scurvy, namely, great prostration, emaciation, a pale muddy 
skin, darting pains in the limbs, the scurvy sore mouth, and the petechial 
spots, will be added to the dysenteric symptoms, and the stools will contain 
blood from the very onset, and are as fetid as in the malignant variety. In 
scorbutic dysentery, profuse and fatal hemorrhages are liable to occur after 
the first few days. 



DYSENTERY. 



307 



Chronic dysentery is, in most instances, the direct sequela of the 
acute form. In a few cases dysentery is chronic from the beginning, and 
its cause then lies in fatty or waxy degeneration of the liver or spleen, or 
both, or in a strumous or scorbutic taint. The temperature usually ranges 
above the normal. In some instances hectic fever may attend it. The 
evacuations are scanty and frequent, tormina and tenesmus are present in 
most cases, and the stools contain mucus. . At times they are serous, pale, 
slimy, or frothy, but always fluid ; occasionally they contain faecal matter 
and are brown and watery. The patient progressively loses flesh and 
strength, although the appetite may remain good. Defective nutrition is 
shown by furuncles, a dry, scaly skin, a red, glazed, and often deeply fis- 
sured tongue, falling of the hair, and a worn and feeble expression of 
countenance. 

Differential Diagnosis. — Dysentery may be mistaken for acute rectitis or 
intestinal catarrh, for diarrhoea complicated with hemorrhoids, and for can- 
cer or polypus of the rectum. Acute rectitis begins with colicky pains and 
constipation ; while dysentery commences with a distinct chill or rigor, 
diarrhoea, and a permanent elevation of temperature. Dysenteric dis- 
charges contain mucus, pus, blood, and scybalae. 

In acute intestinal catarrh there is no blood mingled with mucus in the 
discharges, and the latter do not have the dysenteric odor which is so 
characteristic of dysentery. Tenesmus is always present in dysentery, 
and never in intestinal catarrh. The discharges are profuse in intestinal 
catarrh, scanty in dysentery. The pain in acute enteritis is more intense 
and paroxysmal than in dysentery. The constitutional symptoms are much 
more severe in dysentery than in enteritis. 

A simple diarrlma in one suffering from hemorrhoids may be accom- 
panied by bloody discharges and tenesmus, but the absence of constitutional 
symptoms and an examination of the rectum will readily establish the diag- 
nosis. 

In the same way cancerous or polypoid growths in the rectum, from 
which pus or blood is frequently discharged, can readily be differentiated 
from dysentery. 

Prognosis. — The prognosis in simple, acute, and malarial dysentery is 
good. In the malignant, or asthenic and scorbutic varieties, it is exceed- 
ingly bad. The ordinary duration of acute dysentery is from eight to ten 
days ; malignant dysentery may terminate fatally in two or three days. 
Sporadic dysentery in children usually lasts about a week. Chronic dys- 
entery may continue for years. The favorable symptoms in any case are 
absence of a gangrenous odor to the stools, absence of great nervous 
depression and of an anxious, sodden expression of countenance, the gradual 
subsidence of the tenesmus and of the peculiar dysenteric stools. The. unfa- 
vorable indications are a large quantity of blood in the discharges, a sunken 
aspect of the countenance, hiccough, vomiting, a distended, tympanitic 
abdomen, great nervous depression, a typhoid condition, great restlessness, 
suppression of urine, and marked cerebral disturbances. Dysentery may 
be complicated by extreme anaemia, by prolapsus ani, by hepatic ab- 



308 



DISEASES OF THE DIGESTIVE SYSTEM. 



scess, by bronchitis and lobular pneumonia, by malaria, typhoid fever, pur- 
pura, scurvy, the hemorrhagic diathesis, enlargement of the spleen and 
liver, any one of which renders the prognosis unfavorable. Death may occur 
from exhaustion, from hemorrhage, from perforation and peritonitis, or 
from secondary pysemic abscess. In all cases, however, the immediate 
cause of death is asthenia. 

Treatment. — The preventive treatment of dysentery consists in disinfect- 
ing the evacuations as soon as they are discharged, in the same way as in 
typhoid fever, and the avoidance of all those conditions, such as bad 
hygienic surroundings, insufficient clothing, and improper food, which act 
as predisposing causes. A patient with dysentery must be kept in bed, 
and all irritating matter removed from the intestinal tract by a full 
dose of castor-oil ; to accomplish this an enema of one to two quarts of warm 
water is recommended by East Indian physicians. The diet should be 
chiefly of milk with light meat broths ; no solids should be allowed. 
If at the very onset there is great tenesmus, two or three leeches about 
the anus will often give great relief. Medicinally, opium is the drug 
almost universally employed, and should be given to semi-narcot- 
ism. 1 

Its direct action is three-fold — narcotic, sedative and astringent ; secondly, 
it controls the inflammatory process by its action on the sympathetic nerv- 
ous system. When the rectum is chiefly involved, it is best administered 
per rectum, but when the temperature is high and the tenesmus is intense, 
the rectal use of opium is contra-indicated. In such cases ipecacuanha in 
large or small doses has been found most efficacious. Some recommend 
that it should be given in thirty-grain doses, 2 but it seems to me just 
as efficacious when given in -|-grain doses every half-hour. When larger 
doses are. given, it must be administered when the stomach has been 
empty for some hours, and no fluid should be taken for some time after 
its administration ; my own experience has led me to rely upon the 
J-grain doses of ipecacuanha with sufficient morphine hypodermically to 
relieve the pain and restlessness* Ipecacuanha is markedly beneficial in 
children, combined with bismuth, chalk, or bicarbonate of soda. 

Hot fomentations or poultices over the abdomen are always grateful to 
the patient and are not contra-indicated. Finely pounded ice introduced 
into the rectum and ice-bags externally are recommended, but they have 
seemed to me to increase, rather than arrest the inflammatory process. In 
malarial dysentery, quinine must be given in full doses with the ipe- 
cacuanha, and when there is evidence of hepatic congestion one or two 
grain doses of calomel act beneficially. All treatment of malignant 
dysentery is unsatisfactory ; it is summed up in the treatment of symp- 
toms, and in supporting the patient with concentrated nutrition and 
stimulants. In the scorbutic variety, in addition to the opium and 

i Opium may, by semi-narcotism, mask the true picture of the disease, and sudden death may unexpect- 
edly occur when the friends regard the case as doing well. 

8 Ewart states that we possess in ipecacuanha "a non-spoliative antiphlogistic, a certain cholagogue 
and unirritating purgative, a powerful sudorific, and a harmless sedative to the heart and muscular fibres 
of the intestines.'" Quain's Dictionary, pp. 414-415. 



TYPHLITIS. 



309 



ipecacuanha, lemon and lime-juice, fresh vegetables and milk, and ripe 
fruit should be freely given. The "grape cure " has received a deserved 
reputation in the treatment of this variety. During convalescence iron, 
bark, and the mineral acids are indicated. 

Patients with chronic dysentery should reside in a mild, dry, equable 
climate, and wear flannel next the surface, especially over the abdo- 
men. With some a sea-voyage will effect a cure. The diet should be 
most carefully regulated ; each case is a law unto itself ; and the 
articles of diet can only be determined by trial. Astringents, as 
the acetate of lead, sulphate of copper and nitrate of silver, combined 
with small doses of opium, are recommended, but I have found the 
greatest benefit from the prolonged use of cod-liver oil and the pernitrate 
of iron. Quinine is recommended by East Indian physicians. 

TYPHLITIS. 

Typhlitis, sometimes called ei caecitis," although a catarrhal inflamma- 
tion of the caecum and vermiform appendix, might properly be classed 
under the head of intestinal ulcerations, since the inflammation of the 
mucosa is commonly accompanied by ulceration. 

Morbid Anatomy. — Typhlitis begins as an acute local catarrh of the 
mucous membrane of the caecum, which soon involves the submucous tis- 
sue ; the muscular coat loses its contractile power, so that the intestine 
becomes dilated and allows of large faecal accumulations, which are 
usually attended by ulceration of the mucous and submucous tissue. The 
faecal accumulation constitutes a typhlitic tumor. The catarrh may extend 
to the vermiform appendix, or an independent inflammation of the appen- 
dix may occur ; in either case it becomes dilated and forms a sac with 
thin walls, which is filled with a semi-transparent fluid. The termina- 
tions of the ulcerations which occur in the caecum are, 1st, rupture and 
general peritonitis ; 2d, an extension of inflammation through the intes- 
tinal walls to its peritoneal covering, and a local peritonitis ; 3d, exten- 
sion of the inflammation to the connective- tissue at the posterior wall of 
the caecum, where the peritoneum is wanting, and a consequent suppura- 
tion or adhesive cellulitis, which may bind the colon to the iliac fascia, 
and develop a suppurative " perityphlitis ; " or, 4th, adhesions may form be- 
tween the caecum and small intestine, matting them together, and binding 
them to neighboring organs. 

Etiology. — More than two-thirds of the cases of typhlitis are excited by 
the presence of foreign bodies, or by impaction of faecal matter, from mus- 
cular atony of the intestine, the result of the habitual distention accom- 
panying constipation ; bilious and intestinal concretions and masses of lum- 
brici sometimes cause it. It may also result from acute or chronic intestinal 
catarrh. It is most frequently met with in males from twelve to thirty 
years of age. 

Symptoms. — The premonitory signs of typhlitis are vague : sometimes 
there may be dull, uneasy pains in the right iliac fossa, usually of a distinct 



310 



DISEASES OF THE DIGESTIVE SYSTEM. 



colicky character, or a dull, heavy, dragging sensation ; diarrhoea of ten al- 
ternates with constipation ; the abdomen is more or less distended and tym- 
panitic. The faeces, for some time before the attack, will be described by 
the patient as hard round balls ; if it end in resolution, these symptoms 
gradually subside, and after a week or two the patient regains his former 
health. In some cases, these premonitory signs are absent. In either case, 
the actual symptoms begin with a severe pain in the caecal region and right 
hip, increased by pressure and by motion of the parts. On account of a 
loss in the contractile power of the muscular coat of the intestine, there is 
nausea and vomiting. At first, the contents of the stomach are ejected, 
then bilious matters, and finally (in some instances) the ejected matter is 
stercoraceous in character. The pain is often remitting ; the patient is 
most comfortable on the right side. With these symptoms there may be 
a slight rise in temperature, but this is not constant, nor does it follow any 
rule ; the temperature may rise to 102° or 104° F., accompanied by a pulse 
of 130 per minute ; with these symptoms the patient often suddenly passes 
into a condition of collapse. 

If recovery now occurs, the bowels will move spontaneously, and large 
quantities of faeces are discharged, accompanied by severe griping pains, and 
the typhlitic tumor may entirely disappear ; sometimes it remains, after 
copious discharges from the bowels, on account of the infiltrated state of 
the intestinal walls. This is called "chronic typhlitis." A local perito- 
nitis may remain after the typhlitis has disappeared, but if peritonitis has 
occurred, it usually subsides with the typhlitis. When peritonitis occurs 
it will mask the ordinary symptoms of typhlitis. 

Physical Signs. — Inspection may show a swelling in the right iliac fossa. 

Palpation discovers a superficial, sausage-shaped tumor just above Pou- 
part's ligament, its long axis pointing inwards and downwards, and some- 
times reaching laterally to the median line, and vertically to the free border 
of the ribs. It is tender, slightly movable, and may give a "gurgling " on 
pressure. It is not to be forgotten that in chronic typhlitis with peritonitis, 
the tumor loses its characteristic sausage-shape and grows broader. 

Percussion. — There is dulness on slight percussion over the tumor, and 
the limits of the tumor can be well defined. 

Differential Diagnosis. — If a typhlitic tumor develops slowly, it may be con- 
founded with other abdominal tumors, as ovarian, renal, cancerous and an- 
eurismal. But in all cases the latter are covered by the intestine, whereas 
typhlitic tumors are superficial. The perforating peritonitis of typhlitis may 
be mistaken for peritonitis from other causes, when it comes on suddenly, 
and a diagnosis is only reached by careful study of the previous history, 
which in typhlitis is characteristic. 

Prognosis. — The prognosis is always doubtful, but in the majority of cases 
favorable, statistics showing 75 per cent, of recoveries. The duration in 
severe cases may be only three days, and again it may continue for three or 
four weeks ; the average duration is from eighteen to twenty days. The 
peritoneal changes may be permanent. Typhlitis may be complicated by 
perityphlitis, peritonitis, periproctitis, perinephritis, faecal fistula, pylephle* 



APPENDICITIS. 



311 



bitis and thrombosis of the femoral vein. Death always occurs from some of 
the complicating conditions. 

Treatment. — Typhlitis demands prompt treatment. Leeches should be 
applied over the caecum, and followed by hot fomentations over the tumor. 
If there are no evidences of peritonitis, large enemata of tepid water may 
be administered, preceded by a full dose of castor oil; drastic purges should 
never be employed. If free evacuations from the bowels are obtained, the 
case soon terminates in recovery, for the swelling, which often goes on in- 
creasing afterward, is not due to faecal accumulation, but to a local inflam- 
mation. If there are evidences of local or general peritonitis, opium must 
be administered in sufficiently large doses to give complete relief from pain, 
and it should be continued until all signs of peritonitis have disappeared. 
If the bowels do not then move spontaneously, a full dose of castor oil may 
be given, followed by an enema of warm water. 

APPENDICITIS. 

Morbid Anatomy. — Primary inflammation of the appendix may be catarrh- 
al, ulcerative, or gangrenous. In the former case the cavity is distended 
by catarrhal or purulent inflammatory products ; its walls are tense and 
thinned. Simple ulceration seldom follows : the inflammation subsides 
or the appendix sloughs. Localized ulceration more commonly depends 
upon the presence of a foreign body, and is often followed by perforation. 
In either case a peritonitis is developed which agglutinates the adjacent peri- 
toneal surfaces. When perforation or sloughing has occurred, the resulting 
peritonitis may be local ; but if it become general the inflammatory prod- 
ucts are often encysted. Simple appendicitis may subside and leave no 
evidences save in adhesions of the appendix to the colon or pelvic wall. 

Etiology. — Catarrhal appendicitis may attend typhlitis or develop with- 
out obvious cause. The ulcerative and gangrenous forms are quite invari- 
ably, and the catarrhal often, excited by foreign bodies, small masses of 
inspissated faeces, fruit seeds, foreign bodies, worms, gall-stones, etc. 
Traumatism is occasionally the exciting cause, and straining — as in lift- 
ing or jumping — is the etiological factor in about 20 per cent, of the cases. 
It is most frequent in young male adults from fifteen to thirty years 
of age. 

Symptoms. — The earlier stages often pass entirely unnoticed. If any 
symptoms are present, they are either a slight localized pain and tenderness 
in the iliac fossa, or the symptoms just given as those of typhlitis without 
the sausage-shaped tumor. 

In such cases it cannot be distinguished at first from typhlitis. 

The symptoms which are diagnostic are, first, a sharp, sudden, intense pain 
localized in the iliac fosssa, but possibly extending to the navel, liver, or into 
the back. This is usually attended by nausea, vomiting, and chill. These 
symptoms mark the time of perforation or the advent of an acute peritonitis. 
Fever is the next most constant symptom, but the temperature is seldom 
above 103° F. and averages from 101° to 102° F. Micturition is often 



312 



DISEASES OF THE DIGESTIVE SYSTEM. 



disturbed, and there may be complete retention, possibly dependent upon 
the opium given to control pain. 

On physical examination a circumscribed tumor is detected, which is 
composed of inflammatory exudation. It is distinctly different from the 
tumor of typhlitis, being more oval, doughy, or fluctuating, and not sausage- 
shaped. Usually located in the iliac fossa, it may extend towards the 
median line or to the iliac crest. When the appendix has become adherent 
to the pelvic wall, it will be situated deeper, and best recognized by rectal 
examination. The tenderness of the parts renders an examination with 
an anaesthetic advisable in all cases. Fluctuation is a late rather than an 
early sign, and often can be obtained only by rectal examination. The 
tumor is dull as a rule, but gives a tympanitic note when covered by dis- 
tended intestines, or when the contents of the abscess are partly gaseous. 
The inflammatory products become fluid, and abscess is formed in from 
two to four days. The purulent products are usually encysted, and seldom 
invade the peritoneal cavity unless rupture has occurred. The course of 
these cases is exceedingly acute. Over 50 per cent, of deaths occur in the 
first week. 

Differential Diagnosis. — This is principally from simple typhlitis and 
perityphlitis. An early diagnosis is not always possible. Appendicitis, 
however, is usually insidious, and attended by few if any symptoms before 
its sudden and severe explosion. Then all the symptoms are intense, and 
the nervous shock is prominent. Typhlitis begins with mild but distinct 
symptoms of constipation, iliac lameness, and tenderness, and the sausage- 
shaped tumor, and there is no sudden and severe exacerbation until the 
condition is well established. When abscess has formed in appendicitis, 
rectal examination may differentiate the tumor from that of perityphlitis. 
Quite frequently the diagnosis cannot be made. 

Prognosis. — Eesolution may possibly take place, but is exceedingly 
rare. When perforation has occurred and is followed by general peri- 
tonitis, then death is almost inevitable, even when operative procedures are 
resorted to. 

Treatment. — When an exact diagnosis of appendicitis can be made before 
perforation, antiphlogistic measures locally, and opium internally, may be 
employed with the hope of arresting or limiting the inflammation ; but my 
experience leads me to the opinion that it is better to make an explorative 
incision as soon as there is reasonable evidence that appendicitis exists. 
After the advent of sudden pain, shock, and other symptoms of perforation, 
surgical measures employed before general peritonitis has developed offer 
the only efficient means of relief. 



PERITYPHLITIS. 



313 



PERITYPHLITIS. 

Perityphlitis is an inflammation of the connective- tissue which attaches 
the ascending colon to the iliac fascia, rarely extending beyond the region 
of the caecum. By some it is regarded as a form of peritonitis, and it has 
also received the name of pericecal abscess. In nearly all cases the inflam- 
mation is propagated from the caecum, the vermiform appendix, or the as- 
cending colon. It may occur as a primary inflammation from traumatic 
causes. 

Morbid Anatomy. — The ulcerative processes within the caecum are usu- 
ally accompanied by localized congestion of the peritoneum over it. Fre- 
quently the congested peritoneum is covered with a thin layer of partially 
organized lymph. The new connective-tissue formation binds together 
the appendix vermiformis and the caecum, and attaches either or both of 
them to the adjacent parts. When typhlitic ulceration extends into this 
new tissue a perityphlitic abscess is formed. In rare instances recovery 
takes place without an abscess. If an abscess forms, its seat is in the 
cellular tissue between the colon and quadratus lumborum, or in the cell- 
ular tissue between the iliac fascia and the caecum. Many perityphlitic 
abscesses are undoubtedly peritoneal abscesses. These abscesses are deep 
and irregular in shape, owing to the great resistance of the fascia in this 
neighborhood. 

The pus may infiltrate the connective-tissue as far up as the level of the 
eleventh rib, and reach the under surface of the liver, or may extend as far 
down as the rectum. It may burrow and point near the anus, or it may 
make a direct external opening in the groin or loin, or, as most frequently 
happens, it may perforate the adjoining wall of the caecum and be voided 
through the bowel and anus. After the pus has burrowed it may form a 
sinus or a series of sinuses which never become obliterated, although they 
grow smaller and smaller as time advances ; faecal matter may at times 
escape from such sinuses. In many instances a peri typhli tic abscess opens 
into the bladder. The pus may escape through the skin of the thigh, 
or it may perforate the peritoneal sac and induce general and quickly 
fatal peritonitis. In most cases peritoneal adhesions prevent the opening 
of the abscess into the peritoneal cavity. When the veins are pressed 
upon by the abscess there will be more or less oedema of the extremity. In 
some cases the inflammation does not assume an intense or acute form, but 
is rather sub-acute in character, and then its area is limited, and the ac- 
companying adhesions are firmer and more extensive. 

Etiology. — Perityphlitis is usually the result of extension of inflamma- 
tion from the vermiform appendix, or is secondary to a typhlitis. It may 
be due to the extension of tubercular, typhoid, or dysenteric ulcers in the 
caecum, and to the lodgment of foreign bodies in the vermiform appendix. 



314 



DISEASES OF THE DIGESTIVE SYSTEM. 



Caries of the spine or of the pelvis has induced it. Traumatism is an oc- 
casional cause ; it is rarely of spontaneous origin. 

Symptoms. — In a few instances of perityphlitis, especially those super- 
vening on typhlitis, there will be a history of colicky pains which radiate 
outward from the caecal region, with more or less irregularity in the ac- 
tion of the bowels. There is pain in the thigh, accompanied by numb- 
ness and a sense of formication in the right lower extremity, due to 
pressure of the tumor upon the nerves. This pain is deep-seated and 
much increased by flexing the thigh upon the abdomen. Eigors and fe- 
brile movement are usually slight. In extensive perityphlitis the patient 
cannot raise the right thigh, either on account of the pain, or from inter- 
ference with functions of the nerves from the pressure. When the abscess 
is of large size there may be oedema of the limb. The parts in the vicin- 
ity of the caecum are very tender to pressure, and the patient usually lies 
on the right side, with his thigh semi-flexed so as to relax the psoas and 
iliac muscles. As the abscess increases in size, there is in adults consti- 
pation, and a tendency to vomit. In children the bowels are commonly 
loose, and pain in the stomach will have been an early and prominent 
symptom. When a perityphlitis arises as a typhlitis is disappearing, a 
painful tumor, more deeply seated than in typhlitis, will make its appear- 
ance. 

Physical Signs. — Inspection reveals a tumor in the right iliac region, 
which may extend upward and to the left, as far as the umbilicus. In chil- 
dren the tumor is often elongated, reaching from the ramus of the pubis to 
the free border of the ribs. 

Palpation. — If suppuration has occurred, palpation may show the exist- 
ence of fluctuation over, and to the right of the tumor. In children 
these tumors sometimes have a brawny hardness. Careful manipulation 
shows the tumor to be deeply seated. 

Percussion may give a tympanitic resonance on account of the gaseous 
distention of the caecum, the tumor being behind this portion of the intes- 
tine. More often the percussion note has an obscure tympanitic resonance, 
for the caecum is either tumefied, or contains faecal matter. 

Differential Diagnosis. — Perityphlitis may be mistaken for typhlitis. In 
typhlitis there will be a history of colicky pains, dyspepsia, irregular action 
of the bowels, and tympanitis, all of which are present before a tumor is 
developed ; in perityphlitis a tumor is present before any other symptoms 
are developed. In typhlitis the pain is superficial and unaffected by the 
motion of the thigh, in perityphlitis it is deep-seated and increased by 
motion of the right thigh. There is no sense of numbness or formication 
in the right lower extremity in typhlitis, but this is more or less marked 
in perityphlitis. There is no evidence of suppuration (fluctuation), etc., 
in typhlitis, while evidence of fluctuation is present in perityphlitis as 
soon as suppuration occurs. The tumor of typhlitis is superficial and 
sausage-shaped, that of perityphlitis deep and irregular. A typhlitic 
tumor gives a flat percussion sound, a peri typhlitic tumor an obscure tym- 
panitic resonance. 



INTESTINAL ULCERS. 



315 



A psoas abscess has no intestinal symptoms, and the purulent discharge 
is of a very different character, lacking the faecal odor. Renal and ova- 
rian tumors will not be mistaken for perityphlitis if the early history of 
the case is carefully analyzed. 

Prognosis.— In the majority of cases in which the peritonitis is localized, 
and intestinal perforation does not occur, recovery takes place. If a peri- 
typhlitic abscess opens externally, or into the ascending colon, or if the 
pus burrows and points in the region of the thigh, buttock, or scrotum, 
the prognosis is more favorable than when it opens into the peritoneal 
cavity, or into the bladder. . If chills, hectic, emaciation, and extreme ex- 
haustion are present the prognosis is unfavorable. The average rate of 
mortality is about 25 per cent. If recovery from the primary attack 
occurs, there still may be narrowing of the intestine, or such alteration in 
the relative position of the parts that there will be more or less intestinal 
obstruction for the remainder of the individual's life. One of the most 
unfortunate sequelae of perityphlitis is the formation of a faecal sinus. 

Treatment. — The first and most important thing, after aspiration has 
determined the character of the tumor and shown the presence of pus, is 
to make an incision into the abscess, cutting cautiously through the 
abdominal wall at the seat of the swelling. Free drainage must be kept 
up by means of a drainage tube. Previous to the evidences of suppu- 
ration, leeches may be applied over the tumor, followed by warm poul- 
tices. Absolute rest is all important to the successful management of 
these cases. Some prefer to open at once, i. e., before fluctuation 
occurs. After an artificial or spontaneous opening, or after the occur- 
rence of absorption, care must be taken to avoid any pressure upon that 
part of the intestine for some time. The exhaustion from the suppura- 
tion must be combatted by iron and the vegetable tonics. The diet 
throughout should be highly nutritious and easy of digestion. Opium 
should be employed when the least indication of peritonitis, local or gen- 
eral, appears, and laxatives and purgatives must not be administered un- 
til the reparative processes are well established. 

INTESTINAL ITLCEKS. 

The Duodenal Ulcer. — The round or perforating duodenal ulcer may be 
regarded as the analogue of the peptic gastric ulcer. 

Morbid Anatomy. — This ulcer in its nature and appearance closely resem- 
bles the gastric ulcer, and its subsequent changes are the same. Its most 
frequent seat is the ascending portion of the duodenum, it is rarely found 
in its descending or transverse portions. Not infrequently duodenal and 
gastric ulcers coexist. The cicatrix which results from the healing of a 
duodenal ulcer may cause dilatation of the stomach, and of that portion 
of the duodenum between the cicatrix and the pylorus. This constric- 
tion and subsequent dilatation will induce chronic gastric and duodenal 



316 



DISEASES OF THE DIGESTIVE SYSTEM. 



catarrh. In rare cases the vena portae is completely obliterated by the 
constriction of a duodenal cicatrix, or the ductus communis may be oc- 
cluded, thus giving rise to obstructive jaundice. Atrophy of the pancreas 
has resulted from occlusion of the pancreatic duct, and in this connection 
it may be mentioned that duodenal ulcers near the head of the pancreas 
rarely, if ever, perforate. Another result is the formation of a fistula 
communicating with the gall-bladder. A duodenal ulcer may perforate 
the duodenal walls into the peritoneal cavity and cause peritonitis, or hav- 
ing perforated the walls of the duodenum it may involve the liver, pan- 
creas or gall-bladder, which becomes adherent to it at the seat of the 
ulcer. It may perforate directly outward at the seventh intercostal space, 
or indirectly outward after having first opened into the loose cellular tis- 
sue behind the bowel. Abscesses resulting from such perforation have bur- 
rowed through the mediastinum into the tissues of the neck and opened 
posteriorly near the shoulder-blade. 

Etiology. — Compared with gastric ulcers, duodenal ulcers stand in the 
proportion of one to thirty. The cause of the round duodenal ulcer is the 
same as that of round ulcer of the stomach. An embolus obstructs a ves- 
sel, or blood is extravasated, necrosis results, and the action of the intestinal 
juices rapidly establishes the ulcerative process, just as the gastric juice 
causes a gastric ulcer ; an ulceration resulting from burns is much more lia- 
ble to be duodenal than gastric. Duodenal ulcers occur more frequently 
in males than in females ; occasionally they are met with in children. 

Symptoms. — The symptoms of duodenal ulcers are obscure, the first and 
only symptom, in many cases, being a sudden and fatal peritonitis. When 
perforation occurs, it ordinarily takes place after a hearty meal, or from ef- 
forts made in vomiting or defecation. The patient rapidly passes into a 
condition of collapse, the face becoming " Hippocratic," the pulse small or 
imperceptible, the extremities cold, and suppression of urine often precedes 
the fatal issue. A fatal gastric hemorrhage has been the only sign of duo- 
denal ulcer. Pain is less pronounced than in gastric ulcer. The pain may 
be limited to the right hypochondrium, or it may be localized over the du- 
odenum. It commences from two to four hours after eating. The loca- 
tion of the pain and the time of its occurrence, are the diagnostic signs of a 
duodenal ulcer. It gives rise to intestinal hemorrhages more frequently 
than to peritonitis. If jaundice occur with these symptoms, it aids in its 
diagnosis. If the pancreas is secondarily enlarged and indurated, there 
will be a tumor in the right hypochondrium. 

Prognosis. — The prognosis is not as good as in gastric ulcers, for cicatriza- 
tion is not so likely to occur. Duodenal ulcers are to be treated in the same 
manner as gastric ulcers. 

Follicular Ulcers. — Though the morbid anatomy of this variety of in- 
testinal ulcers is almost inseparable from that of enteritis (q. v.), its symp- 
toms are distinct, and are better considered under a separate head. 

Symptoms. — Following a long-continued intestinal catarrh, especially in 
cachectic subjects, where the diarrhoeal discharges have been distinctly mu- 



INTESTINAL ULCERS. 



31? 



co-purulent, and have alternated with natural faecal discharges coated with 
blood and mucus, there will appear in the dejections transparent masses of 
mucus, looking like "boiled sago/'' and having the form of the conical- 
shaped ulceration of the follicles of Lieberkuhn. With follicular ulceration 
there is great emaciation and marasmus. In children, where this form of 
ulceration is often extensive, death often results from inanition. If long 
continued, there may be tormina and tenesmus, while the stools become 
uniformly opaque, puriform and yellowish white. If recovery takes place, 
the resulting cicatrices give rise to obstinate constipation. Death may 
occur from perforation, peritonitis, or from marasmus. 

Diffused Catarrhal Ulcers are never met with apart from acute enteritis. 

Morbid Anatomy. — Acute intestinal catarrh may be accompanied by a sup- 
purative process, which will cause the destruction of an irregularly circular 
portion of the intestinal wall, including the mucous, submucous, and often 
the muscular coats, and lead to perforating peritonitis. The margin of 
these ulcers is usually well defined. Their centres, which are irregularly 
depressed, contain a grayish shreddy mass ; between the ulcerated patches 
the mucous membrane is congested. If cicatrization takes place rapidly, 
stricture of the intestine at the corresponding point may result. If cicatri- 
zation takes place slowly, portions of the intestine will be matted together 
in coils, and will become more or less adherent to the adjacent organs.' 

Etiology. — The etiology of catarrhal ulcers is the same as that of catarrhal 
enteritis. They are especially liable to be induced by foreign bodies and 
faecal impaction. The condition occurs most frequently when an acute be- 
comes ingrafted on a chronic intestinal catarrh. The symptoms, prognosis 
and treatment are identical with those of chronic enteritis. 

Tuberculous Ulcers. — Under this head I shall consider the so-called "fol- 
licular " or strumous enteritis. 

Morbid Anatomy. — The caecum is the region which is most frequently 
the seat of these ulcers ; next the lower portion of the ileum. The large 
and small intestines are often equally affected. Peyer's patches and the 
solitary follicles are the primary points of invasion. At first they become 
swollen and congested, hyperplasia of their lymphatic elements causing nu- 
merous projections on the mucous surface. These projections are small, 
gray, translucent, elastic nodules, " the gray miliary tubercle." They usu- 
ally occur in isolated patches, but may become confluent over a consider- 
able portion of the intestine. After a time these gray nodules become 
yellow, dry, and cheesy, increase in size and constitute the "yellow tuber- 
cle," and afterward soften and form ulcers. 

The primary tubercular ulcer is a small, round, crater-like cavity, with 
indurated base and walls. Several primary ulcers in one Peyerian patch 
may be separated from each other only by thin septa, and then the 
patch presents a honeycomb-like appearance ; or several follicles form an 
elevated patch, which ulcerates in points. Diffuse inflammation of the 
submucous tissue occurs in the vicinity of these patches. The villi are 
matted together at their base, and free at their apex. Tuberculous ulcers 



318 



DISEASES OF THE DIGESTIVE SYSTEM. 



spread by the development of small fresh nodules in the walls of the 
blood-vessels, so that they extend transversely, sometimes forming girdles 
half an inch wide around the whole internal surface of the intestine. In 
this way the oval tuberculous ulcers outside of Peyer's patches have their 
^ „ : - - '•'^^^:^^r\ ax i g transversely. As these ulcers 

P^-~~~ "'•'^^^^^^/ > ^ \ i ncrease i 11 s * ze > tne y cause contraction and 

-43 narrowing of the calibre of the intestine. 



These ulcers rarely cicatrize and rarely 
fS^y^P^^I^J8f^tf|tJ cause hemorrhage or perforation of the 

intestine. If a tuberculous ulcer extends 
to the serous coat of the intestine, the lat- 
ter becomes thickened, reddened, and some- 
what clouded, and is covered with a fibrin- 
ous exudation which mats the intestines 
together. It is at these points that the peri- 
toneum is covered with minute tubercle 
granules. A more or less severe intestinal 
catarrh accompanies tubercular ulceration. 
The process may extend to the mesenteric 
glands, or these may be primarily involved, 
constituting what is called "tabes mesen- 
terica." 

Etiology. — As the primary manifest a- 
tion of tubercle it appears almost exclu- 
sively in children under five years of age, 
while tubercular inflammation of the 
intestines and mesenteric glands of adults 
is always secondary to tubercle else- 
where, especially pulmonary tuberculosis. 
The causes which in non-tubercular sub- 
jects would excite simple enteritis may in this class predispose to tuber- 
cular development. 

Symptoms. — The symptoms of tubercular intestinal ulceration are never 
diagnostic. Diarrhoea is its most constant symptom. Pain in many cases 
precedes the diarrhoea, which consists of thin green mucus, or more rarely 
is yeasty in character. Blood is not often present in the discharges. An 
inordinate desire for food is often a prominent symptom. There is early 
tympanitic distention of the abdomen, which causes it to become round 
and protuberant, and this pot-belly presents a marked contrast to the 
wasted chest and limbs. Ascites is sometimes present, and enlargement 
of the abdominal veins is quite common. The general health is much 
impaired, and there is progressive emaciation, although there are inter- 
vals of apparent improvement. The sleep is disturbed, and muscular 
twitchings and convulsions occasionally occur in children. During 
the whole course of this disease there is a continuous rise of a degree 
or two in temperature. When the end is near, the diarrhoea which has 




B. 

Fig. 65. 

Tubercular Ulcers of the Ileum. 

A. Mucous coat. 

B. Peritoneal coat. 



INTESTINAL HEMORRHAGE. 



319 



continued through the disease in many cases gives place to obstinate con- 
stipation. 

Physical Signs. — Palpation may reveal localized tenderness, especially 
about the caecal region. The enlarged mesenteric glands may sometimes 
be felt through the abdominal walls, although tympanitic distention often 
so interferes with the examination that they cannot be detected. 

Differential Diagnosis. — Tubercular disease of the intestine may be mis- 
taken for tubercular meningitis and tubercular 'peritonitis. The abdomen 
is distended in tubercular intestinal ulceration and retracted in meningitis 
There is constipation in tubercular meningitis, and diarrhoea in intestinal 
ulceration. Vomiting, projectile in character, is a marked and constant 
sign of tubercular meningitis, while vomiting is rare in intestinal ulcers, 
and when present is retching in character. The pulse is slower than nor- 
mal early in meningitis, while it is accelerated in tuberculous ulcer of the 
intestine. The pupils are normal in size in intestinal disease, and con- 
tracted or dilated in meningitis. 

Tubercular peritonitis is often associated with intestinal ulceration. If 
peritonitis exists, the abdomen is more rigid than in intestinal ulceration, 
the tenderness and paroxysmal pain are much more severe, and emaciation 
is not so prominent a sign or so progressive. Enlarged cervical glands are 
more frequent with ulceration than with peritonitis. 

Prognosis. — This is always unfavorable. It is essentially a chronic disease. 
Death may occur from exhaustion incident to the diarrhoea and maras- 
mus, or from intercurrent tubercular complications. 

Treatment. — The prophylactic treatment is similar to that of general tuber- 
culosis. If the diarrhoea is copious and exhaustive, astringents with opium 
may be employed. Inunctions of cod-liver oil and iodine may be made 
over the abdomen, which should be covered with a flannel bandage. When 
pain is severe anodyne poultices may be applied locally to relieve it. 



INTESTINAL HEMORRHAGE. 

Intestinal hemorrhage may be a symptom of local or of general disease. 
The bleedings may be slight when they are capillary, profuse when they 
come from vessels of considerable size. Blood from the stomach which is 
passed with the dejections cannot strictly be regarded as intestinal hemor- 
rhage. 

Morbid Anatomy. — At the post-mortem of one who has died during or 
soon after an intestinal hemorrhage the intestinal mucous membrane may 
be found either hyperaemic or anaemic, according as the hemorrhage has 
been slight or profuse. The intestinal canal will contain dark grumous 
blood or small clots. If the hemorrhage is caused by ulcers in the intes- 
tine, coagula generally adhere to the ulcers, and the edges and base of the 
latter are suffused with blood. In a few instances the mucous membrane 



320 



DISEASES OF THE DIGESTIVE SYSTEM. 



appears normal, especially when the hemorrhage is due to obstruction of 
the portal circulation. 

Etiology.— Any disease in which there is extensive obstruction to the 
portal circulation may be a cause of intestinal hemorrhage ; with the ex- 
ception of intestinal ulcers, cirrhosis or atrophy of the liver is its most fre- 
quent cause. It is a very frequent attendant upon typhoid and dysenteric 
ulcerations. Foreign bodies and traumatism act mechanically in producing 
it, and it may be induced by powerful chemical and mechanical irritants 
acting directly on the intestinal mucous membrane. It occurs in waxy de- 
generation of the intestine, and may be caused by the rupture of an aneu- 
rism into the intestinal canal. 1 It frequently attends the development of 
intestinal cancer, and is a common symptom of internal hemorrhoids. It 
occurs in yellow fever and in the pernicious malarial fevers, and a vicari- 
ous hemorrhage may take the place of the menstrual discharge. Subsidence 
of the fiery-red tint of the face in erysipelas has been followed by remit- 
tent intestinal hemorrhage. Chronic constipation and the pressure of large 
tumors may cause it by impeding the venous return. It has occurred in a 
few cases of intestinal invagination and with embolism of the mesenteric 
artery. It is a common symptom in purpura hemorrhagica, and in that 
condition known as haemophilia. Acute yellow atrophy and splenic leuco- 
cythaemia may be attended by intestinal hemorrhage. Those affected with 
a scorbutic or syphilitic taint are always predisposed to it. It occurs oft- 
ener in men than in women. The aged are subject to a passive intestinal 
hemorrhage, without apparent cause. 

Symptoms.— If the hemorrhage is slight it frequently passes unnoticed, 
for it gives rise to no symptoms. When it occurs in dysentery, typhoid and 
yellow fevers, the symptoms which attend it will vary with the amount, num- 
ber and persistence of the bleedings as well as with the stage of the disease in 
which it occurs. Its color will be determined by its seat and the length of 
time it remains in the intestinal canal. When it comes from the upper 
portion of the intestinal tract, it is of a dark red color, grumous and tarry, 
when its seat is near the rectum it is of a bright red color and fluid. The 
tarry color and consistence given to the faeces by the presence of blood is 
called " nielaena." 

The symptoms which attend a large intestinal hemorrhage are a feel- 
ing of faintness, a feeble pulse, a deadly pallor, ringing in the ears, bright 
flashes before the eyes and coldness of the surface, followed by syncope 
which may end in death. Immediately following or preceding these 
symptoms there may be a large discharge of blood from the bowels. In 
most instances, after a few hours the patient recovers from the shock 
of the hemorrhage. There may be abdominal pain at the time of the 
hemorrhage, accompanied by a sensation as if warm water was being 
poured into the abdominal cavity. A continuation or succession of large 
hemorrhages will rapidly give rise to the characteristic signs of anaemia. 



i Bamberg places diphtheritic inflammation of the intestines as its second most frequent cause, dys- 
entery being the first. 



INTESTINAL OBSTRUCTION. 



321 



If the normal dejections are coated with blood, the origin of the hemor- 
rhage is within the large intestine. When the hemorrhage is from intes- 
tinal ulcers, pus will be mingled with the blood. Intestinal hemorrhages 
may cause death when there has been no discharge of blood from the 
,-inus. 

Differential Diagnosis.— The diagnosis of intestinal hemorrhage is not dif- 
ficult, it is usually made by the patient. Its source can only be determined 
by a careful history of the case. In acute infectious diseases its seat is in 
the small intestine ; in chronic disease it usually has its seat in the large 
intestine. When diseases of the liver can be excluded, local causes in the 
rectum should be sought for. 

Prognosis. — The prognosis will depend upon the seat and cause of the 
bleeding. In yellow, typhoid and malarial fevers, in dysentery and cirrho- 
sis, it is always unfavorable. Arterial hemorrhages are far graver than 
capillary. The condition of the patient at the time of the hemorrhage 
influences the prognosis. It is less dangerous in vigorous than in feeble 
and anaemic subjects. Death may occur from a single large hemorrhage, 
or from the asthenia produced by repeated smaller bleedings. 

Treatment. — The first, and perhaps the most important, indication is ab- 
solute rest. The patient should be kept in bed in a cool, quiet room, and 
should not be allowed to change the position of the body. Peristalsis must 
be arrested by opium ; fluid nourishment should be given at short intervals 
and in small quantities. Cold compresses or ice-bags should be placed over 
the abdomen, and styptics should be administered by the mouth or by the 
rectum, according to the supposed seat of the hemorrhage. Alum -whey, 
perchloride of iron, acetate of lead, tannin, or any of the haemostatics may be 
given by the' mouth or rectum. Ergot internally or ergotine hypodermatic- 
ally should be administered in sufficient quantities to produce the physio- 
logical effect of the drug. When the bleeding has been excessive, stimu- 
lants—alcohol, ether or musk— should be administered, and it may be 
necessary to practice transfusion. Everything taken by the patient by 
the mouth or rectum must be ice-cold. The use of the mineral acids as 
beverages has been advocated. No irritating food or drinks should be 
allowed for many days after all signs of hemorrhage have ceased. If 
intestinal hemorrhage occurs in one who gives the evidence of purpura or 
haemophilia, the salts of iron or potassa, combined with vegetable acids, 
are serviceable. 



INTESTINAL OBSTRUCTION. 

By the term intestinal obstruction is meant a narrowing, closure, invagi- 
nation, or twisting of some portion of the intestine, so that its calibre is 
diminished and the passage of its contents retarded or prevented. In all 
cases there is a mechanical impediment situated either within or without, 
or in the wall of the intestine. When a foreign body prevents the onward 
progress of the contents of the intestines, by becoming an actual plug, the 



322 



DISEASES OF THE DIGESTIVE SYSTEM. 



obstruction is said to be within the intestine ; when some abdominal tumor 
presses on, and narrows almost to closure, some portions of the bowel, it is 
said to be without the intestine ; and when a deep ulcer, involving the whole 
wall of the intestine, contracts and forms a stricture, or other changes take 
place in its walls which diminish or obliterate its calibre, it is said to be in 
the intestinal walls. It is impossible to separate the etiology of intestinal 
obstruction from its morbid anatomy, and they can best be considered to- 
gether. 

Morbid Anatomy. — I shall first consider intestinal obstruction from causes 
which have their seat in the wait of the intestine. In this group stricture 
and intussusception are the chief lesions. Intussusception, or invagination, 
consists in the descent or prolapse of a portion of the intestine into that 
which immediately succeeds it, like a glove-finger drawn partially within 
itself. It always occurs from above downward. In this condition the two 
mucous and the two serous surfaces are opposed to each other, so that a 
section exhibits three cylinders, one within the other, called respectively — 
the receiving layer, the entering layer, and the returning layer. Sometimes 
the intussusception is lateral and partial. The me- 
sentery belonging to the invaginated portion lies 
between the middle and internal layers. By the 
traction of the mesentery, the central part of the in- 
testine is curved laterally. Invagination which occurs 
during the last moments of life is unimportant ; it is 
chiefly found in children who die of brain disease. 
The occurrence of intussusception is regarded by most 
as the result of the sudden passage of a spasmodically 
contracted portion of the intestine into a flaccid 
or paralyzed portion. An exaggeration of the 
normal peristaltic wave can produce it, especially 
when there is great gaseous distention of the in- 
testine. Some observers state that it is the par- 
alyzed portion which is thrust forward by a sudden 
increase in peristaltic action of the intestine. 

Its most frequent seat is in the neighborhood of the ileo-cascal valve. It 
may occur in any portion of the intestine. The whole colon may be filled 
by the ileum, and the latter may even project outside of the anus. It is 
more common in the young ; 50 per cent, of all the cases occur in child- 
hood. Males are more subject to it than females. 1 The mucous membrane 
of the invaginated portion is intensely congested, its villi are swollen, soft- 
ened, friable, and sometimes united by a pseudo-membrane. The single and 
theagminated glands are hypertrophied, infiltrated with fluid, and ulcerated 
at the centre. The sub-serous cellular tissue is infiltrated with blood, and 
is ecchymotic. The intestine above the obstruction, when the latter has 




Fig. m. 

Diagram Illustrating Intus- 
susception. 

M. Mucous surface of intestine. 

A. Entering layer. 

B. Returning layer. 

C. Receiving layer. 



1 In the Croonian Lectures, 1857, intussusception appears to be ileo-caecal in 50 per cent., iliac in 28 
per cent., jejunal in 4 per cent., and colonic in 12 per cent. 



INTESTINAL OBSTRUCTION. 



323 



existed for some time, is dilated. In many cases there is more or less 
twisting besides the invagination. Sometimes blood extravasates into the 
mucous tissue and into the mesentery. The invaginated portion may 
become gangrenous, slough, and be discharged per rectum. During the 
sloughing the peritoneal cavity may be opened. 1 In the neighborhood of 
the obstruction the mucous membrane may be the seat of intense catarrh. 
Sometimes the intussusception is restored. Polypoid growths in the rectum 
or sigmoid flexure, besides inducing intussusception, may themselves cause 
intestinal obstruction. 

Other common causes in the intestinal wall which induce obstruction are 
cancerous and non-cancerous stricture. These diminutions in the calibre 
of the intestine may be due either to contraction of cicatrices, or to infiltra- 
tion of the intestinal walls. Such obstructions are developed gradually, 
and are rarely complete. Intestinal stricture may be merely a thin fold of 
mucous membrane, or four or five inches of intestine may be included. 
Above the stricture there is well-marked dilatation and hypertrophy ; below, 
atrophy of the intestine. The accumulation of matter above a stricture 
often leads to ulceration and perforation. About seventy-five per cent, of 
all strictures are in the large intestine, and most of these are in the rectum. 
About half of all intestinal strictures are of cancerous origin. Congenital 
stricture is a surgical disease. 

Intestinal obstruction may, secondly, have its cause outside the wall of the 
intestine. Folds of the intestine may be caught in bands of adhesion formed 
by an old peritonitis, or may be forced through openings in the abdom- 
inal walls and become strangulated, causing internal or external hernia. 
The small intestine is strangulated by hernise, diverticula, and bands of 
new formation, more frequently than the large intestine. Internal 
strangulation occurs oftener in men than in women. It may occur at 
any age, although it is met with most frequently in those about thirty. 
Volvulus or twisting of the intestine may occur, so as to produce in- 
testinal obstruction ; the mesentery or a coil of intestine may be the 
axis about which certain parts revolve. Again, a coil of intestine may, 
with another, form a knot. Both of these occurrences are most frequent 
about the sigmoid flexure. An abnormally relaxed mesentery predisposes 
to it. Half a turn is sufficient to cause obstruction. In the old the sig- 
moid flexure may become twisted, by shrinking of the mesentery. Any 
abdominal tumor may induce by pressure more or less diminution in the 
calibre of the intestine and intestinal obstruction. 

The third class of causes which give rise to intestinal obstruction 
are situated within the intestinal canal. Under this head are included 
obstruction from gall-stones, impacted fasces and foreign bodies of various 
kinds. Gall-stones are most frequently impacted in the ileum near the 
ileo-caecal valve and in the duodeno-jejunal region. The larger and thin- 
ner the calculus, the more liable is obstruction to occur. In some cases 



1 In one instance the whole of the caecum and ascending colon sloughed away, and recovery took 
place.— Guy's Hosp. Reports. 



324 



DISEASES OF THE DIGESTIVE SYSTEM. 



gall-stones cause a fatal obstruction, but usually the obstructions continue 
only for two or three clays. Gall-stones of immense size have been found 
completely plugging an intestine. These obstructions rarely have their seat 
in the large intestine and are met with more frequently after fifty years of 
age, and in females oftener than in males. 

Hardened faecal masses mixed with the phosphate of magnesia and lime, 
concretions of chalk and magnesia, ammonio-magnesian phosphate, inspis- 
sated mucus, and large oyal masses consisting chiefly of cholesterin, are 
among the commoner forms of the so-called "enteroliths." Concretions 
of hardened faeces rarely cause fatal obstruction. The list of foreign bodies 
which have caused intestinal obstruction is very large, but they all act in 
the same way. 

The changes which follow all forms of intestinal obstruction, are dila- 
tation of the intestine above, and atrophy below, the seat of the obstruc- 
tion. The peritoneum over the site of the obstruction is the seat of acute 
or chronic peritonitis. Gangrene may occur at the point of greatest press- 
ure. There is always more or less extensive intestinal catarrh in every 
case of intestinal obstruction. 

Symptoms. — The symptoms of intestinal obstruction vary with its seat, 
extent, and cause. The symptoms which are common to all varieties 
are obstinate constipation, and vomiting. The matters vomited consist 
first of the contents of the stomach, then mucus, and after a time bile 
and stercoraceous matter. The accompanying pain varies in character 
and intensity : sometimes it resembles that of a colic, sometimes that of 
peritonitis. When the obstruction is low down there is tympanitis. When 
the upper part of the small intestine is obstructed there is hiccough. Ac- 
companying these symptoms there is prostration and often collapse. The 
skin is cold and the countenance assumes an Hippocratic expression. In 
a few cases, portions of the intestine that have become invaginated can 
be seen projecting from the anus. A careful analysis of these prominent 
symptoms will often enable one to determine the seat and character of the 
obstruction. When gall-stones and other foreign bodies or intestinal 
worms obstruct the intestine, constipation will come on suddenly. 

In intussusception, constipation does not occur suddenly, for thin liquid 
faeces are able to pass the narrowed orifice. When invagination occurs in 
the small intestine, the discharges are accompanied by a copious flow of blood. 
But when the lower bowel is invaginated the blood is mingled with the dis- 
charges, and they are dysenteric in character. When intussusception be- 
comes chronic, diarrhoea may develop and become exhausting, especially 
in children. When sloughing occurs gangrenous masses mingled with 
mucus and blood will be discharged. 

If thin bands of faeces are passed, it indicates the existence of an in- 
complete stricture of the large intestine. Slow but steadily increasing 
constipation, the bands of the faeces becoming gradually smaller, indicates 
the growth of a stricture or the enlargement of a tumor compressing the 
intestine, If obstruction occurs suddenly, the rectum retains its contrac- 



INTESTINAL OBSTRUCTION. 



325 



tile power and is empty, while if the obstruction comes on gradually it is 
patulous. Vomiting is present in most cases ; when the obstruction is 
high up the vomiting is bilious, and occurs within an hour or two after its 
occurrence ; when near the caecum, the obstruction is accompanied by 
faecal or stercoraceous vomiting ; when low down, two or three days may 
elapse before the vomiting occurs. In the so-called chronic forms of 
obstruction, vomiting occurs at intervals, and is more persistent the higher 
the obstruction. Copious stercoraceous vomiting is evidence that the 
obstruction is at the ileo-caecal valve. 1 In children vomiting occurs very 
readily, and, with the pain, is the first well-marked sign of the obstruc- 
tion. When gall-stones are lodged high up, vomiting comes on early and 
continues until death occurs, or the stone is dislodged. 

Enteroliths usually give rise to typhlitic symptoms. The pain which 
accompanies or precedes the vomiting is colicky or paroxysmal at first, after- 
ward it becomes constant and severe. Sometimes patients can locate the spot 
where the pain originates, at other times it resembles a stitch in the side. 
When the constriction has come on slowly the pain resembles that of ordi- 
nary colic. If the small intestine near the caecum or jejunum is strangulated, 
there is pain in the region of the umbilicus. When the colon is obstructed 
the pain is located at the seat of the obstruction. Pain in the groin or in 
the left iliac fossa indicates obstruction at the sigmoid flexure. There is 
usually no tenderness at the onset. When tenderness, local or diffuse, is 
extreme, peritonitis is indicated. 

In all cases except those where the obstruction is near the duodenum, the 
abdomen gradually becomes distended from gaseous accumulation in the 
intestine above the seat of the obstruction, — tympanitis. It occurs first near 
the obstruction. When twisting of the intestine occurs the portion consti- 
tuting the loop often forms a tympanitic tumor. The tympanitic note is 
readily elicited as the abdominal muscles become rigid. Vomiting relieves 
the tympanitis to a greater or less degree. The higher the obstruction 
the greater the relief from the vomiting. 

Intestinal cancer, large gall-stones, faecal masses, and other abdominal 
tumors which gradually compress the intestine may usually be accurately 
located and definitely mapped out. Invagination sometimes gives rise to a 
soft, sausage-shaped tumor, which can be distinctly felt, especially when it 
occurs at the caecum. In intussusception of the small intestine a central 
tumor may often be felt near the umbilicus. If invagination occurs low 
down, the slit-like opening in the in vagina-ted portion may be felt per rec- 
tum. Faecal tumors along the line of the colon are quite distinct on pal- 
pation, and, while firm, continued pressure gives no pain, their situation 
and form may gradually be altered ; attention to these points will prevent 
mistaking faecal for malignant tumors. 

Percussion over these tumors elicits dulness corresponding to their extent. 
If the obstruction is in the duodenum, there is an almost total suppression 

5 Brinton suggests that a double current is produced ; the intestinal contents are propelled along the 
wall of the intestine until they meet the obstruction, and then a return current passes up in the centre of 
ine intestine. This retrograde movement continues until the vomited matters are the same as those at the 
seat of the stricture. 



326 



DISEASES OF THE DIGESTIVE SYSTEM. 



of urine ; when in the jejunum or ileum, there is marked diminution ; 
but when the lower bowel is occluded the flow is abundant and limpid. In 
many cases of intestinal obstruction there is a sudden shock at the time of 
its occurrence, similar to the shock in peritonitis ; this is often followed by 
symptoms of collapse. During the whole course of intestinal obstruction, 
the temperature is rarely elevated. If the obstruction is complete, the face 
becomes " drawn," the extremities and the surface cool, the pulse rapid 
and small, the patient lies on his back with the knees flexed, and carefully 
avoids movements which induce pain and vomiting. Later on symptoms of 
collapse are developed, the breathing becomes rapid and superficial, thirst 
is intense, the voice is husky, the pulse becomes imperceptible, and the 
patient dies as in collapse, from peritonitis which will be found in most 
cases after death. If the obstruction is in the small intestine hiccough is 
a constant and annoying symptom. The mind is undisturbed to the 
last. In slowly developed intestinal obstruction, as in cancer-strictures 
and compression from tumors, the patient loses flesh and strength, becomes 
anaemic and melancholic, and the countenance bears the aspect of one 
suffering from malignant disease. Torsion or twisting of the intestine 
is attended by acute and rapidly fatal enteritis. 1 In these cases all the 
symptoms of severe enteritis are present. 

Differential Diagnosis. — It is important in every case to determine the seat 
and cause of the intestinal obstruction. Intussusception occurs most fre- 
quently in children, it begins suddenly with intense colicky pains, and there 
is blood mingled with the scanty mucous discharges. Faecal vomiting occurs 
early, and there is commonly a distinct tumor, firm pressure on which some- 
times relieves the pain ; in a few cases the invagination may be determined 
by a rectal examination. The patient rapidly passes into collapse. When 
this train of symptoms occurs suddenly in a child, previously healthy, and 
without appreciable cause, intussusception may be suspected. 

Internal hernia occurs suddenly. The pain is fixed at one point and 
paroxysmal in character, faecal vomiting comes on after a few hours, accom- 
panied by obstinate constipation and rapidly developing tympanitis ; in a 
day or two the patient may pass into a state of collapse. The large in- 
testine is usually empty. In a few cases the patient will have "felt some- 
thing give way in the abdominal cavity." Its symptoms resemble those of 
an external strangulated hernia and intussusception combined. 

Twisting, volvulus, and the sudden incarceration of loops of the intestine 
under bands of adhesion or diverticula are attended by similar symptoms. 

Foreign bodies usually have their seat in the caecal region and give rise 
to typhlitic tumors. When gall-stones are the cause of the obstruction 
there is usually a history of hepatic colic, and the seat of the obstruction is 
high up ; this will be indicated by the vomiting and urinary suppression. 

Obstruction from cicatrices, and from the pressure of tumors is of slow 
growth, there will be the history of frequent attacks of constipation, gradu- 
ally increasing in duration and severity, coils of distended and displaced 



1 Bristowe supposes the enteritis may occur first, may weaken the parts, and that the volvulus is a 
secondary phenomenon. 



INTESTINAL OBSTRUCTION. 



327 



intestine are easily detected, the centre of the abdomen has a doughy feel, 
and a tumor can often be made out. 

Intestinal obstruction may be mistaken for colic (or enter algia) peri 
tonitis, external hernia, acute poisoning (as from arsenic, antimony, etc.), 
hepatic or renal colic, and enteritis. In colic the discharges from the 
bowels will be normal, or there may be diarrhoea. In intestinal obstruction 
there is obstinate constipation. The pain of colic is of short duration and 
is usually relieved by pressure, while in intestinal obstruction the pain is 
persistent and as a rule not relieved by pressure. Faecal vomiting, tympani- 
tis, and symptoms of collapse are present in obstruction and absent in colic. 

Peritonitis is attended by a rise in temperature, by great tenderness on 
pressure, by a tense, hard, wiry pulse, and by rigidity of the abdominal 
walls ; while obstruction, if it begins with colicky pains, is soon attended 
by faecal vomiting, the pain is localized, there is a sub-normal temperature 
and more distention of the abdomen. 

Internal hernia may be confounded with femoral or inguinal hernia ; a 
careful examination of the inguinal regions and the history of the case are 
usually sufficient to establish a diagnosis. 

In cases of acute poisoning there will be evidences in the mouth and phar- 
ynx of the action of an irritant poison ; the gastric symptoms, especially the 
sense of heat in the epigastrium, will be marked ; there will be diarrhoea, no 
faecal vomiting, no tympanitis, and the vomited matters will contain traces of 
the poison. 

In hepatic colic the pain is persistent and radiates from the region of the 
gall-bladder to the back. There is no faecal vomiting and no tympanitis, 
but the stools are clay-colored, and the calculus may be detected in the 
fasces after the attack ceases. The urine contains bile, and if the attack is 
prolonged jaundice occurs. 

In renal colic the bowels are normal, the pain shoots from the back down 
the ureter to the end of the penis, and the testicle on the affected side is re- 
tracted. Eelief immediately follows the passage of the calculus into the 
bladder, which is followed by a copious flow of bloody urine ; in intestinal 
obstruction there is no haematuria, no symptoms referable to the urinary or- 
gans, the bowels are constipated, and there is tympanitis and faecal vomit- 
ing. 

Enteritis is distinguished from intestinal obstruction by copious mucous 
discharges from the bowels, by the rise in temperature, and the absence of 
faecal vomiting, excessive tympanitis, and the symptoms of collapse. 

Prognosis. — The length of time for which an intestinal obstruction may 
exist before causing death varies with its seat and its character ; a weak child 
may die in eight or ten hours from the shock of intussusception, and an 
adult whose intestine is gradually being occluded by the presence of some 
slow-growing tumor, may live for months. As a rule, the nearer the stom- 
ach the obstruction, the more rapidly death ensues. Volvulus, strangula- 
tion, internal hernia of the small intestine, and obstruction by large gall- 
stones and enteroliths induce death more rapidly than stricture, compres- 
sion, and intussusception, especially of the large bowel. Intussusception 



328 



DISEASES OF THE DIGESTIVE SYSTEM. 



may be recovered from when a gangrenous process throws off the in vagina* 
ted portion, and it is possible for it to slip back into its normal relations. 
The prognosis is favorable in intussusception when a portion of the invagi- 
nated bowel is discharged. It is better, the lower the seat of the obstruc- 
tion. Of all forms of obstruction, faecal tumors are the least grave. The 
complications of intestinal obstruction are enteritis, with or without per- 
foration, septicaemia, phlebitis, ulceration and gangrene within the canal, 
and perforation of the intestine above the stricture. After recovery from 
the primary obstruction, the attending peritonitis may cause permanent 
constriction of the intestine. Another sequela is the formation of internal 
fistulae. 

Treatment. — Whenever there is reason to suspect intestinal obstruction 
of a non-faecal origin, free catharsis should be avoided. It is better not to 
relieve a simple constipation, than to attempt to force faeces through an 
internal hernia. Whatever may be the seat or character of the obstruction, 
the therapeutical indications are the same, whereas a knowledge of the site 
and variety of the obstruction is demanded before surgical interference 
should be resorted to. Eest is demanded in every case ; hence opium is to 
be given in sufficient quantities to relieve pain. The more sudden and 
severe the onset, and the more urgent the symptoms, the more serviceable 
is opium. The condition of the patient alone regulates the quantity to be 
administered. 

Nourishment should be given per rectum in the form of defibrinized 
blood, and peptonized fluids. Each injection should contain from three to 
five grains of chloral, to retard decomposition. Ice may be given to relieve 
the thirst. If the tympanitis is excessive, it may be relieved by aspiration, 
or by the introduction of a tube into the colon. Instead of ice, warm com- 
presses seem to relieve the pain and soreness, but they have no other value. 
There is no objection to saline laxatives in stricture or in compression, 
where, though not wholly occluded, the intestine is gradually narrow- 
ing, and only a small opening remains through which liquid faeces can 
pass. 

When the obstruction is faecal, opium should not be given ; the bow- 
els should be acted on by those drugs Avhich produce copious watery 
evacuations without drastic action ; at the same time the rectum must be 
emptied by mechanical means, or by enemata of warm water and glycerine. 
Much patience is often required to remove these faecal obstructions. The 
most efficient method of mechanically overcoming obstruction is to make 
large injections of warm water through long rubber tubes, which must be 
inserted as far as possible. In order, however, to overcome by enemata an 
obstruction situated high up, the patient must be brought under the influ- 
ence of ether or chloroform, and during the administration of the enema 
careful manipulation of the bowels must be practised. Taxis is to be prac- 
tised according to the rules which surgery lays down for the reduction of 
hernia. Instead of warm water, air and gas have been injected in order to 
distend the intestines. Whatever injection is employed, it should be thrown 
in very slowly, and in very large quantities. It has been suggested to de- 



WAXY DEGENERATION OF THE INTESTINES. 



329 



velop gas inside the patient by successively injecting solutions of soda 
bicarbonate and of tartaric acid ; rupture of the intestine may result from 
such a procedure. Before injections are given or taxis practised, it is well 
for the patient to take a prolonged and moderately hot bath. As an aid to 
the reduction of an intestinal obstruction, the hips may be elevated or the 
patient may assume the knee-elbow position. The use of the constant cur- 
rent is advocated by some, to produce active peristalsis ; this must not be 
resorted to unless there is no danger of exciting peritonitis by the active 
peristalsis. If the long tube is used for the purpose of giving injections, it 
must be introduced with the utmost care, for perforation has been caused 
by its careless introduction. 

If at any time symptoms of collapse come on, alcoholic stimulants, musk, 
ammonia, etc., should be freely administered. As regards surgical meas- 
ures, colotomy and laparotomy are the proceedings which have been pro- 
posed. The mortality after laparotomy is not exactly known, some statistics 
showing 6S per cent., others 73 per cent., and still others 75 per cent, of 
deaths. Laparotomy is especially applicable in acute intussusception, and 
should be performed with as little delay as possible. The dangers from co- 
lotomy seem to be less than those of any other operation. The statistics of 
lumbar colotomy exhibit the low rate of 33 per cent, of deaths. Laparo- 
enterotomy has a mortality-rate below sixty, but concerning laparo-colot- 
omy, laparo-typhlotomy, etc., the number of operations is too small to give 
reliable statistics. 

WAXY DEGENERATION OF THE INTESTINES. 

Statistics show that after the kidney, spleen, and liver, the intestines are 
most frequently the seat of waxy degeneration. 

Morbid Anatomy. — The primary seat of amyloid change in the intestines 
is in the arterioles. The small intestine is more often involved than the large. 
The mucous membrane is pale, shining, and slightly cedematous ; on the 
application of the iodine test small maroon colored spots appear in the villi, 
where the earliest changes occur ; later the muscular coat is involved, and 
finally the entire wall of the intestine is fused into a homogeneous mass. 
Peyer's patches are less affected than the surrounding tissues, but there is 
annular infiltration about the solitary glands. 

Etiology. — Its causes are all those conditions which predispose to waxy 
changes in other organs. It is usually a late complication of waxy kidney 
and liver. 

Symptoms. — Its symptoms are masked by those of waxy liver and kidney, 
with which it is always associated. When general amyloid degeneration of 
the entire intestinal canal exists, the nutritive disturbances are great ; ex- 
haustion, emaciation, and anaemia are more marked than in any other con- 
dition. The countenance, the appearance of the skin, and the other consti- 
tutional symptoms are identical with those of waxy liver and kidney, but 
in addition to these there is a serous diarrhoea which is persistent an£ 
exhausting. 



330 



DISEASES OF THE DIGESTIVE SYSTEM. 



Differential Diagnosis. — The diagnosis is made by the presence of diar 
rhcea associated with the evidences of waxy changes in other organs. 

Prognosis. — This is very unfavorable ; more so than when the amyloid 
change is confined to other organs, for it indicates that the changes which 
usually precede a fatal termination have already occurred in those organs. 

Treatment. — The treatment is altogether palliative ; the diet should be re- 
stricted to meat and milk taken in small quantities and at short intervals. 
In addition to the general constitutional treatment of waxy degeneration, 
the diarrhoea may be checked by the vegetable astringents — haematoxylon, 
tannin, and catechu, or when these fail, the mineral astringents can be 
given. Iodide of potassium and iron will be found especially beneficial in 
these cases. 

CANCER OF THE INTESTINE. 

Carcinoma is the most common variety of intestinal neoplasm. It is less 
frequent than carcinoma of the stomach, and is almost always primary. In 
rare instances, it may be secondary to cancer of the peritoneum, uterus, or 
bladder. It almost exclusively affects the large intestine ; the rectum is 
its most frequent seat, then the anus, the caecum, the sigmoid flexure of 
the colon, and lastly the duodenum and jejunum. 

Morbid Anatomy. — The primary development of intestinal cancer is com- 
monly in the mucosa and extends into the submucous connective-tissue ; 
the infiltration extends in a ring around the intestine. Sometimes its 
primary development is in the epithelium of the follicles. It may involve 
an inch or three or four inches of the intestine. In any case it causes 
more or less diminution in the calibre of the intestine ; the intestinal wall 
becomes infiltrated and ulceration may bs established, which will destroy 
the mucous membrane covering the cancerous mass, and temporarily re- 
move the intestinal obstruction. Frequently cancerous masses project from 
the anus looking like cutaneous growths about its margin, or they may 
project from the anus in the form of fungous masses. 

Before ulceration occurs scirrhus cancer presents a smooth, nodulated 
surface ; encephaloid is soft, vascular, and often forms a tumor or series of 
tumors projecting into the intestine ; these tumors are round, lobuiated or 
villous. Often where the upper part of the rectum seems to be the seat of 
cancer, the disease will be found to have its seat at the sigmoid flexure, 
which has been pushed down into the pelvis, as the result either of the 
obstruction which it has caused, or of its own weight. 

When ulceration occurs, fungoid masses may spring up upon the elevated 
surface and lobuiated tumors may rapidly develop, or a smooth excavation 
may be foimed, with hard, well-defined edges. Cancerous ulcerations may 
extend through the intestinal walls, and cause peritonitis or fsecal abscess, 
or establish communication with the bladder, urethra, uterus, vagina, or 
with other portions of the intestine. Scirrhus, more often than either of 
the other varieties, produces stricture of the intestine. In a few cases both 
large and small intestines are studded with small cancer-nodules, whose fa- 
vorite locality seems to be the Peyerian patches. In any form of cancer, 



CAKCER OF THE INTESTINE. 



331 



especially scirrhus, there may be great distention of the intestine above the 
seat of the cancer. There may be catarrh of the intestinal mucous mem- 
brane above and below the seat of the cancer. In cancer of the rectum the 
disorganization may be so rapid and extensive that dilatation occurs at the 
site of the cancer. Stricture, hemorrhage, perforation, fistulae, and matting 
together and deformity of the organs in the neighborhood, are common 
pathological sequelae of intestinal cancer. The neighboring lymph glands 
are always more or less involved. If cancer commences outside of the in- 
testine and extends inward, it will be most extensive along the line of the 
attachment of the mesentery. The loose tissue around the rectum, cae- 
cum, or duodenum may be so extensively infiltrated that the intestine 
within is merely a narrow rigid channel. 

Etiology. — Intestinal cancer is rare before thirty, and more frequent be- 
tween forty and sixty. Sex has no marked influence over its development ; 
statistics give cancer of the rectum as occurring three and one-half times 
as often in males as in females. Its etiology is obscure ; cancer of the 
colon seems to develop most frequently in the cicatrix of an ulcer or after 
traumatism. 

Symptoms. — The symptoms of intestinal cancer vary with its seat. It 
comes on insidiously, with vague abdominal pains, a sense of unrest, and a 
marked decline in health and strength. 

Duodenal cancer simulates hepatic and gastric cancer; it is often 
attended by coffee-ground vomiting coming on several hours after taking 
food. Sometimes there will be jaundice from pressure of the tumor on 
the common bile ducts. The tumor may be felt near the cartilage of the 
right tenth rib. 

Cancer of the ccecum is attended by pain in the right iliac fossa and a 
tumor will be felt in the region of the caecum, usually much larger than the 
cancerous mass and formed by the accumulation of faeces above the stenosed 
portion. Manipulation in these subjects causes movement, and diminution 
in size of the faecal tumor, leaving distinct the cancer nodule, which is ten- 
der. In colloid cancer of the caecum, the tumor is large, hard, and smooth. 
In most instances there is "tympanitic dulness" on percussion, over the 
tumor. 

Cancer of the rectum first causes the symptoms due to a stricture, the bow- 
els are constipated and the stools are not cylinders, but narrow bands. " Sa- 
cral pains darting down the limbs, of a stabbing, lancinating character, 
giving rise to most intense suffering, are often present. When the bowels 
move, there is a sensation as if the parts were being burned, accompanied by 
more or less tenesmus. The bowels usually are at first constipated, but some- 
times an irregular diarrhoea is present from its commencement ; later in all 
cases, there is diarrhoea, the thin stools containing blood, pus, mucus, and 
shreds of sloughing and gangrenous matter. The invasion of the sphincter 
is followed by loss of power to retain the faeces, and then a brownish, watery, 
offensive fluid continually oozes from the anus. Communications with the 
vagina or urethra are followed by the escape of liquid faeces through these 
channels. A physical examination of the rectum (the patient being ether- 



332 



DISEASES OF THE DIGESTIVE SYSTEM. 



ized) reveals numerous hard nodular masses, with a cartilaginous feel, or a 
soft, fungoid, friable mass having a hard base. A portion of the mass 
removed and examined microscopically, will usually decide its character. 
At times, an irregular, angry red, fungoid mass protrudes from the anus, 
and on inspection it is readily recognized as cancer. The finger may 
detect a septum thrown across the gut, or, in colloid disease, a large, 
round, smooth tumor projects forward, to occlude the rectum. The 
symptoms of epithelial cancer of the rectum are the least urgent and 
serious in appearance of all forms of rectal cancer. It may exist for a 
long time without producing either constipation, pain, or cachexia. 

The prominent symptoms, which are common to all varieties of intes- 
tinal cancer, are pain, cachexia, constipation, and the presence of a tumor. 
As soon as the cancerous development has reached sufficient size to cause 
pressure, there is constant pain, which may be dull, vague, and dragging 
in character, or sharp and lancinating. In upper rectal and sigmoid can- 
cer, the seat of pain is in the left iliac fossa and loins ; in lower rectal can- 
cer, it is in the loins, upper part of the thigh, and sometimes in the testes. 
In other situations the pain is at the site of the cancer. A cachexia 
usually develops with the commencement of the cancerous development, 
accompanied by emaciation, loss of strength and flesh ; the skin is dry, 
"scaly," and assumes the dirty greenish "cancer color," the hair and 
nails become harsh and dry, and easily split. With the growth of the 
cancerous mass, exhaustion and cachexia gradually and steadily increase, 
and in some cases are the direct cause of death. As with cancer elsewhere, 
the disease may run its entire course without pain, anaemia, or marasmus. 
Constipation is the rule : at first there is flatulence, nausea, and vomiting ; 
later these symptoms vary according to the locality of the obstructions, as, 
for example, if the cancerous growth is high up in the rectum, or at the 
sigmoid flexure there is marked distention of the colon. A free evacu- 
ation of the bowels temporarily relieves the distress ; diarrhoea may alter- 
nate with the constipation, attended by rapidly increasing exhaustion. In 
some instances intestinal cancer is attended only by the symptoms of intes- 
tinal obstruction. Cancer high up in the colon is more often attended by 
diarrhoea than in the other localities. In long-standing cases of intes- 
tinal cancer, the lymphatic glands in the neighborhood of the cancer 
will be found enlarged, and there will be occasional intestinal hemor- 
rhages, dropsy, and thrombosis of the neighboring veins. The discovery 
of a tumor along the line of the intestine is essential to the diagnosis of 
intestinal cancer. When it is developed in the ascending and descending 
colon and caecum, the tumor is always felt in the normal position of the 
intestines, but when it is developed in the small intestine and transverse 
colon, the mobility of the parts and the weight of the tumor may cause it 
to occupy an abnormal position. 

Differential Diagnosis. — Cancer of the duodenum cannot at first be dis- 
tinguished from hepatic or gastric cancer ; later on, however, the situation 
of the tumor, the character of the vomiting, and the time of its occurrence 
after meals will often enable one to recognize its seat and character. 



EECTITIS I PROCTITIS. 



333 



Cancer of the pancreas cannot be distinguished from that of the duo- 
denum. Abdominal aneurism may be distinguished from a pulsating 
duodenal cancer by the alteration which it causes in the pulsation of the 
femoral artery. 

Cancer of the intestine is to be distinguished from floating kidney by the 
absence of the cancerous cachexia in the latter, and from the fact that the 
kidney tumor is behind and the cancer tumor in f ront of the intestine. Can- 
cer maybe distinguished from enteritis, colic or intestinal ulceration by the 
cachexia, tumor, and constipation. The age of the patient and a history of 
gradual development will aid in the diagnosis. The diagnosis of cancer of 
the rectum from other growths in it, or from proctitis or hemorrhoids, is 
made by a digital and ocular examination of the rectum and by a microscop- 
ical examination of a portion of the mass. 

Prognosis. — The prognosis is always unfavorable. When the disease is 
situated in the rectum or at the anus, surgical interference may prolong 
life. After it is possible to recognize the existence of cancer of the intestine 
a fatal termination will generally be reached within a year. 

Duodenal cancer gives rise to more distressing symptoms, and is more 
rapidly fatal on account of its situation, than any other variety. Death 
may result from exhaustion and anaemia (" cancer marasmus") from small 
hemorrhages, or from a single large hemorrhage, from rupture of the 
intestine and peritonitis, and from secondary complications. Death some- 
times occurs with all the symptoms of sudden intestinal obstruction, at- 
tended by large accumulations of faeces above the site of the cancer. 
Pyaemia, thrombosis, and embolism are sometimes the immediate causes of 
death. 

Treatment. — The treatment of intestinal cancer is only palliative. The 
diet should be restricted to such articles as will produce the least faecal 
matter, such as milk, nutritive broths, and eggs ; saline waters should always 
be taken freely to keep the faeces semi-fluid, without at any time causing 
diarrhoea. Pain must be relieved by the hypodermatic use of morphine ; 
hemorrhages may be checked by balsams and astringents. If at any time 
hardened faeces collect at the sigmoid flexure, warm water injections are to 
be given through a long tube. The formation of an artificial anus, the 
operations of colotomy, typhlotomy, etc., are surgical means for prolonging 
life. Extirpation of the rectum for cancer has been performed with suc- 
cess. 

EECTITIS : PKOCTITIS. 

Eectitis, or proctitis, is a localized catarrh of the rectum ; it rarely occurs 
except as the result of traumatism, or from the pressure of foreign bodies. 
It may be acute or chronic. 

Morbid Anatomy. — The morbid changes in rectal catarrh are similar to 
those which occur in catarrh of other portions of the intestinal canal. The 
colon is distended, and there may be faecal impaction above the sigmoid 
flexure. The results of chronic rectal catarrh are periproctitis, peritonitis, 
abscess, fistulae into the adjacent tissues and organs, cicatricial contrac- 



334 



DISEASES OF THE DIGESTIVE SYSTEM. 



tions, and thrombosis of the hemorrhoidal veins, with subsequent emdolie 

hepatic abscess. 

Etiology. — Acute catarrh of the rectum may result from blows, the pres. 
ence of foreign bodies, irritation produced by hardened faeces, and the long 
continued use of purgatives which act on the lower bowel. It may arise 
from an extension of inflammation, as in enteritis or dysentery ; in the 
latter case it will be accompanied by ulceration ; some regard rectitis as a 
mild form of dysentery, but it has none of the constitutional symptoms of 
dysentery, although it is attended by tenesmus, and blood may appear in 
the stools. Hemorrhoids may excite it, and then it is often called " the 
hemorrhoidal catarrhal flux." 

Syphilitic disease of the anus or rectum, fistula in ano, mucous patches, 
ulcerations of tertiary syphilis, and exposure to cold, as sitting on the damp 
earth or on wet sand-bags, may cause it. 

Symptoms.— The first symptom of proctitis is tenesmus, — a feeling of ful- 
ness and heat in the rectum with straining at stool, which gives rise to 
burning, scalding pains that shoot from the anal region into the loins and 
back. The stools contain gelatinous mucus, and frequently there are quite 
profuse hemorrhages. There is spasm and excessive tenderness of the 
sphincter ani, and, after violent efforts to expel supposed contents, rectal 
prolapse occurs, and causes the most intense suffering. At no time does 
the patient feel that the rectum has been completely emptied. There is 
frequent urination without relief. After these symptoms have existed for 
some time, scybalous masses are mingled with the muco-purulent dis- 
charges, and strangury, hemorrhoids, headache, nausea and restlessness 
may be present. Hard faecal masses can often be felt along the line of the 
colon. It may terminate in recovery in from four to eight days, or it may 
become chronic. 

Chronic proctitis is attended by purulent or sero-purulent discharges, in 
which are scybalous masses and shreds of sloughing mucous tissue. The 
discharges are foul smelling. It is usually accompanied by constipation. 
A digital examination of the rectum gives the sensation of a rigid cicatrical 
tube. 

Differential Diagnosis. — Proctitis may be mistaken for dysentery, hemor- 
rhoids, or cancer of the rectum, and, in women, for displacement of the 
uterus. Dysentery is an acute febrile disease, attended by severe pain in 
the abdomen and great exhaustion, and the discharges have a characteristic 
dysenteric color and odor. On the other hand, the symptoms of proctitis 
are local, and a digital examination of the rectum readily establishes the 
diagnosis. The presence or absence of hemorrhoids is also determined by a 
digital examination ; the two conditions, however, may frequently be asso- 
ciated. 

Cancer is accompanied by the characteristic cachexia ; it develops slowly, 
and the form of the stools is for a long time modified by the constriction. 
A small portion of the cancerous mass may sometimes be removed, and 
when examined microscopically will exhibit the characteristics of the can- 
cer-tissue. In mal-positions of the uterus, symptoms analogous to those 



PERIPEOCTITIS. 



335 



of rectitis are often present, but the introduction of a uterine sound at once 
determines the condition. 

Prognosis.— The prognosis in acute proctitis is good ; its average duration 
is about a week, and its only dangers are chronic proctitis, peritonitis, fis- 
tulae, and abscess. When proctitis is the result of cancer, or of tumors 
pressing on the rectum, the prognosis is unfavorable. Chronic rectal ca- 
tarrh is difficult to cure, and cicatrices following attendant ulceration may 
lead to intestinal obstruction. When any disease of the liver, lungs, or 
heart is present which interferes with the venous return, recovery is rarely 
reached. 

Treatment. — A patient with acute rectitis should be kept in bed ; a mild 
laxative, castor-oil, should be given, and the intestine thoroughly evacua- 
ted ; a milk and farinaceous diet only should be allowed. Sedative enemata, 
opium and belladonna, cocaine, or morphine, alternating with copious warm 
water enemata, are the most successful methods of treatment. If there is 
intense pain, with tenesmus and local engorgement, a hypodermatic of mor- 
phine may be given, and leeches applied about the anus. Hot hip baths 
often give marked relief. Chronic rectal catarrh, if mild, is to be treated 
by the local application of any of the vegetable astringents ; and when 
severe, the tough and ulcerating membrane should be brushed over every 
few days with a forty-grain solution of nitrate of silver. Constipation 
should be avoided, and aperient enemata should be employed rather than 
cathartics. Local treatment is always more successful than internal med- 
ication. 

PERIPROCTITIS. 

Periproctitis is an inflammation of the connective- tissue surrounding the 
rectum, and is usually suppurative in character ; the resulting abscess may 
open either into the lower bowel or internally. 

Morbid Anatomy. — The manner of the extension of the inflammation 
through the coats of the intestine to the adjacent connective-tissue, and the 
course of the morbid processes excited, are identical with those of perityph- 
litis following typhlitis. The infiltrated tissue forms a tumor which can 
readily be detected through the rectum. After fluctuation occurs in the 
tumor, its subsequent course varies. A spontaneous cure by absorption and 
induration may take place, or the abscess may open and a complete fis- 
tula be established, having an internal opening communicating with the rec- 
tum. These fistulous tracts are very tortuous, and are always accompanied 
by a suppurative cellulitis in the adjacent cellular tissue. These fistulous 
openings in the rectum are high up, and the tracts are separated from the rec- 
tum by indurated connective-tissue. Fistulas may also be established with 
the bladder or vagina. Suppurating granulations surround the irregular 
sinuses, and in cases of long standing they may have an epithelial lining 
similar to that of the anal mucous membrane. Chronic periproctitis may 
lead to stricture and intestinal obstruction. 

Etiology. — Periproctitis is very often a result of proctitis. It also occurs 
with cancer^ intestinal ulcers, and other structural diseases which may in- 



336 



DISEASES OF THE DIGESTIVE SYSTEM. 



volve the rectal mucous membrane. It may be traumatic in origin. It is 
especially liable to develop in phthisical subjects at a point remote from the 
rectum, and it may be one of the changes in metastatic pyaemic inflamma- 
tion. 

Symptoms. — The existence of periproctitis is determined by a physical 
examination. There is local pain, heat, and tenderness ; a tumor develops, 
which soon fluctuates and either gradually disappears or opens externally. 
If extensive, the formation of the pus-cavity will be attended by hectic, 
rigors and irregular sweats. There may be a well-marked febrile move- 
ment, with nausea and vomiting. If a recto-vesical fistula form, then the 
urine will infiltrate the adjacent tissues, and septic symptoms will be de- 
veloped. In all cases, defecation causes intense suffering. The tumor pro- 
duced by the abscess has been, in some cases, so prominent and resistant 
that symptoms of intestinal obstruction have resulted. These patients can- 
not sit erect ; and all pressure about the pelvic region is attended by pain. 
When the abscess opens internally, foul-smelling, purulent masses will be 
mixed with the faecal discharges, and the tumor gradually diminishes. 

Differential Diagnosis. — Periproctitis may be mistaken for any of those 
affections of the mucous membrane of the rectum which cause constipa- 
tion, local pain, and tenesmus ; but a careful examination of the parts will 
show disease of the mucous membrane, and palpation with one finger over 
the rectal region will discover a fluctuating tumor that is found in no other 
disease. 

Prognosis. — When occurring with structural and malignant disease of the 
rectum, the prognosis is determined by the primary disease. Its prognosis 
is often unfavorable, on account of its painful and annoying sequelae, such 
as fistulai and stricture. Fistulous openings communicating with any other 
parts than the skin or intestine, are very grave results ; when they occur in 
phthisical or enfeebled anaemic subjects the prognosis is always unfavora- 
ble. In idiopathic and traumatic periproctitis, the prognosis is good. The 
lower down the suppurative process, the better is the prognosis. 

Treatment. — Before fluctuation occurs, the rules of treatment are the 
same as in perityphlitis— rest and opium. When fluctuation occurs, the 
abscess must be opened at its most prominent point ; subsequent fistulae 
should be freely opened. The abscess should be opened early, to prevent 
its being discharged into the bladder, rectum, or vagina. 

HEMORRHOIDS. 

Hemorrhoids, or piles, are tumors formed at or near the anus by dis- 
tended hemorrhoidal veins, or by connective-tissue and skin, which have 
been distended by blood and indurated by local inflammation. The anas- 
tomoses of the superior, middle, and inferior hemorrhoidal veins about the 
anus form a channel through which venous blood flows, either to the 
liver or to the cava ascendens. Hence any obstruction in the liver, or 
cava, may cause distention of these veins. 

Morbid Anatomy.— Hemorrhoids are internal or external ; the former are 



HEMOREHOIDS. 



337 



within the rectum, the latter are at its anal margin. Piles are " dry " or 
"bleeding;" internal piles are usually bleeding. External piles are usu- 
ally dry ; they may be large, smooth, tense, dark blue tumors, congested 
and painful, or smaller, shriveled tabs of skin, quiescent and usually pain- 
less. The latter represent a later form of the former after partial spontane- 
ous cure. 

On section these tumors exhibit a congeries of dilated veins, sometimes a 
central cyst containing a blood clot, and sometimes free extravasated blood. 
Their size varies from that of a pea to that of a walnut. Internal hemor- 
rhoids are sometimes merely flat patches of the mucous membrane with 
dilated capillaries, and bleed at the slightest touch. Any internal pile 
may be extruded during defecation, and, if not directly replaced, become 
congested and inflamed through partial strangulation by constriction of the 
sphincter. Thrombi forming in the large varicose tumors may lead to 
ulceration and obliteration. A strangulated hemorrhoidal tumor may 
slough, and pyaemic symptoms may follow, or a hemorrhoidal ulcer may 
form. Again, the process may cause periproctitis, abscess, or a rectal fis- 
tula. 1 

Etiology. — Hemorrhoids are oftenest met with after the fiftieth year. 
There is often an hereditary tendency to their development. A sedentary 
mode of life, luxurious living, and a tropical climate are predisposing causes. 
Anything retarding blood-return from the rectum, such as impacted faeces, 
habitual constipation, a gravid uterus, or pelvic tumor, leads to their devel- 
opment. Cirrhosis, atrophy, and passive hyperemia of the liver, or ob- 
structive hepatic disease will cause hemorrhoids. In diseases of the heart 
or lungs, causing obstruction in the venae cavae, hemorrhoids will develop. 
Proctitis, cancer, ulceration about the rectum, and the excessive use of drastic 
purges are causes of hemorrhoids. They may be produced by prolonged 
attacks of diarrhoea or dysentery. Excess in venery is a frequent cause, 
and they often develop just after the menopause. 

Symptoms.— The symptoms of hemorrhoids vary with the size, number, 
stage, and seat of the tumors. At first there is a feeling of weight and ful- 
ness in the rectum, or a sensation as if a foreign body were present. Dur- 
ing and after a hard stool, there is a throbbing, aching or burning pain, ra- 
diating to the loins or down the limbs. There is heat, soreness and tingling 
about the anus, and as the tumor increases in size, sitting becomes uncom- 
fortable, and the individual grows restless, depressed, and anxious. The 
pain soon becomes constant, and is always more severe after a passage or 
after a moderate walk. 

Internal hemorrhoids have, as their chief symptom, Heeding, when the 
bowels are evacuated. From this symptom the name is derived. Slight 
internal piles may exist for years and only produce local itching and heat. 
Large internal piles are almost always extruded during a passage, but at 
first are easily replaced. Later on, standing or walking may cause them to 

1 Among pathological sequences of hemorrhoids, are anal fissures, prolapsus ani, and changes in the 
mucous membrane described by Virchow as relaxation, with the formation of puffs or folds, slightly thick- 
ened and grayish white. The submucous tissue is increased and relaxed and very vascular. The mem- 
brane is usually covered with a tough, whitish mucus. 
22 



DISEASES OE THE DIGESTIVE SYSTEM. 



protrude. Wfoen they are congested and protrude, they appear as dark pur- 
ple, soft, vascular tumors. The amount of blood lost in internal hemor- 
rhoids varies from a couple of drachms to a quart ; in the latter case there 
is marked exhaustion and anaemia. Bleeding may be venous or arterial, 
regular, irregular, or periodical. The latter relieves renal and hepatic con- 
gestion, and may ward off gouty and apoplectic seizures. Many "reflex 
symptoms " accompany hemorrhoids ; such as irritable bladder, urethra, 
and vagina. This class of patients are usually low-spirited, irritable, sal- 
low and anaemic. They may become subjects of melancholia. 

Differential Diagnosis. — Hemorrhoids may be mistaken for proctitis, can- 
cer of the rectum, stricture of the rectum, prolapsus ani, venereal ex- 
crescences, or intestinal hemorrhages. The points in the differential diag- 
nosis of the first three have been given. A caref al examination of the everted 
but normal mucous membrane in prolapse readily distinguishes it from 
hemorrhoids. Venereal growths are hard, have well-defined borders, a 
cauliflower-like surface, are exceedingly slow in their development, and are 
accompanied by other evidences of syphilis. Intestinal hemorrhage is dis- 
tinguished from bleeding hemorrhoids by an ocular examination of the rec- 
tum. Internal hemorrhoids may be distinguished from rectal polypus by 
the fact that rectal polypus occurs chiefly in the young, as a large solitary 
m&pale colored tumor, having a well-marked pedicle. 

Prognosis. — The prognosis in uncomplicated hemorrhoids is good ; long- 
standing piles in the aged are rarely permanently cured. Copious bleed- 
ings from internal hemorrhoids often hasten a fatal termination in chronic 
diseases of the liver and lungs. 

Treatment. — Those who have hemorrhoids should never allow themselves 
to become constipated. The diet should be nutritious, and so regulated 
as to induce free daily evacuations from the bowels. Violent exercise, espe- 
cially lifting heavy weights, long walks, sitting on damp, warm seats, alco- 
holic stimulants, and highly seasoned food should be avoided. The best 
cathartics for this class are rhubarb, senna, sulphur, glycerine, and aloes. 
The careful use of mineral water is of service in those who are the subjects of 
hepatic disease. In external piles, a cold sitz-bath should precede the use 
of astringents, and these, combined with opium and chloroform, will often 
give marked relief. Inflamed external piles call for the application of leeches 
and poultices about the anus. Eecently, the topical application of iodoform, 
and the injection into the hemorrhoidal tumors of carbolic acid has been 
recommended. A surgical procedure is the only sure and permanent relief. 

INTESTINAL PARASITES. 

( Worms.) 

The history of intestinal worms dates from the earliest medical writings. 
In the middle ages the history of the tape-worm was closely associated with 
the doctrine of spontaneous generation. It is within the last fifty years 
that the doctrines of metamorphosis and migration have been established. 
There was a time when nearly every malady was attributed to worms, — while 



INTESTINAL PAKASITES, 



339 



■a- reaction of sentiment ascribed the utmost benefit to their presence. Every 
year discovers some new parasite ; of the fifty or sixty now known, only 
about ten per cent, are common in, or peculiar to man. The worms which 
have their habitat within the intestinal canal of the human subject are 
comparatively few. I shall only give a brief history of those which are of 
frequent occurrence. 

Tarnia Solium, or tape-worm, is the final development of an embryo, 
usually lodged in the flesh of some animal. It is from seven to thirty feet 
long, has a globular head, connected by a slender neck to its numerous 
flat segments or joints. The neck is an inch in length, and gradually widens 



into 




The head measures about l-40th of an 
convexity is arranged a double coro- 
net of booklets, — the 4 i armed tape- 
worm," — and it is provided with 
some two or four suckers. The flat, 
thin joints vary from one-half to one- 
eighth inch in length, being smallest 
near the neck. The lower border of 
each segment is larger than the upper. 
Each mature joint contains both male 
and female sexual organs (hermaphro- 
dite). The uterus is a long tube, with 
seven or ten branches on either side, 
in which the ova develop. An ordi- 
nal-sized tape-worm contains five 
millions of ripe ova. These ova, 
l-1700th inch in diameter, become in 
the pig cysticercus celluloses (measly pork) 



inch ; around its 




Mature Segment of Tsenia 
Solium. 

A. Genital pore. 

B, B. Uterus. 

C, C. Lateral branches of 
the uterus, x 30. 



From one 

to forty T. solium may be present in the same intestinal 



Fig. 67. 
Head of Taenia Solium. 

A. The Rostellum. 

B. uovble row of hooks. 

B\ S com^nSng segments tract ; their hooklets and suckers are firmly embedded in 

below the neck. , , £ 77 . , , • , , 

Enlarged about 12 times mucous membrane oi the small intestine — they are 
' almost exclusively confined to its upper third. The pro- 
glottides sometimes hang far down into the large intestine ; the terminal 
ripe oaes are constantly falling off, and are discharged with the fasces. T. 
solium is the development of the C. cellulosus from measly pork, the em- 
bryo being swallowed, and its vesicular annex removed by the stomach 
juices, the hooklets become fixed just below the pylorus, and in a few 
months the tape-worm reaches considerable size. 

Tceuia saginata, or T. medio-cannellata, also called "unarmed tape- 
worm, 7 ' is larger, stronger, and thicker than T. solium. The segments are 
broader, far more opaque, and harder than those of T. solium ; the head 
has no hooklets, measures about l-10th inch, and has four strong and prom- 
inent suckers. The uterus is more finely divided, and there are from fifteen 
to twenty dichotomous branches. The head of the medio-cannellata is more 
club-shaped than that of the T. solium. The neck is very short. The 
larval form of this worm is the cysticercus T. saginata, or cysticercus bovis, 
the embryo being found in beef. The ova of T. saginata are oval, and 



340 



DISEASES. OE THE DIGESTIVE SYSTEM. 




Head of Taenia Sagi- 
nata, or Unarmed 
Tape-worm. 

A. Rostellum. 
B, B. Four discs, x 8. 



larger than those of T. solium. In their larval state they occur not only 
in beef, but in the sheep, goat and giraffe. Its mode of entrance, locality, 
and development are precisely the sa?ne as the T. solium. 
It occurs far more frequentty, and more extensively than 
T. solium, which formerly was the variety always meant 
when tape-worm was mentioned. 

The Bothriocephalus lotus is the largest worm infesting 
man; the head of this tape-worm is club-shaped, deeply 
grooved on either side, and is "unarmed." The head is 
shaped like an egg, l-10th of an inch long and l-26th of an 
inch wide. The neck is very short and thread-like ; the 
joints are about three times as broad as they are long, 
but toward the end of the worm they are square. The 
genital pores look like a small rosette, and are situated 
about the centre of the segment, and, being all placed on 
the same side of the worm, this cestoid can be said to have 
a belly and a back. The eggs are oval, from l-350th to 
l-550th inch, brown in color and at first ciliated. They 
possess six hooklets. This worm sometimes reaches sixty 
feet in length ; its color, unlike the others, is a dull bluish-gray. The seg- 
ments do not drop off when ripe, and have not an independent life, It is 
estimated that ten feet of this worm can produce twelve million ova. The 
development of this worm is unknown ; some suppose its embryo to be 
found in a fish or mollusk. It is found in the small intestine singly, or 
with the other two varieties ; several may inhabit the same individual. 

Round worms, or the hematoids, are more highly organized than the ces- 
toids; the common round worm, or A scar is luiribricoides, is of a brown 
color, with a cylindrical body, 10 x 1-8 inch in length and breadth in the 
male, and 15 x 1-4 in the female. The head terminates in three thick 
semilunar lips, each lip having about 200 teeth. The mouth opens into 
the alimentary canal, which can be seen through the transparent body. 
The tail is curved strongly toward the abdomen in the male, this, with its 
small size, distinguishing it from the female. The female contains two 
long coils of ovary and oviduct, the length of the generative tubes being 
eleven times the length of the animal. At the end of the tail, in the male, 
two projecting spiculse can be seen connected with the generative organs, 
which are coils of tubes eight times as long as the worm. The ova are oval 
in shape (1-340 to 1-440), are produced in immense numbers (sixty millions 
in a mature female), and are discharged with the faeces. The vitality of 
these ova is wonderful. How they obtain entrance into man is not known, 
but it is probable that they previously pass through an intermediate state, 
and that they attain their full development after entrance. The worms 
inhabit the small intestine, and vary in numbers from one to thousands. 
They wander, however, through the tract, may pass through the nose or 
mouth, or may enter the hepatic, gall or pancreatic duct, into the gall- 
bladder, or into any fistulous channel, and reach the kidneys, spleen, lung, 
larynx, etc. The round worm occurs in the ox and pig as well as in man. 



IKTESTIKAL PARASITES. 



341 




a 



The "thread worm," "maw-worm," Oxyuris vermicularis, looks like an 
ordinary piece of thread ; the male (like the 
round worm) is smaller than the female, and 
is about one-sixth of au inch long. The fe- 
male is from one-third, to one-half an inch 
long. The body is cylindrical, the tail is much 
sharper than the head. The head terminates 
in a mouth surrounded by three lips, from 
which extends the alimentary tract. The end 
of the tail, in the male, is curved up toward 
the abdomen. The eggs are oval, 1-100 to 
1-500 inch, each female containing about ten 
thousand. They are very hardy, having a 
stout envelope. All their stages of develop- 
ment take place within the intestinal canal. 

The "seat-worm " as its name indicates, 
has its habitat in the large intestine, especial- 
ly about the rectum, whence it may pass into 
the vagina or insinuate itself into narrow 
folds of skin in the anal region. Mature 
females especially inhabit the caecum. They 
vary in number : sometimes the mucous 
membrane is completely covered with them. 
The ova enter by means of tbe food or di- 
rectly through personal contamination ; they 
die in a few hours after they are placed in 
water. 

The Trichocephalus dispar, or " whip-ivorm" is a small worm about one 
and one-half to two inches in length, the female being the larger. It has 
been called the "hair-headed" worm because its head, which constitutes 
about two-thirds of its length, is thread-like. The thick body contains the 
genitals and the intestinal canal ; the body of the male is curved into a. 
spiral. The male organ presents a spicula projecting from the cloaca ; it is 
set with numerous sharp points, and is surrounded by a sheath. The uterus, 
when distended with eggs (60 ova), fills nearly the whole posterior part of 
the body. The eggs are brown and oval (1-5,000 — 1-12,000 inch) with a 
nipple-like appearance at either pole. Its mode of entrance into the body is 
unknown. There is probably no intermediate state of the ova of T. dispar. 
The embryos are probably liberated in the stomach, and, developing as they 
travel onwards, reach the large intestine. Their numbers vary from fifty 
to one thousand. The T. dispar is found in some varieties of apes ; and 
the T. crenatus of the pig is probably the same as this worm. 

Trichina spiralis belongs to general diseases, and will not be considered 
here. 

The Anchylostomum duodonale, or dochmius duodenalis, is a small cylin- 
drical worm, the females being seven-tenths and the males four-tenths inch 
in length. It is thicker than the seat-worm, almost as thick as the body of 



Oxyuris vermicularis, or thread worm, 
female. B, Same, male— both natu- 
ral size. 

Female of same, magnified about ten 
times, containing ova. a, anus; b, 
vulva. 

D. Mature egg of the thread worm, x 250. 

E. Ascaris lumbricoides, male, natural 

size. F, head, and G, tail of same, 
magnified about four diameters. 



342 



DISEASES OF THE DIGESTIVE SYSTEM. 



the whip-worm. The mouth is furnished with eight teeth. The armature 
of the mouth, and the capsule about the head are yery complex. The male 
terminates in a lobate enlargement, but the female is pointed. The eggs 
are oval (1-350 to 1-1000 inch), have a very thin shell, but regarding their 
development little is known. It inhabits the lower part of the duodenum 
and the upper part of the jejunum. It probably has no intermediate 
bearer, but as soon as developed attaches itself to the villi and may become 
encysted between the mucous and muscular coats. It may cause intestinal 
hemorrhage. 

Etiology. — Worms develop in the intestines of man, either by the en- 
trance of ova which grow into the mother parasite ; or by the entrance 
of what are called "intermediate parasites." Their entrance into the 
intestinal tract is only effected through food and drink. Butchers, and 
those who handle raw meat, are more subject to them than others. Filthy 
surroundings, squalor, and personal uncleanliness are conditions which 
favor their development. 

Cestoids occur at all ages ; tape-worm has been found in a five-day-old 
infant. Botliriocephalus latus is found chiefly in Scandinavia, Eussia, and 
Poland. T. solium occurs wherever the pig is domesticated. T. saginata 
is found wherever raw beef is used for food. The Taenia are not found 
among Jews and those who eat no pork. The monks of the Carthusian 
order, who eat only fish, are free from worms. Iceland is the only country 
in which the hsematoids are not found. The round worm occurs in warm 
climates oftener than in cold. Their number and extent are in direct pro- 
portion to the filth of the surroundings. They are more common in women 
and children than in men ; in those who live in the country than in those 
who live in cities. The oxyuris vermicularis is everywhere prevalent. It 
occurs especially in young children, but is not uncommon in adults. The 
itching which these worms cause, especially at night in a warm bed, induces 
so much scratching, that when two or more children sleep together the 
worms may be carried from one to another by the hands. Those who have 
charge of children, nurses, etc., often become infected in this way. 

T. dispar abounds in this country, Europe, Syria, and Egypt ; it is 
present at all ages, but, strangely enough, in the first and second years of 
life it is rare. The whip-worm produces so few symptoms, and can be so 
readily overlooked at a post-mortem, that its etiology is obscure. The 
Anchylostomum duodenale (or the dochmius or strongylus duodenalis) was 
discovered by Dubini in 1838, in Northern Italy. It prevails in Brazil and 
Egypt. The negro is oftener subject to it than the white ; but it can be 
shown that bad food and drink are of more importance in causing it than 
race. Women are affected oftener than men. The conditions known as 
cachexia Africana, mal d'estomac, etc., are due to the presence of this 
parasite. 

Symptoms. — The only symptom which gives positive evidence of the ex- 
istence of intestinal worms or their ova is their discovery in the stools or 
about the anus. Taenia produces no constant symptoms. The bowels are 
usually irregular. There may be colicky pains in the abdomen ; the appe- 



INTESTINAL PARASITES. 



343 



tite is capricious, the face may be pale and the mouth drawn. Often the 
stomach feels weak, and there is nausea, perhaps vomiting. In some in- 
stances these stomach symptoms, with colic, occur after certain articles of 
food ; in others, certain kinds of food relieve them. Among the reflex 
svmptoms are headache, dizziness, ringing in the ears, sudden sweatings, 
irregular attacks of palpitation, depression of spirits, lassitude, ocular spec- 
tra, sadden salivation, and itching about the nose and anus. Chorea, 
grinding the teeth, hysteria, anomalies in menstruation, epileptiform and 
maniacal actions have occurred in those in whom tape-worms were found 
to be present. The special senses may be temporarily involved :— deafness, 
blindness and loss of speech have occasionally occurred. All the senses are 
enfeebled to a marked degree. These symptoms are more those of hypo- 
chondria and hysteria than of taenia. The subjective sensations which one 
who believes he has taenia may describe are innumerable, and each patient 
will have his own peculiar group of special notions. Often patients with 
one large or several small taeniae enjoy perfect health so long as their exist- 
ence is not suspected. The diagnosis can only be made by the discovery of 
detached joints or segments of the worms in the faeces. 

The ascaris lumlricoides or round worm may be present in large num- 
bers, and yet give no symptoms of its presence. Usually, however, there 
are certain symptoms which are regarded as " signs of worms," such as 
itching and picking at the nose, foul breath, colicky pains, especially 
about the umbilicus, bloody mucous diarrhoea, perverted appetite, restless- 
ness, disturbed sleep in which the child grinds its teeth, with nausea and 
vomiting,, which is regarded as evidence that the " worms have passed into 
the stomach. " The vomiting, however, is reflex. The abdomen is usually 
tumid, distended, and doughy to the feel. The urine looks somewhat like 
rice-water, the lower eyelid is of a dark purple color, or there may be rings 
about the eyes ; the pupils are often unequal. Later there are hysterical 
convulsions, with choreal movements, and the child becomes emaciated. 
These worms, by coiling themselves into a bundle, have caused intestinal 
obstruction. They have entered the larynx and induced death by suffoca- 
tion, have reached the ductus communis and caused jaundice and hepatic 
abscess, and they may take their way through any artificial opening into 
the peritoneal cavity or bladder, but they cannot cause intestinal perfora- 
tion. It is a question if lumbrici can induce catarrh and ulceration of the 
intestine. At an autopsy, where large colonies of lumbrici have been found, 
the intestine has been intensely congested in the neighborhood, leaving no 
doubt as to the cause. Attacks of laryngismus stridulus are sometimes 
induced by lumbrici in highly nervous children. While the existence of 
these worms may be suspected, their diagnosis can only be made by their 
discharge from the stomach or intestine. 

The seat-ivorm, or oxyuris vermicularis, when present in small numbers, 
produces few symptoms. When they are numerous in nervous and suscep- 
tible patients, there is intense itching about the anus, especially on retiring, 
when the increased warmth causes them to be very active, and by this sleep 
is more or less disturbed. They often cause a frequent desire to go to stool, 



344 



DISEASES OF THE DIGESTIVE SYSTEM. 



and sometimes there is an abnormal amount of mucus mixed with the faeces 
showing that they have produced extensive local irritation. In such cases^, 
there will be punctate redness about the anus, and in female children, where 
the worm wanders into the vagina, there will be irritation of the vulva, 
which leads to vulvitis. Sometimes with the itching there will be pain and 
tenesmus, and the fetid stools will be bloody and streaked. The genito- 
urinary disturbance may cause such abnormal excitement of the sexual 
organs, that it may lead to onanism, seminal loss, and nymphomania. Hys- 
terical, epileptiform, choreal, and cataleptic symptoms have been induced 
by the irritation produced by these worms. On account of the local irrita- 
tion which they produce and their easy detection on careful examination, 
their diagnosis is not difficult, for their ova or the parasites themselves 
will be found in the faeces, or in the folds at the margin of the anus. A 
careful inspection of the rectum in those who suppose they are suffering 
from hemorrhoids will often disclose the presence of the seat-worm as the 
cause of the anal irritation. 

Trichocephalus dispar produces no symptoms. Either the worms or their 
eggs must be found in the faeces to establish a diagnosis. 

Anchylostomum duodenale induces a chlorosis-like anaemia; the skin and 
mucous membranes are pale, and the cardiac and venous murmurs of anae- 
mia are well marked. The loss of flesh and strength is constant and pro- 
gressive. Dyspepsia and anorexia, alternating with bulimia, and an appe- 
tite for certain and peculiar articles of food, are early symptoms. In most 
cases there is a sense of weight or pain in the abdomen ; the stools are fre- 
quently colorless, and the urine is pale and abundant. Sometimes slight 
intestinal hemorrhage will occur. 

Differential Diagnosis. — The diagnosis of the presence of intestinal para- 
sites is made by the discovery of the parasites or their ova in the stools or 
the matters vomited. Acute hydrocephalus may be mistaken for worms, 
but in hydrocephalus the projectile vomiting, the slowed pulse, the fever 
with irregular exacerbations and remissions, the constipation, the hydro- 
cephalic cry, and the retracted abdomen, all stand in marked contrast to 
the symptoms of intestinal parasites. 

Prognosis. — Intestinal parasites may cause death, first by their entrance 
into the larynx, the ductus communis (causing abscess of the liver), or when 
they collect in masses and cause fatal intestinal obstruction ; secondly, 
when extreme anaemia and exhaustion are produced by anchylostomum 
duodenale. The prognosis in taenia is good, except in very young children, 
and in the enfeebled. When parasites have resided a long time in the in- 
testines, some of the reflex symptoms may remain after their removal. It 
is thought that the ascaris lumbricoides does not remain longer than a year 
in the human body, unless there is an exposure to new sources of infection. 
Death occurs with symptoms of exhaustion, greatly increased by the intes- 
tinal hemorrhage, profuse diarrhoea, and persistent vomiting. 

Treatment. — Prophylaxis demands that all raw or "underdone" meat 
shall be avoided. Measly pork should not be allowed to be sold in the 
markets, and wells and springs from which drinking water is obtained 



IKTESTIXAL PARASITES. 



345 



should be removed from the neighborhood of stockyards. A point in prophy- 
laxis that has never been mentioned is the washing of green vegetables, such 
as lettuce, as the Swiss and Germans sprinkle their growing vegetables with 
the water drained from human excrements. 

The means to be employed for the expulsion of the tape-worm have for 
their object the dislodgment of its head ; so long as this remains, it is use- 
less to hope for cessation of the symptoms. Whatever anthelmintic is 
administered for this purpose, the bowels must be thoroughly evacuated. 
This can be effected by some of the saline purges, or by a copious draught 
of some purgative mineral water. The diet should be restricted for two or 
three days before its administration, and then either pomegranate, Kousso, 
male fern, or pumpkin-seeds may be given in full doses. As the adminis- 
tration of anthelmintics may induce vomiting, a cup of black coffee may be 
given a few minutes before they are taken. The cortex radicis punicm 
granati is used in the form of a decoction (three ounces to a pint and a 
half of water). When boiled down one-half, it should be given in three 
divided doses. To this may be added filix mas, gamboge, or tansy ; and in 
case the worm is not dislodged, a dose of castor-oil should follow. Kousso, 
the flower of the Brayera anthelmintica, is given in one-half oz. doses 
mixed with water ; or in an infusion (one-quarter oz. to four oz. of water). 
The odor of the Kousso is very offensive. 

The male fern (aspidium filix mas) is one of the oldest and best known 
vermifuges. The ethereal extract — oleoresin — is given in capsules ; dose, 
one-half drachm. It maybe given as the powder of the rhizome, 60 to 100 
grains. It should also be followed by a dose of castor-oil, gamboge, or cal- 
omel. Oil of turpentine, in one-half or one-ounce doses, is very effective ; 
it may produce headache, giddiness, or a kind of intoxication. Petroleum, 
in 20 to 30-drop doses, has been used in Egypt. Kameela (Bottler a tine- 
toria) is to be given in one-third drachm doses every three hours. Carbolic 
acid (5 grains) and salicylic acid (12 grains) have also been found efficacious. 
An emulsion of pumpkin-seeds frequently acts efficiently. The active prin- 
ciple of pomegranate-root bark, pelletierine, is thought by some to possess 
all the powers of the root. All the above-named drugs are efficacious, and 
when they fail it is usually because they are not properly administered. 

For round worms, besides the vermicides mentioned, santonin, spigelia, cal- 
omel, and chenopodium may be used. Santonin is by far the most reliable, 
but it requires care in its use, on account of the severe gastric and nervous 
symptoms which it causes ; one-half grain for a child and three to six grains 
for an adult is a maximum dose, The oil of chonopodium is recommended, 
— dose, five to ten drops ; and the fluid extract of senna and spigelia is often 
effective. 

The thread or seat-worm may be destroyed and washed away by enemata 
of quassia, oak-bark, alum, salt and water, or carbolic acid. At the 
same time the vermifuges should be given, and the bowels gently moved 
by castor-oil. Thoroughly washing the anus and the parts around it with 
a one per cent, solution of carbolic acid, and subsequent attention to clean- 
liness, suffice in the majority of instances. It is said that turpentine and 



346 



DISEASES OF THE DIGESTIVE SYSTEM. 



calomel are the best means of getting rid of the A. duodenale. Following 
the expulsion, tonics should be used. For either the round, seat, or whip- 
worm, santonin is the best remedy ; and for the last two varieties, thorough 
local treatment and absolute cleanliness will generally suffice. 

FUNCTIONAL DISEASES OF THE INTESTINES. 

The principal functional diseases of the intestines are constipation and 
colic or enter algia. 

CONSTIPATION. 

Constipation is a relative term, for some perfectly healthy persons have 
only one movement from the bowels every second or third day, while others 
have two stools daily. 1 It is difficult to explain these differences, and to 
say what constitutes constipation in an individual unless his habit is known. 
No standard can be applied indiscriminately to all persons. Those who 
suffer from constipation are always able to make their own diagnosis. In 
the majority of instances constipation is due to a deficiency in the peristal- 
sis of the large intestine. 

Morbid Anatomy. — There are no lesions which are constant in functional 
constipation, but if it has been of long standing it may cause changes which 
after a time become an additional cause, such as dilatation of the intestine 
and hypertrophy of its walls. The colon may become so dilated as to meas- 
ure from twelve to fifteen inches in circumference. If hypertrophy occurs 
it is usually most marked at the upper part of the rectum and at the sig- 
moid flexure of the colon. More or less paralysis of the muscular coat pre- 
cedes and accompanies dilatation, and pouches may form along the colon 
containing masses of mucus and faecal matter. These pouches occur most 
frequently at the sigmoid flexure, and may be arranged in rows. Ulcera- 
tion and perforation of the dilated and weakened intestinal wall may cause 
fatal peritonitis. Sometimes the intestines rupture ivithout ulceration from 
prolonged and severe peristalsis at the seat of the faecal obstruction. Typh- 
litis and perityphlitis may be a result of faecal impaction due to habitual 
constipation. Many diseases of the rectum and adjacent viscera are also 
among its results, such as haematuria, rectal abscess, fistulae, anal fissures, 
prolapsus ani, and passive hyperaemia of the pelvic viscera. ' Hemorrhoids 
usually complicate long-standing constipation. 

Etiology. — Constipation often results from the same habits and mode of 
life which cause dyspepsia, and it is a very frequent accompaniment of it. 
It may arise from the prolonged use of opium and the abuse of laxatives. 
It occurs with certain diseases of the brain and spinal cord. In those who 
have what is called a " costive habit " collections of pills which have been 
taken for its relief sometimes form a nucleus about which masses of im- 
pacted faeces collect. A change in habits of life or diet is frequently 
followed by temporary constipation. Those who lead a sedentary life, the 
feeble, infirm, the bed-ridden, and child-bearing women are predisposed to 



1 Cases are recorded where periods of three months have elapsed between two successive movements, 
and yet tbe individual was apparently in good health. 



COKSTIPATIOK. 



347 



constipation. Loss in the contractile power of the abdominal muscles from 
any cause may induce constipation. Abnormalities in the intestinal se- 
cretion, as in chronic alcoholismus, and organic or functional disturbances 
of the liver lead to constipation; heart disease, bronchitis, emphysema, and 
asthma are included in this list. It may also result from unnatural dry- 
ness of the faeces, such as occurs in diabetes, where large quantities of fluid 
are carried off by the kidneys. This dryness may also occur in those whose 
occupations cause profuse perspiration. General anaemia and chlorosis 
cause it. Many conditions giving rise to reflex irritation, more especially 
diseases of the genito-urinary organs, induce atony of the intestine and 
consequent constipation. 

One of its most frequent causes is anxiety and prolonged mental labor, 
especially in those leading a sedentary life. It is common in melan- 
cholia and insanity, and may occur with hysteria. The long-continued use 
of cathartics is a frequent cause of obstinate constipation. Hereditary pre- 
disposition may be classed as a cause. Old age is always a predisposing 
cause. Cases are on record where from boyhood until the seventieth year 
the bowels did not move more than once a week, and yet the individual en- 
joyed perfect health. In those accustomed to large doses of opium the 
bowels have been known to move only four times in the year. Departure 
from the standard natural to each individual will determine the existence 
or non-existence of constipation. 

Symptoms. — Usually when a person whose bowels have been accustomed 
to move daily habitually passes two or three days without defecation he 
complains of a sense of fulness in the rectum, with flatulence, headache, 
vertigo, a foul breath, anorexia, and well-marked dyspeptic symptoms. 
Nervous subjects become hypochondriacal, and there is mental inactivity 
with insomnia, or the individual awakes unrefreshcd from a broken sleep. 
The skin becomes parched, shrivelled, sallow and pasty. Eruptions such as 
psoriasis, eczema, prurigo, erythema and urticaria often appear upon the 
surface. There are frequent flushings of the face, and the eyes are sur- 
rounded by deep purplish rings. The tongue is flaccid, often indented by 
the teeth. The breath and the perspiration have an offensive odor, and 
frequent attacks of cardiac palpitation cause the patient to become anxious 
about himself. Those who are habitually constipated are subject to fits of 
vertigo and temporary loss of consciousness. 

Besides the subjective symptoms of constipation there are those produced by 
the mechanical interference caused by the hard faecal masses. If the colon is 
distended there is more or less pain, which is nearly always located in " the 
chest." A distended transverse colon may cause such pressure upon the 
duodenum as to interfere with its function and give rise to dyspeptic symp- 
toms. The pressure of large faecal collections in the descending colon and 
caecum sometimes causes irritation along the genito-urinary tract, irrita- 
bility of the bladder, and neuralgic pains in the groins, ovaries, testicles, loins, 
and lower extremities. At any time the symptoms of intestinal obstruction 
may occur. Diarrhoea may follow prolonged constipation, from the catarrh 
excited by the irritation of the mucous membrane produced by the fascal 
mass, and pressure on the biliary duct may cause an obstructive jaundice. 



348 



DISEASES OF THE DIGESTIVE SYSTEM. 



The impacted faecal masses may give rise to one large tumor, or to 
several small yet distinct masses which can easily be detected along the 
line of the large intestine ; they may be felt often in the transverse or 
ascending colon as movable tumors, but generally the largest accumula- 
tions collect in the sigmoid flexure and caecum. These tumors are often so 
large that they cause tenesmus. In the aged, torpor of the rectum is often 
marked by spurious diarrhoea, acute pain in the lower part of the abdomen, 
great tenesmus and bearing down at stool, accompanied by dysuria, and, 
often, retention of the urine. 

Differential Diagnosis.— The method of the diagnosis of impacted faecal 
masses has been given under the head of "Intestinal Obstruction." Im- 
pacted feces in the rectum may be mistaken for cancer; a digital examina- 
tion of the rectum will establish the diagnosis. 

Prognosis. — When the constipation is functional, and not the result of 
malignant growths, or intestinal obstruction other than faecal, the progno- 
sis is good. In very old people it is almost impossible to overcome habitual 
constipation, on account of their constant indolence and apathy. Inflam- 
matory complications always render the prognosis unfavorable ; and after 
long-continued constipation the symptoms of intestinal obstruction are 
apt to be followed by peritonitis of a low type, which may not be suspected 
during life. 

Treatment. — The treatment of temporary constipation consists in the ad- 
ministration of a dose of Epsom or Rochelle salts, or a tumbler of any one 
of the many efficient natural waters ; or, if indicated, a mercurial purge 
followed by a saline. It is not often that a physician is consulted for sim- 
ple constipation ; care, diet, and exercise, with an occasional cold water 
enema, are usually all that is required to keep the bowels open. 

Habitual constipation, however, frequently attains the dignity of a disease, 
audit requires much care and patience, both on the part of the physician and 
patient, to overcome it. One who suffers from habitual constipation should 
endeavor to establish a regular hour for the evacuation of the bowels. Strain- 
ing at stool should be avoided. Eegular habits in this respect are most effi- 
cient for overcoming obstinate constipation ; the success of any plan of 
treatment will depend largely upon the perseverance of the individual. 
The dietetic measures consist in partaking freely of those articles of food 
which leave a bulky residue, such as the coarser vegetables, cracked wheat, 
oatmeal, etc. Fruits which have fine seeds (figs, strawberries) that will stim- 
ulate the intestinal mucous membrane, are of service if they do not cause 
indigestion. Prunes sweetened with molasses are sometimes very efficient. 
Great care should be exercised not to overload the stomach with food difficult 
of digestion, and each individual is a law unto himself in this matter. A 
goblet of cold or hot water just before retiring and on rising will often over- 
come a long-standing constipation, while the daily use of saline waters is to 
be avoided, for such use often makes the constipated habit more inveterate. 
Daily exercise in walking or horseback riding, is a most efficient means for 
overcoming constipation in those who are strong and vigorous. Water 
should be taken freely before and after the exercise. The tonic effects of a 



INTESTINAL COLIC. 



349 



cold sponge or shower-bath on rising are often of great service. The mechan- 
ical means consist in friction and kneading of the abdomen. In the old 
and bed-ridden, bending the body backward and forward will be fonnd to 
provoke and aid defecation. The galvanic current is especially beneficial in 
the aged and paralyzed. Included in the list of mechanical means are ene- 
mata and suppositories. Cold water, salt water, soap and water, castor-oil, 
etc., are at first very efficient as enemata, but the rectum very soon becomes 
accustomed to them and ceases to respond to their stimulus. 

If mechanical means, diet and change of habits fail to overcome the con- 
stipation, recourse must be had to medicinal agents. These are very 
numerous ; the rule is to begin with the mildest. Cases are often met with 
where an individual has taken stronger and stronger cathartics without 
avail, and until the great object of his life seems to be to get a movement 
from the bowels. It will generally be found in such cases that reliance has 
been placed wholly on drugs ; by changing to the milder cathartics, regulat- 
ing the diet, and insisting upon daily exercise, the constipation is easily 
overcome. It is always to be borne in mind that drugs are only aids to 
other measures. Tonics should always be combined with laxatives ; gen- 
tian, strychnine and quinine, combined with aloes, will often effect more 
than the most drastic purgatives. Favorite cathartic combinations are : — 
(1) aloes, myrrh, colocynth, gentian, and quinine ;— (2) aloes, rhubarb 
and strychnia ; — (3) strychnia and aloin ; — (4) nux vomica, aloes, bella- 
donna, and podophyllum. In all combinations for constipation in females, 
belladonna and hyoscyamus are very active agents. Podophyllum produces 
slow and painless evacuations, and acts efficiently for a long time. In very 
obstinata cases, colocynth, scammony, or one-sixth of a drop of croton-oil 
may be required until the habit of daily evacuation is established. Rhu- 
barb and magnesia is a favorite cathartic in children and young girls. In 
old age and in children, drastic cathartics are always to be avoided. If a 
large focal mass becomes impacted in the lower part of the colon, it 
will often have to be scooped out with the finger or rectal scoop. If 
the mass is exceedingly hard, it is best to throw a steady stream of moder- 
ately hot water and glycerine against it before attempting to remove it. 
Enemata are adjuvants to all plans of treating constipation, where there 
is evidence of a large faecal accumulation in the lower bowel. 

INTESTINAL COLIC. 

The term intestinal colic, in its wider sense, includes all painful affec- 
tions of the intestines which are not caused by structural changes in the in- 
testinal walls. Its varieties are flatulent, lilious, lead, copper, gouty and 
rheumatic colic. It belongs to the class of neuroses, and is purely func- 
tional in its nature. It is attended by irregular spasmodic contraction of 
the muscular coat of the intestine. 

Etiology. — It occurs most frequently in the young, the liability to it stead- 
ily decreasing with advancing years, and in females oftener than in males. 
Neurotic temperaments and a sedentary mode of life, rheumatism, chronic 



350 



DISEASES OF THE DIGESTIVE SYSTEM. 



alcohol ism us, and gout predispose to it. Its most frequent direct cause is 
excessive distention of a portion of the intestinal canal. It is apt to occur 
in the hysterical and hypochondriacal, and in those who are the subjects of 
malarial and syphilitic cachexia. Hepatic and biliary derangements induce 
it. Cold, especially cold to the feet, is often its exciting cause. Direct 
irritation of the bowels by undigested food, certain articles of food, as cu- 
cumbers, shell-fish, strawberries, etc., will cause colic in some persons. 
Gaseous collections and distention of the intestine by fasces, or by bundles 
of worms, sometimes excite it. Lead and the copper salts cause colica pic- 
tonum and copper colic. All metallic colics seem to result from hyperes- 
thesia of the terminal nerves. 

Symptoms. — An attack of intestinal colic may be preceded by a sense of 
distention in the abdomen, slight nausea and belching, languor, numb- 
ness, irritability of temper, or apathy. The attack itself comes on sud- 
denly. 

In flatulent colic, there is a severe twisting, paroxysmal pain around 
the umbilicus, or in the region of the colon. The abdomen becomes dis- 
tended with the flatus, the bowels are constipated, eructations and borbo- 
rygmi are present, and there may be vomiting. The escape of flatus, change 
of position, and steady pressure over the abdomen relieve the pain ; rarely 
is the abdomen tender. There is no rise of temperature, the surface, if the 
pain is severe, is cold and covered with clammy perspiration. The pulse is 
small and feeble. At the height of the attack the patient groans and rolls 
about, frequently throwing himself across some hard substance, so as to 
cause pressure on the abdomen. In children, convulsions, projectile vom- 
iting, syncope, strangury, priapism, and cardiac palpitation are not infre- 
quent. A large quantity of limpid urine is usually secreted, and there is a 
frequent desire to urinate. After several hours, during which many spasms 
of the colic have occurred, large discharges of flatus, rumbling of the boAV- 
els and milder paroxysms of pain, mark the termination of the attack. In 
the weak and nervous, the expression of the countenance, the condition of 
the pulse, and the signs of collapse may cause one to suspect intestinal per- 
foration. On palpation during a spasm, the intestine at points may be 
felt rigid and hard ; the symptoms disappear as the paroxysm subsides. 

Flatulent colic is often called crapulous, when it follows a too hearty meal 
or the ingestion of indigestible articles of food. In crapulous colic, the 
tongue is either covered with a white fur, is enlarged, showing the red 
papillae through it, or it is bright red at the tip and edge. Crapulous colic 
is accompanied by pains in the head and dimness of sight ; and sometimes 
urticaria and roseola, strophulus, and o^ier lichenous eruptions appear on 
the skin. Flatulent colic is most frequently met with in infants, and the 
picture presented by a child with wind colic is too familiar to need further 
description. In adults, flatulent colic may be due to malarial influence, 
and then the attacks will be periodical. 

Bilious colic is accompanied by nausea and vomiting, the vomited 
matters being greenish and yellow. It is preceded by nausea, anorexia and 
a coated tongue. It sometimes begins with a chill. The bowels" are ob- 



IXTESTIXAL COLIC. 



351 



stinately constipated, there is slight fever, the abdomen is tender and 
slightly distended, or it may be retracted. When prolonged, bilious colic 
may be accompanied by jaundice. Bilious colic occurs in summer and 
autumn, chiefly in malarial districts. A form of colic which is often a 
distinct " cramp, " is obviously due to a gouty or rheumatic diathesis ; 
beyond its etiology, it does not differ from flatulent colic. It may be 
metastatic. 

Of the metallic colics, lead colic, " colica pictonum/' is far the most fre- 
quent ; it is a true colic, no lesions being found in the intestines of those 
who have died of it. The metallic colics are produced by the primary ac- 
tion of the metal on the nervous system, and are preceded by the general 
symptoms of the poisoning. Lead colic comes on with moderately se- 
vere paroxysms of pain, which gradually increase in severity until a series 
of intense paroxysms rapidly follow each other. The pain is located about 
the umbilicus, and is twisting or grinding in character. With the colic 
there may be cramps and pains in the extremities. The abdomen is con- 
tracted and hard ; knots of rigid intestine can sometimes be felt. The 
abdomen is not tender, and forcible pressure markedly relieves the pain. 
The bowels are obstinately constipated, but as the attack passes off diarrhoea 
often occurs. After the subsidence of the pain another attack may be ex- 
cited by taking food, or one may return without any apparent cause. The 
pulse is slow during an attack, and there is no rise of temperature. An 
individual suffering from lead poison is sallow, anaemic, and more or less 
enfeebled. The extensors of the fore-arm are often paralyzed (drop-wrist), 
and there may be amaurosis (due to optic neuritis) and epileptiform con- 
vulsions. Along the edge of the gums is a deep blue dotted line composed 
of lead, formed by the sulphuretted hydrogen produced by decomposing 
food lodged between the teeth reacting on the lead which circulates in the 
capillaries. This is the distinctive sign of lead poisoning. The pain in 
lead colic radiates in all directions, and its point of maximum intensity is 
located at different times in different regions of the abdomen. 

Copper colic may be distinguished from lead colic by the fact that the 
pain is increased by pressure, the abdomen is distended instead of retracted, 
and in place of obstinate constipation there is diarrhoea with greenish stools ; 
there is a purplish line about the gums, and there may be attacks of dysp- 
noea from laryngeal and bronchial spasm. 

Differential Diagnosis. — Intestinal colic may be confounded with peritoni- 
tis, intestinal obstruction, gall-stone colic, intestinal perforation, spinal 
disease, aneurism, labor-pains, hernia and muscular rheumatism. 

In peritonitis there is usually a distinct febrile movement, the pulse 
is accelerated and is tense and wiry in character. In colic there is no 
fever or increase in pulse-rate, the rule being rather a slowed pulse. In 
peritonitis the patient avoids the slightest motion of the body, and firm 
pressure over the abdomen increases the pain, while in colic the patient 
tosses from one side to the other, and firm pressure over the abdomen 
relieves the pain. The pain of peritonitis is constant, that of colic 
is paroxysmal. 



352 



DISEASES OF THE DIGESTIVE SYSTEM. 



Perforation of the intestine is to be distinguished by the intensity and 
rapidly increasing severity of the pain, rapidity of the pulse, rapidly de- 
veloping tympanitis and collapse. 

In spinal disease the pain is along the course of the nerves and all the 
intestinal symptoms of colic are absent. 

Aneurism of the abdominal aorta is distinguished by the physical signs 
of aneurismal tumor, by the change in the femoral pulse, and by constant 
localized pain in the back. 

Hernia has an external tumor, there is stercoraceous vomiting, and only 
great carelessness in the examination will allow of error in the diagnosis. 

Labor -pains may simulate colic, and there are cases on record where — 
in concealed pregnancy — the true state of affairs was not recognized until 
labor was completed. 

Muscular rheumatism is attended by intense and constant pain, aggra- 
vated by motion and pressure, having its maximum intensity at the origin 
and insertion of the muscles. There will be a history of exposure, and also 
of frequent rheumatic attacks in other parts of the body. 

Prognosis. — The prognosis is always favorable. Death has occurred from 
rupture of the intestine from excessive gaseous distention, and from con- 
vulsions in very young children. 

Treatment. — The indications for treatment are to be found in the etiology 
of each attack. In flatulent colic, and in that from impacted faeces and 
undigested food, evacuants are indicated. The internal administration of 
castor-oil and an aperient enema generally give relief. If the colic is due 
to exposure of the feet or abdomen to cold, hot aromatic teas and diapho- 
retics are indicated. In all forms, opium, chloroform, hydrate of chloral, 
or ether may be given to relieve the pain and spasm. In hysterical and 
nervous subjects, at the onset of the attack, Hoffman's anodyne, musk, 
asafoetida, valerian, and the essential oils often quickly relieve the pain and 
remove the flatus. In children, bromide of potassium in carminative 
waters, often affords speedy relief. In some cases it will be necessary to re- 
lieve an overloaded stomach by administering an emetic. Malarial colics 
demand for their relief quinine combined with calomel. Gouty colic is best 
treated with oil of cajeput, Warner's cordial, and carminatives. The feet 
are to be placed in a mustard bath, and a mustard plaster is to be placed 
on the abdomen. Anti-gout remedies are to be given as soon as the sever- 
ity of the colic is relieved. 

In lead colic, opium is the most efficient remedy. It will often relieve 
the constipation. My rule is to combine it with belladonna and croton 
oil (1 grain of opium, l-6th grain of the extract of belladonna, and 1 drop 
of croton oil), every two hours, until relief is obtained. Sulphate of mag- 
nesia is preferred by some to the croton oil ; a warm bath will often give 
immediate relief and hasten the action of the croton oil. As soon as the 
bowels are acted upon the pain disappears. Faradic electricity and pilo- 
carpin are advocated by some German authorities. A milk diet acts as a 
prophylactic and curative agent, and workmen in lead factories should 
drink large quantities of it. It is claimed by some, that sulphuric-acid 



PERITONITIS. 



353 



lemonade is a good preventive, as it forms insoluble lead sulphate. A long 
time elapses before all the lead is removed from the system. 

In copper colic sulphur baths, turpentine stupes or sinapisms, ether and 
opium, and a milk diet, with the casual indications, are all that is ne- 
cessary for its successful management. In all forms there are two prom- 
inent indications for treatment, viz. : to relieve pain with opium, and to 
evacuate the bowels. Warm fomentations and sinapisms to the abdomen 
are always of service. Cold applications are contra-indicated. Always 
seek for, and, if possible, find the cause before cathartics are given. 

PERITONITIS. 

Peritonitis is an inflammation of the whole or a part of the serous mem- 
brane which lines the abdominal wall and covers the viscera contained in 
the abdominal cavity. It may be acute or chronic; local (circumscribed) 
or general. The acute form usually begins at one point and rapidly spreads 
over the entire membrane. The chronic may result from the acute, or it 
may be interstitial, hemorrhagic, tubercular or cancerous. 

Morbid Anatomy. — Acute, general (or diffused) peritonitis begins with an 
intense injection of the capillaries of some portion of the visceral or parietal 
layer of the peritoneum. Sometimes the injection is so intense that the 
capillaries rupture at points and cause small blood extravasations. The in- 
flamed portion at first presents a mottled appearance ; the redness is most 
intense at the starting point of the inflammation. With the capillary 
hyperemia there is desquamation of the endothelial cells, and the perito- 
neum loses its natural glistening appearance, becomes dry and lustreless, 
and there is swelling and an increase in the number of its fixed connective- 
tissue cells. Following this, a more or less abundant exudation takes place 
upon its free surface, into its substance and underneath it. This exudation 
may be fibrinous, sero-fibrinous, or purulent. The changes in general peri- 
tonitis are usually most marked in the parietal portion of the peritoneum, 
in layers of the omentum, and in the meso-colon. 

With the advance of the disease, the fibrinous exudation increases in 
amount, and assumes a distinctly yellowish tinge ; as it increases in thick- 
ness it presents the appearance of a roughened false membrane, which may 
vary in thickness from a mere film to a quarter of an inch or more ; its 
consistency varies from a pulpy mass to a coherent, elastic membrane. It 
may form a continuous layer over the visceral or parietal portion of the 
peritoneum, and agglutinate its opposing surf aces more or less firmly to each 
other. If a serous effusion occurs at the same time, it tends to gravitate to 
the most dependent portion of the peritoneal cavity ; it is usually small in 
quantity. After a time cells appear in the layer of fibrinous exudation, 
probably derived from the connective-tissue of the peritoneum, which 
cause the development of a layer of new connective-tissue, which may give 
rise to permanent thickenings and adhesions between the surfaces. Pap- 
illary connective-tissue growths may also form and cause adhesions; 
these adhesions are usually in patches. The new connective-tissue is most 
23 



354 



DISEASES OF THE DIGESTIVE SYSTEM. 



extensive and thickest over the solid viscera, as the uterus, liver and 
spleen. 

The bands of adhesion may bind down a portion of the intestine and 
cause fatal obstruction, or they may form tense cords underneath which a 
loop of intestine may be suddenly incarcerated. On the surface of the solid 
viscera the new tissue gradually becomes indurated, resembling cicatricial 
tissue. Sometimes the new connective-tissue bands are so slight that the 
peristaltic motion of the intestines causes them to disappear. Firmer adhe- 
sions may cause displacement of the viscera or twisting of the intestines, or 
the whole contents of the abdominal cavity maybe matted into one globular 
mass. Acute peritonitis may cause a general thickening of the peritoneum 
without adhesions, its tissue becoming dense, white and fibrous. In these 
cases the fibro-cellular developments are chiefly in the substance of the 
peritoneum — not on its surface. 

The changes in the intestines. vary: at first, vascular lines are seen running 
along their long axis, and in very acute cases their whole surface is red- 
dened. Interstitial cell-growth of the sub -peritoneal coat, accompanied by 
inflammatory oedema, causes their peritoneal surface to present an opaque 
appearance. The muscular coat loses its contractile power, and they become 
distended with gas, so that when the abdomen is opened they protrude 
through the incision. The abdominal muscles and the surface of the vis- 
cera, especially the liver and spleen, are paler than normal. The intestinal 
mucous membrane is sometimes paler than normal, sometimes intensely 
hyperemia 

In non-adhesive or sero-fibrinous peritonitis, with the plastic exudation 
there is a more abundant effusion of fluid, containing flocculi of lymph 
and cells which are most abundant in the most dependent portions of 
the abdominal cavity. Its color varies from a delicate straw color to a 
grayish red. Underneath the fluid on the surface of the peritoneum there 
is a layer of exudation which in its anatomical arrangement is the same as 
that in adhesive peritonitis, and it undergoes similar changes. Displace- 
ments of the abdominal and thoracic organs often occur from the pressure 
of a large fluid effusion. The fluid effusion may undergo absorption, and> 
the two plastic layers coming in contact, adhesions will form as in the 
adhesive variety. 

Acute suppurative peritonitis may have for its product a fibro- or sero- 
purulent exudation. In this variety, the parietal and visceral layers of 
the peritoneum are partially or completely covered and infiltrated with 
a gray, opaque, soft, fibrous exudation, which is infiltrated with pus 
cells. The effusion varies in color and consistency ; it may be thick, 
creamy, and viscid, or turbid, thin and watery. It collects in the de- 
pendent portions of the pelvic cavity. The purulent exudation may be 
spread out over the entire surface of the membrane, or it may be associated 
with adhesions when it occurs in distinct collections ; it is bounded by or- 
ganized septa, and appears as if there were numerous separate abscesses. An 
ulcerative process may be established, and the purulent accumulation may 
be discharged through the abdominal walls into the intestinal canal, blad- 



PERITONITIS. 



355 



der, vagina, or even into the thoracic cavity. The purulent accumulation 
may find exit, in rare instances, along the plane of the psoas muscle. In 
"puerperal peritonitis," the uterus and its appendages are thickly covered 
and infiltrated with pus. Sometimes the ovaries and the Fallopian tubes 
contain pus. In nearly every instance of acute suppurative peritonitis the 
surfaces of the viscera present evidences of lymphangitis, phlebitis, or super- 
ficial abscesses. If recovery takes place without a discharge of the purulent 
accumulation, a part of it is absorbed, and the remainder becomes cheesy 
and encysted. 

If acute local peritonitis is secondary to visceral inflammation, the in- 
flammatory process in the viscus reaches its surface and involves the peri- 
toneum covering it. These inflammations have received various names, 
as perihepatitis, perisplenitis, perimetritis, etc. ; the inflamed peritoneum 
in this variety is usually sharply defined. Adhesions are quickly formed, 
and encysted purulent effusions frequently result. By the establishment 
of local peritonitis, ulcers of the stomach or intestine and abscesses of 
the liver are prevented from penetrating the abdominal cavity and causing 
a rapidly fatal general peritonitis. 

General Chronic Peritonitis. — An acute general peritonitis may run a 
protracted course, become chronic, and cause sero-purulent collections, 
or it may be chronic from the onset. An extensive adhesive or sero- 
fibrinous peritonitis may become chronic, causing numerous adhesions 
and thickenings of the peritoneum, and a more or less abundant 
collection of fluid contained in the spaces formed by the adhe- 
sions. The fluid after a time usually becomes sero-purulent or puru- 
lent, and in the latter case may be converted into a cheesy mass. Coils of 
intestine are matted together, or very firm adhesions with organs or with 
the abdominal parietes occur. In all cases of chronic peritonitis there are 
extensive peritoneal adhesions and thickenings. When a considerable quantity 
of pus is circumscribed by fibrous septa, either an external opening takes 
place or it becomes encapsulated. In some cases of chronic general perito- 
nitis, there is a gradual ascitic accumulation. In most cases, pigmented 
and hemorrhagic spots stud the thickened peritoneum. Local or circum- 
scribed chronic peritonitis may be developed over an enlarged spleen, or a 
cirrhotic liver, or in connection with chronic intestinal diseases. Its ana- 
tomical changes are similar to those of general chronic peritonitis. 

In hemorrhagic sub-acute peritonitis, the new tissue formations are exceed- 
ingly vascular, and the thin walls of the vessels may rupture. The new mem- 
brane may consist of one thin layer, or of several strata with elfused blood 
between them. Sometimes the new tissue is infiltrated, and the entire sur- 
face of the peritoneum may assume a dark brown color, the fluid in its 
cavity having a distinct chocolate hue. This form of peritonitis is especially 
liable to occur with hypertrophic cirrhosis. 

In tubercular peritonitis there may be only a few tubercular 
nodules on the surface of the peritoneum, or there may be a gran- 
ular infiltration of the entire membrane. In its milder form only 
a few gray, semi-transparent tubercles will be found in that portion 



356 



DISEASES OF THE DIGESTIVE SYSTEM. 



of the peritoneum which overlies intestinal ulcerations. In severe or 
extensive tubercular peritonitis, the surface of the peritoneum is studded 
with tubercular granulations, w T hich are also disseminated through the new 
tissue formation, and in the subjacent peritoneal and subperitoneal tissue. 
The mesentery and omentum are also studded with granules. The adhe- 
sions formed in tubercular peritonitis divide the cavity into compartments, 
which contain the effusion. The effusion may be sero-fibrinous or puru- 
lent ; in some instances it is hemorrhagic, and varies in color from a light 
pink to a deep chocolate. In very severe cases tubercular peritonitis is 
always hemorrhagic. Ecchymotic spots and petechise are frequently pres- 
ent in the new membrane. No form of diffuse peritonitis, except can- 
cerous, causes such extensive thickenings, adhesions, and distortions as 
tubercular. 

Camerous Peritonitis. — Cancer of the peritoneum is rarely primary, but 
is propagated to the peritoneum from adjacent organs. When peritonitis is 
the result of cancer in the peritoneum, it commences with the primary cancer- 
ous developments, or is established when cancer of the abdominal or pelvic vis- 
cera reaches their surface and involves the peritoneum covering them. The 
cancerous developments may begin in the omentum and gradually involve 
the entire peritoneum. Cancerous peritonitis may begin as a diffused sup- 
purative peritonitis, in connection with rapid cancerous developments in 
some of the abdominal viscera, especially in the uterus. Sometimes, in 
cancerous peritonitis, the peritoneum may be distended with a serous, lemon- 
colored or whey-like fluid, accompanied by a more or less abundant plastic 
exudation with hemorrhages into the exudation. The hemorrhage into the 
effusion colors it as well as the cancerous nodules on the surface of the per- 
itoneum. Adhesions are formed as in the other varieties of peritonitis, and 
collections of fluid may thus become encapsulated. This variety of peri- 
tonitis is not only attended by the development of tough, leathery mem- 
branes, hut entire organs may be enveloped by the new tissue formations ; 
in these cases the mucous membrane of the intestinal tract is usually the 
seat of chronic enteritis. 

Etiology. — Peritonitis may occur at any age, in the strong and robust as 
well as in the weak and feeble. It is met with more frequently in females 
than in males ; certain localities predispose to it, and the tendency to it is 
greater in those suffering from chronic diseases. Karely, if ever, is acute 
peritonitis of spontaneous origin. But the discovery of its cause during 
life is often very difficult, yet very important, for on the cause depends the 
prognosis and to some extent the treatment. 

The exciting causes of acute peritonitis are : first, intestinal obstruc- 
tions and perforations. Under this head may be included typhlitis 
and perityphlitis, with ulceration; rupture of hepatic and other 
abscesses ; ulceration and rupture of the stomach, the gall or urinary 
bladder; rupture of hydatid and ovarian cysts; ulceration and per- 
foration of the intestines in typhoid fever, syphilitic or tubercular in- 
testinal ulcers ; and the rupture of an abdominal aneurism. In rare 
instances, hydatids of the lung or purulent pleural accumulations open 



PERITONITIS. 



357 



into the cavity of the abdomen and set up a diffuse peritonitis. Injections 
into the uterus may pass through the Fallopian tubes into the peritoneal 
cavity and cause peritonitis. Rupture of an organ from a blow or fall, and 
penetrating wounds of the abdomen, are causes of traumatic peritonitis. 
Abscesses of the abdominal parietes, of the vesiculae seminales, or psoas and 
lumbar abscesses from caries and necrosis of the spine, ribs or pelvic bones, 
may open into the peritoneal cavity and cause general peritonitis. 

Secondly, the extension to the peritoneum of inflammation of organs 
covered by peritoneum is a common cause of local peritonitis. In this 
class of cases the peritonitis is first local, and then it may become general. 
Inflammation of the stomach or intestines may, by extension, involve the 
peritoneum covering them. Peritonitis may result from extension of in- 
flammation from the uterus and its appendages, liver, spleen and kidneys. 
In typhlitis, perityphlitis, proctitis, periproctitis and chronic ulcer of the 
rectum, peritonitis may occur by extension of inflammation without per- 
foration. Venous thrombi, especially lymphangitis and phlebitis of the 
uterus, or severe contusions of the abdomen may cause peritonitis by exten- 
sion. Intestinal intussusceptions, vol villi, hernias, etc., quickly induce per- 
itonitis even when no rupture has occurred. Gangrenous and inflammatory 
processes in the umbilical vessels often give rise to peritonitis in the new- 
born. In the very young, incomplete descent of the testicle may cause 
it. Diverticula from hernia of the mucous membrane of the lower bowel 
through the muscular coat, may become filled with fasces and excite peri- 
tonitis. 1 

Thirdly, in many instances acute general peritonitis is the immediate re- 
sult of infection ; pyaemia, septicaemia, and puerperal fever are the condi- 
tions in which infectious peritonitis is most likely to occur. Puerperal peri- 
tonitis may occur with or without pyaemia. Intra-uterine peritonitis can 
often be traced to a syphilitic taint, and to puerperal sepsis in the mother. 
Exposure to cold and wet rarely, if ever, directly causes peritonitis. Serous 
inflammations of a rheumatic character are very interesting in their com- 
binations ; we may find peritonitis with pericarditis and pleurisy, or with 
pneumonia and dysentery. Erysipelas has been complicated by peritonitis. 
Chronic general peritonitis may result from acute diffuse, or from acute 
local peritonitis, or from tubercle and cancer. It may be caused by long- 
standing ascites, in connection with cirrhosis of the liver and chronic 
splenitis. Chronic local peritonitis follows inflammatory conditions in or- 
gans which have a serous covering, by simple contiguity of tissue, as in 
hepatitis, hobnailed liver, enlarged spleen, chronic dysenteric ulcers, 
chronic typhlitis, etc., etc. Tumors may excite local chronic peritonitis 
when they are in contact with the peritoneum, as ovarian tumors. Chronic 
peritonitis has occurred, according to Yirchow, in intra-uterine life. Ex- 
tra-uterine pregnancy without rupture, when the foetus undergoes degen- 
eration, may lead to chronic peritonitis. Hemorrhagic peritonitis occurs 
most frequently with hypertrophic cirrhosis of the liver, Bright's disease, 
general tuberculosis, and acute articular rheumatism. Tubercular peri- 



1 American Clinical Lectures, page 221. 



DISEASES OF THE DIGESTIVE SYSTEM. 



tonitis is met with most frequently in early life, and cancerous peritonitis 
between the ages of forty and sixty-five. 

Symptoms. — The symptoms of acute peritonitis vary with its extent, 
severity, and the causes which produce it. If it is the result of intestinal 
perforation, its onset will be marked by excessive pain over the whole ab- 
domen. In infectious peritonitis, the first symptom will be a severe chill. 
Peritonitis resulting from the extension of an already existing visceral in- 
flammation begins with local and gradually increasing pain. All varieties 
of acute peritonitis from whatever cause are ushered in by pain as one of 
the earliest symptoms. The pain may be local or diffuse. In severe cases, 
if local at first, it becomes diffuse in a few hours. It is described as a 
cutting, burning pain, aggravated by pressure and by movements of the 
abdomen. The more sudden the onset, the more intense the pain. In some 
cases, the weight of the bedclothes cannot be borne. The pain causes the 
patient to remain motionless, he lies on his back, with the knees drawn 
up, the breathing is wholly thoracic, the respirations are rapid and super- 
ficial, and the face, by its pallid, drawn and anxious look, is almost 
diagnostic of the disease. In most cases, the pain is at first paroxys- 
mal. , 

If the peritonitis is general the abdomen soon becomes distended and tym- 
panitic, the tympanitis increasing as the disease advances. At the onset of 
acute peritonitis, the abdominal muscles are rigid and contracted ; after 
this tonic rigidity they relax and allow of abdominal distention. Some- 
times the distention is so great that the diaphragm is pushed up as far as 
the third or fourth rib, the lungs are compressed, and the heart, liver and 
spleen are displaced. In local acute peritonitis, the tympanitis is usually 
slight ; in diffused it is excessive and increases the pain and causes dysp- 
noea, the respirations often being increased to forty or sixty per minute. 
As the intestines become distended with gas, percussion elicits a tympa- 
nitic note over the whole abdominal cavity. If there is a rapid effusion of 
serum, it will gravitate to the most dependent portion of the peritoneal 
cavity and an abnormal area of dulness will mark its position, the line of 
which will change with a change in the position of the patient. If a large 
amount of coagulable lymph is poured out over that portion of the.perito- 
neum which covers the liver or spleen, a distinct fremitus may be com- 
municated to the hand as it passes over the hepatic and splenic regions, 
accompanied by distinctly audible friction sounds. 

The temperature in acute peritonitis has no typical range ; it may not 
rise above the normal. In most cases it ranges from 102 to 103° E. ; it is 
of the remittent type, being lowest in the morning. If recovery takes 
place, it gradually falls to normal. In fatal cases it may fall below the 
normal during the period of collapse. The pulse is accelerated, often reach- 
ing 140 per minute. For hours before a fatal issue it may beat 200 per 
minute. It is small, hard and wiry in character, and when very rapid is 
hardly perceptible at the wrist. In exceptional cases it is tolerably full and 
strong, and does not rise to more than 90 beats per minute. 

Vomiting is a prominent symptom ; if that portion of the peritoneum 



PERITONITIS. 



359 



covering the stomach is first involved, it precedes all other symptoms. It 
usually comes on about the second day ; the vomited matters at first con- 
sist of the contents of the stomach, later they are a mucus mingled with 
a spinach-green material, which by some is regarded as characteristic. 
Whenever stercoraceous vomiting occurs in peritonitis, it is evidence of 
intestinal obstruction, such an obstruction being the cause or the result of 
the peritonitis. Total paresis of the lower bowel in rare instances may 
cause stercoraceous vomiting when the muscular wall of the intestine 
above is still active. Sometimes there is constant nausea without vomit- 
ing ; hiccough and gaseous eructations indicate that the diaphragmatic 
portion of the peritoneum is involved. The tongue is covered with a 
thick coating, and anorexia is present from the onset. Constipation due 
to paralysis of the muscular coat of the intestine is the rule, especially 
in the early stage of peritonitis. Yet diarrhoea may not only occur during 
the later stages of the disease, but it may exist throughout its entire course. 
In puerperal peritonitis there is usually watery diarrhoea, and diarrhoea is 
often present in the peritonitis of children. 

The urine is scanty and deposits urates ; "scalding" frequently occurs, 
and if the peritoneal covering of the bladder is involved there may be 
retention of urine or painful micturition. The tendency to heart failure 
and to collapse is one of the most striking characteristics of acute peritonitis. 
In all varieties it must be remembered that the disease rarely runs a typical 
course ; even pain may be absent. A sudden collapse attended by a soft, 
feeble pulse and brown tongue, quickly terminating in death, may be fol- 
lowed by an autopsy which shows the intestines matted together by recent 
inflammatory products. When peritonitis follows intestinal perforation, all 
the symptoms from the onset are severe. The face quickly becomes haggard, 
drawn, and dejected; the eyes are sunken and surrounded by dark 
purple rings ; the nose and cheeks are pinched, the lips are blue, 
the upper one being lifted and tightly drawn across the teeth, 
the voice becomes feeble, or the patient speaks in a husky whisper, 
the extremities are cold and covered with a clammy perspiration, the 
radial pulse is hardly perceptible, the respirations assume the type known 
as " Cheyne-Stokes " respiration, general cyanosis supervenes and death is 
reached within forty-eight hours. Sometimes death occurs within three 
or four hours from the shock of the perforation. The mind is usually 
clear throughout the entire course of the disease ; in infectious peritonitis 
loss of consciousness, apathy, or delirium may precede death by a few 
hours. The pulse and the amount of cyanosis are measures of the heart 
failure. In cases where there is a large amount of fluid effusion the pain 
subsides with the occurrence of the effusion, and this sometimes leads to a 
mistake in prognosis on account of the supposed subsidence of the peri- 
tonitis. In suppurative peritonitis the pain is not infrequently absent, but 
typhoid symptoms are present from the onset, delirium is the rule rather 
than the exception, recurring rigors are common, the fever increases 
toward evening, and the pulse becomes very rapid. Occasionally in typhli- 
tis, gastric ulcer, and intestinal perforation, the shock of the perforation. 



360 



DISEASES OF THE DIGESTIVE SYSTEM. 



or the feeling as if something had suddenly burst, or been torn within the 
abdomen, is distinctly appreciated by the patient. 

Local or circumscribed peritonitis usually pursues a sub-acute rather than 
an acute course. Chronic peritonitis (non-tubercular and non-cancerous) 
is usually the sequela of an acute attack. If convalescence is not established 
during the first week of an acute general peritonitis, the character of the 
inflammation changes and it becomes chronic. Rigors alternate with irregu- 
lar sweats, and a steady increase in the size of the abdomen marks the pas- 
sage from an acute to a chronic peritonitis. There is rapid loss of flesh and 
strength, and a marked diminution in the general vital powers. The face 
assumes the haggard, drawn look so often found with chronic abdominal 
disease. The intense pain of the acute attack subsides, and a " dull ache " 
with more or less tenderness remains. The pain assumes a colicky character 
and not infrequently is increased by taking food. The abdominal muscles 
remain rigid and tense. The temperature ranges from 99° to 104° F. The 
pulse continues rapid and feeble. There is anorexia and progressive ex- 
haustion ; diarrhoea alternates with constipation. Fluid accumulates in 
the peritoneal cavity, sufficient in some cases to cause dyspnoea. The 
thickenings and adhesions which develop may so interfere with the ve- 
nous return that oedema, thrombosis and albuminuria may result. In 
latent general chronic peritonitis there may be large ascitic accumulations 
accompanied by abdominal tenderness, loss of appetite and progressive 
anaemia. The pulse is small and rapid, the vomiting is persistent, and with 
the accompanying diarrhoea exhausts the patient. Recurring attacks oi 
acute local peritonitis hasten the fatal issue. 

In tubercular peritonitis the pain is paroxysmal in character. Its onset 
is often sudden, attended by fever and well-marked- constitutional disturb* 
ance, the pulse is rapid and feeble, there is nausea, vomiting and diarrhoea. 
The tongue is heavily coated, thirst is intense, and there is rapid loss of flesh 
and strength. The skin becomes harsh and dry. Typhoid symptoms appear 
early, fluids gradually accumulate in the peritoneal cavity and the patient 
dies of asthenia. Redness and oedema about the umbilicus are regarded as 
characteristic of tubercular peritonitis. In some cases the pain is so slight 
as to amount only to a sense of tension and fulness in the abdomen ; and 
yet there may be a large effusion into the peritoneal cavity. The tongue 
becomes red and shining, the stomach is irritable ; hectic fever is accom- 
panied by profuse sweats during sleep, and the abdomen has a doughy feel. 
Some cases are unattended by ascites, and knots of intestine embedded in 
firm hard masses are felt in the region of the umbilicus. Friction sounds 
may be heard over these masses. Tubercular peritonitis may have for its 
chief and only symptoms, ascites, anaemia, and the evidences of geneial 
tuberculosis ; its progress is interrupted, now there is marked improvement 
and cessation of all the abdominal symptoms, and then there follows a period 
when death seems imminent. As a rule, there is moderate fever and slight 
pain, with considerable ascites. The mesenteric glands are usually en- 
larged. 

Cancerous peritonitis is attended by the same local symptoms as tuber- 



PERITONITIS. 



361 



euiar. Sometimes a tumor may be felt, especially in the region of the omen- 
tum and mesentery. There is always ascites ; the fluid collects giadually, 
and often in very large quantities ; constipation is more frequent than diar- 
rhoea, and death is often the result of intestinal obstruction. In some cases 
the abdomen is very sensitive, and paroxysms of colicky pains are not in- 
frequent. The temperature rarely reaches 100° If the peritonitis has 
extended from the stomach, liver or intestine, the symptoms of the primary 
disease will have been well defined before the development of the peritoni- 
tis. At any period in the course of cancerous peritonitis all the symptoms 
of acute general peritonitis are liable to be developed. The diagnosis rests 
on the presence of a gradually increasing tumor and the cancerous cachexia. 

Differential Diagnosis. — Peritonitis may be mistaken for colic, intestinal 
obstruction (without peritonitis), enteritis, abdominal neuralgia, hysteria, 
rheumatism of the abdominal muscles, renal and biliary colics, and suppu- 
rative cellulitis of the abdominal walls. The ascites of chronic peritonitis 
may be mistaken for that of the last stages of cirrhosis of the liver. The 
differential diagnosis of colic, intestinal obstruction, and enteritis has al- 
ready been given. 

The pain in abdominal neuralgia simulates that produced by a 
tightly drawn cord about the abdomen, and follows the course of 
the genito-crural nerve. There is tenderness on pressure only at the 
point of exit of the nerve from the spine. There is no tympanitis, no asci- 
tes, no rise of temperature, or acceleration of the pulse, and no signs of 
collapse. The muscular rigidity of commencing peritonitis is absent. 

In hysteria, the patient is ready to complain of increased pain before the 
hand touches the abdomen, yet the firmest pressure does not increase the 
pain if the attention of the patient is engaged. The pulse, temperature, and 
signs of collapse of peritonitis are absent, the countenance is not that of peri- 
tonitis, and there is present the globus hystericus, and the attack is followed 
by the passage of a large quantity of watery, straw-colored urine. 

In rheumatism of the abdominal muscles, the pain and tenderness are 
most intense at the origin and insertion of the muscles. There is no rise of 
temperature, no vomiting, and no signs of collapse ; the pulse is normal, 
and there will be a history of acute or sub-acute articular rheumatism. 

In the passage of a gall-stone, and in renal colic, the patient throws him- 
self about in excruciating agony, and the pain is referred to the region of the 
common bile-duct, or to the course of the ureter. In the passage of a gall- 
stone, it is paroxysmal in character, and will shoot back from the margin of 
the ribs over the gall-bladder to the spinal column. If it continues twenty- 
four hours, the patient becomes jaundiced. In renal colic the pain radiates 
from the kidney along the ureter to the testicle, which is retracted. Both 
are accompanied by characteristic changes in the urine or faeces, neither is 
attended by rise of temperature or great acceleration of pulse, and there is no 
tympanitis or tenderness on firm pressure in either. 

Suppuration of the abdominal parietes is at first difficult to distinguish 
from peritonitis, but after the first two days the superficial swelling and the 
absence of the constitutional symptoms of peritonitis establish the diagnosis. 



362 



DISEASES OF THE DIGESTIVE SYSTEM. 



Prognosis. — Acute general peritonitis is a very fatal disease. Its average 
duration is from four to eight days ; death may occur in a few hours, or be 
delayed two or three weeks. The prognosis in any case is to a great extent 
determined by its cause ; it is most unfavorable when it results from perfora- 
tion, intestinal obstruction, or sepsis. General puerperal peritonitis is almost 
always fatal. The presence of typhoid symptoms, a very rapid and feeble 
pulse, cold extremities, with the other symptoms of impending collapse, in- 
dicate an unfavorable termination. Peritonitis from rupture of an organ is al- 
ways fatal. The prognosis is favorable when the peritonitis is due to extension 
of inflammation from a viscus. When the pain and vomiting cease, the tym- 
panitis subsides, the pulse diminishes in frequency, the temperature reaches 
the normal, and the patient is able to turn in bed, a favorable termination 
is to be expected. Chronic diffuse peritonitis in children, unless purulent, 
usually terminates in recovery. Tubercular peritonitis, after weeks and 
months of anaemia and exhaustion, terminates in death. The same is true 
of carcinomatous peritonitis. Death in acute peritonitis may result from 
shock, from asthenia with typhoid symptoms, and from exhaustion. Among 
its sequela? are collections of pus, stenosis or complete obstruction of the 
intestine, pyaemia, and septicaemia. Permanent jaundice may result from 
narrowing of the bile duct by the contraction of new tissue formations in 
the transverse fissure. 

Treatment. — Acute peritonitis is a severe, rapidly progressive, and dan- 
gerous inflammation, and on this account has always been treated heroic- 
ally. Formerly patients with acute peritonitis were subjected to excessive 
bleedings, tartar emetic was administered in nauseating doses, and to prolong 
the effects of the bleeding, and as an adjunct to these calomel was given 
for its specific effect. At the same time many physicians of recog- 
nized authority were eager to obtain the purgative effects of cathartics, and 
for this purpose recommended and administered large doses of drastic pur- 
gatives. Local bleeding by leeches is often of great service in local perito- 
nitis, but it should be resorted to only at the very onset of the attack in the 
strong and robust. Tartar emetic and calomel, so highly regarded as anti- 
plastics, have fallen into disuse. While acute peritonitis is progressing the 
bowels cannot be moved, and no benefit would result if they were ; so that 
under no circumstance should there be an attempt at purgation. 

The plan of treatment which I have followed for years — a plan which 
gains in favor with me with every new experience — is the opium plan. Prof. 
Alonzo Clark first developed this plan and brought it to the notice of the 
profession. The details of it are as follows : — as soon as the unmistak- 
able symptoms of peritonitis are developed, administer at one dose from 
two to five grains of opium or one-half to one grain of morphine. The exact 
quantity in each case is to be determined by the condition of the patient ; the 
rule is to bring the patient as soon as possible fully under the influence of the 
drug. In the treatment of this disease, it will be observed how greatly pain 
and inflammation modify the effects of this powerful drug. I have adminis- 
tered to patients with peritonitis four grains of opium every two hours for 
twenty-four hours, and then have obtained only a moderate effect of the 



PEEIT0KIT1S. 



363 



drug. The point which must be reached in its administration is moderate 
narcotism, in which state the patient must be kept, not only until all pain 
and tenderness have subsided, but until the pulse has reached its normal 
standard and the tympanitis has entirely subsided. The question arises : 
what are the indications which are to govern the administration of each 
dose of opium ? One must be prepared at the commencement of the treat- 
ment of a case of peritonitis, according to this plan, to be present and de- 
cide upon the quantity of opium to be given at each dose, until the patient 
has fully convalesced. It cannot be trusted to attendants, however intelli- 
gent they maybe. As the patient is brought fully under the influence of the 
opiate, it will be noticed that the entire surface of the body becomes bathed 
in a profuse perspiration. In twenty-four hours a rash, due to the opium, 
will make its appearance on the surface and neck ; this is accompanied by 
an itching of the surface and a constant disposition to rub the nose. The 
pupils become contracted, the eyes suffused, the countenance assumes a dull 
expression, and there is a constant irresistible disposition to sleep. The 
pulse becomes lessened in frequency and force, and the respirations, which, 
before the administration of the opium, may have ranged from 40 to 60 
in a minute, become less and less frequent as the patient comes fully under 
its influence, until they are only twelve in a minute. Now the greatest care 
is to be exercised in the administration of the opium ; the patient is in the 
condition in which it is desirable to keep him. By holding him in this 
state of semi-narcotism, all will be accomplished that can be by the opium 
plan of treatment, and with the respiration at twelve per minute the patient 
is perfectly safe. The amount of sleep is not to be taken into account, but 
the profoundness of the slumber is of great importance. If it is found dif- 
ficult to arouse the patient, the administration of the opium must be stopped 
until he can be easily aroused. If by mistake or negligence the patient be- 
comes fully narcotized, the respirations will sometimes diminish in fre- 
quency to seven or even five in a minute. In this extremity, if the admin- 
istration of opium be stopped, the patient will usually rally from its effects 
after a few hours ; but avoid extremes, endeavor to keep the patient in a 
quiet sleep, not profound, but one from which he can be easily aroused. 
When the pulse begins to diminish in frequency and becomes fuller, one 
may be certain that he is controlling the peritonitis, and as it is controlled 
the patient will become more and more susceptible to the influence of the 
opium. Slowness of respiration and absence of pain cannot be relied on as 
sure indications that the opium is controlling the inflammatory action ; but 
a diminution in the frequency of the pulse, and a subsidence of the tympa- 
nitis are sure indications that the peritonitis is arrested, and that ultimate 
recovery is probable. In most cases, if an acute peritonitis does not depend 
for its exciting cause upon the escape of intestinal gases into the peritoneal 
cavity, or upon complete intestinal obstruction, the inflammatory action 
can be controlled within forty-eight hours from the commencement of the 
attack by adopting, within twelve hours, this plan of treatment. It must, 
however, be continued four or five days longer, for there is still danger of 
a renewal of the inflammation. As the condition of the patient demands 



364 



DISEASES OF THE DIGESTIVE SYSTEM. 



less opium, the dose may be diminished, or the interval between the doses 
lengthened. A safe rule by which to be guided is that, so long as any 
tympanitis exists, the opium should be continued. 

When convalescence is fully established, one should not be too anxious to 
overcome the constipation which usually exists, for a free, spontaneous 
movement of the bowels generally follows a complete subsidence of the 
peritonitis. Wait at least a week for this result before administering a ca- 
thartic, and then, if necessary, employ one mild in its action, such as cas- 
tor-oil. Warm poultices over the abdomen are usually the only local appli- 
cation which I have employed. It is claimed by some that cold compresses 
have a much more beneficial effect than warm applications. My experience 
leads me to doubt the utility of the former, while the latter are far safer, 
and I believe equally efficacious. It has been stated that when the peritoni- 
tis becomes general, excessive gaseous distention of the intestines occurs, 
and this distention greatly increases the danger to the patient ; under such 
circumstances I have recently resorted to minute puncturing of the dis- 
tended intestine with a hypodermic or a very small aspirating needle, and 
have thus relieved the intestinal distention by allowing the gas to escape. 
By so doing, not only is the tension of the peritoneum (which becomes an 
exciting cause of the peritonitis) relieved, but the principal obstruction to 
the respiration is removed, and thus cyanosis is diminished. Immediate 
and marked relief is aiforcled by such a procedure, and as thus far I have 
had no bad results follow, I am disposed to resort to it in all cases where the 
abdomen becomes excessively distended and tympanitic. I remember one 
case in which the gaseous distention was excessive, and the peritonitis was 
supposed to be due to strangulation of a portion of intestine from old peri- 
toneal adhesions, where the relief of the distended intestine by puncture 
was soon followed by a removal of the intestinal obstruction and the rapid 
recovery of the patient. From this circumstance I can readily understand 
how a portion of intestine that was partially constricted by a band of ad- 
hesion might become completely obstructed at the point of stricture by a 
rapid gaseous distention of the intestine above the point of constriction, and 
the relief of the intestinal distention by puncture would very likely liberate 
the constricted portion and thus overcome the strangulation, and so, per- 
haps, save the life of the patient. 

The necessity of absolute quiet, and of the frequent administration of nour- 
ishment and sometimes of stimulants, in small quantities, to this class of 
patients, is apparent. Preceding and during the stage of plastic exudation, 
large doses of quinine are beneficial ; but little nutriment should be admin- 
istered, and that only in a fluid and a highly condensed form. Cracked ice 
may be given to relieve the thirst, and, if there are signs of asthenia, iced 
champagne or brandy should be given in small doses. If hiccough is dis- 
tressing, it should be relieved temporarily by the inhalation of chloroform. 
Vomiting is sometimes allayed by carbonated water, cracked ice and cham- 
pagne, or hydrocyanic acid. Turpentine, as an injection and employed lo- 
cally as an embrocation, will sometimes relieve the tympanitis. W r ith the 
asthenic form of peritonitis, a stimulating plan of treatment should be em- 



ASCITES. 



365 



ployed with the opium. In puerperal peritonitis, great attention should be 
paid to the condition of the uterus and its appendages. Chronic peritonitis 
is treated by local applications of iodine and mercury, and by the internal 
use of iodide of potassium. Its products may be removed by tapping. The 
nutrition of the patient must be carried to the highest point. Tubercular 
peritonitis demands small doses of opium, warm anodyne applications, and 
the administration of tonics, cod-liver oil especially. The treatment of can- 
cerous peritonitis is purely symptomatic ; nausea and attacks of diarrhoea 
and constipation must be promptly relieved. Narcotics may be given for 
the sleeplessness. Concerning the prophylactic and sanitary treatment of 
puerperal peritonitis, the reader is referred to obstetrical works. 

ASCITES. 
{Abdominal Dropsy.) 

Ascites is a local dropsy, — an accumulation of serum in the peritoneal 
cavity. It has also been called peritoneal dropsy, dropsy of the abdomen, 
and hydro-peritoneum. The circumstances under which it occurs are 
similar to those which allow of general dropsy — viz. : obstruction to the 
capillary or lymphatic circulation of the peritoneum, a diminished amount 
of albumen in the blood, and degenerations of the peritoneum. Those 
hydremic conditions which accomjDany exhausting chronic diseases, espe- 
cially diseases of the kidneys, will induce it. One or several of these con- 
ditions may be present in the same case. 

Morbid Anatomy. — The amount of fluid present in ascites may vary from 
a few ounces to four or five gallons. In consistency it may be viscid or 
watery. It is usually of a light straw color, having a faint greenish opal- 
escent tint. It may be opaque and dark, from admixture of blood. With 
disease of the lymphatics it is milky and opalescent. Sometimes it does not 
differ in appearance from pure water. It is alkaline in reaction, and may 
contain albumen, blood, fibrin, fibrinogen, bile-pigments, kreatin, kreatin- 
in, lymph flocculi, and bile acids. Albuminate of soda, leucocytes and pus 
cells are its occasional ingredients. The endothelia of the peritoneum are 
turbid, thick, and in various stages of fatty degeneration. The sub-serous 
tissue is thickened, and the whole membrane has the look and feel of being 
water-logged. The blood changes that cause it consist chiefly in a diminu- 
tion of albumen and an increase of water. Compression, dislocation, and 
diminished function of the abdominal viscera are the results of the ascitic 
accumulation. 

Etiology. — Ascites may be a late symptom of general dropsy. In most 
other instances it results from damming back of the blood in the portal 
tributaries, from pressure on the portal vein — either from hepatic and 
abdominal tumors, or from a diseased condition of the liver substance — 
as in cirrhosis, waxy degeneration, abscess, hepatic atrophy, portal throm- 
bosis, enlarged lymphatics in the transverse fissure, and the constrictions 
due to perihepatitis. These all mechanically impede the blood current in 



366 



DISEASES OF THE DIGESTIVE SYSTEM. 



the portal vessels. Diseases of the heart or lungs which interfere with the 
normal flow of the blood from the cavae will induce it in connection with 
general dropsy ;— under this head are included tricuspid obstruction and 
insufficiency, chronic bronchitis and emphysema, fibrous phthisis, and cer- 
tain forms of mediastinal tumors. Anaemia, hydraemia, chlorosis, malarial 
cachexia, purpura, chronic arsenical poisoning, scurvy, and chronic Bright's 
disease, producing hydraemia— and old age or great exhaustion without 
structural disease — lead to what is often called asthenic ascites or cachectic 
dropsy. Peritoneal dropsy not infrequently accompanies extensive degen- 
eration of the peritoneum, such as tubercle and carcinoma. Finally, ascites 
may occur from unknown causes — from taking cold, after suppression of the 
menses, after the sudden disappearance of acute and chronic cutaneous 
eruptions and ulcers, and perhaps from atmospheric causes. 1 It has been 
suggested that malignant disease of the ovaries and other pelvic organs, and 
of the mesenteric and retro-peritoneal glands, obstructs the capillaries and 
the lymphatic orifices, increasing the functional activity of the endothelia, 
and thus induces ascites. 2 

Symptoms. — The first sign of ascites is a gradual increase in the size of 
the abdomen. The enlargement in simple ascites takes place without pain, 
tenderness, or local subjective symptoms. There is a feeling of fulness, 
and the patient is rendered uncomfortable by pressure of the fluid. The 
respiratory movements are interfered with, and dyspnoea soon results. 
The functions of the stomach may be disturbed, and there may be vomit- 
ing, anorexia, and perhaps haematemesis. Flatulence and diarrhoea are 
frequently present, but when the accumulation of fluid is large it produces 
colicky pains, and often obstinate constipation. All these symptoms are 
relieved as soon as the fluid is removed. Gradually the dyspnoea increases, 
the patient walks with difficulty, with the legs spread widely apart ; the 
urinary secretion is diminished from the pressure on the kidneys and renal 
vessels. The recumbent posture greatly aggravates the dyspnoea. The 
skin and mucous membranes become dry ; the liver and pelvic viscera are 
displaced ; the heart and lungs are pushed upward, and the skin over the 
abdomen becomes tense and shining. The umbilicus is bulged out in the 
form of a globular tumor. The superficial veins are enlarged and tortuous. 
If the inguinal canal is open, fluid may pass into the scrotum ; and ex- 
cessive ascites, by pressure on the vena cava, causes oedema of the feet and 
legs. In hepatic diseases the fluid is chiefly confined to the abdomen, but 
in cardiac and pulmonary dropsies the fluid accumulates first about the feet 
and extends upward, and the abdominal dropsy is then a part of a general 
anasarca. In hepatic dropsies the extremities emaciate while the abdomen 
enlarges ; the skin has a muddy jaundiced hue, and the patient becomes 
exhausted and apathetic. Jaundice, uraemia, delirium, convulsions, coma, 
and cholaemia are prominent symptoms as death approaches. 

Physical Signs. — The physical examination of the abdomen is most im- 
portant in the diagnosis of ascites. 

Inspection. — The abdomen, if distended with fluid, presents the appear- 



i Wagner, Gen. Path., pp. 234-5. 



2 Oppolzer. 



ASCITES. 



367 



ance of a globular or dome-like tumor, the false ribs are elevated and 
pressed out, and the superficial yeins are visible and prominent. The cir- 
cumferential measurement of the abdomen will often be three times as 
great as normal. If the effusion is moderate, the shape of the abdomen 
changes with a change of the position of the patient : it broadens when he 
lies on his back, and when he stands the enlargement will be confined to 
the lower portion. The fluid always gravitates to the most dependent 
portion. 

Palpation. — Fluctuation is obtained when the level of the fluid is above 
the pelvic brim. To obtain the wave most distinctly place the patient on 
his back, place the flat of the hand on one side of the broadened abdomen, 
and with the other hand give one smart tap at a point opposite ; the im- 
pulse of the blow will be felt by the palm of the hand. 

Percussion. — There will be flatness below the level of the fluid, and 
tympanitic resonance above. The line of dulness changes with the 
change of position, and accurately measures the amount of fluid. When 
only a small amount of fluid is present the physical signs of its presence are 
commonly obtained by placing the patient in the " knee-elbow " position. 

Differential Diagnosis. — Ascites may be mistaken for ovarian dropsy, dis- 
tended bladder, pregnancy, hydatid cysts of the liver, and enlargement of 
the spleen. It is important in making a differential diagnosis between 
ascites and ovarian dropsy to have a perfect history of the case. The ab- 
dominal enlargement in ascites is uniform, in ovarian dropsy it is irregu- 
lar. Ascites, however slight, begins at the most dependent portion of the 
abdomen, while ovarian dropsy begins in one of the iliac fossae and gradu- 
ally extends upwards toward the umbilicus. With every change of posi- 
tion, in ascites, the line of dulness changes ; a large ovarian cyst is to be 
recognized by its fixed position and non-gravitation of its fluid. In ascites 
there is fluctuation on palpation ; in ovarian dropsy, fluctuation is absent 
or localized. The abdomen is usually tympanitic above the level of the 
fluid and flat below in ascites, while in ovarian tumor there is often a tym- 
panitic percussion sound at the most dependent portion of the abdominal 
cavity. In ovarian dropsy the outline of the cyst is generally appreciable, 
except in very large tumors where the peculiar form of the cyst may be 
lost, but a rectal or vaginal exploration will generally at once remove all 
doubts. In ascites there will generally be a history of liver, heart, or 
kidney disease, and the uterine organs and functions will be normal. On 
tapping the abdomen a serous fluid will be withdrawn in ascites ; in ovarian 
tumors, it will be a dark, highly albuminous fluid and contain granular 
non-nucleated cells, supposed to be characteristic. 

A distended and sacculated bladder may be mistaken for dropsy, but the 
introduction of the catheter will decide the question. 

Pregnancy will afford ballottement, placental bruit, the sounds of the 
foetal heart, and will be accompanied by distinct mammary changes. The 
uterine tumor can be distinctly mapped out, and a vaginal examination 
combined with external palpation will rarely fail to make a differential 
diagnosis between it and ascites. 



3(58 



DISEASES OF THE DIGESTIVE SYSTEM. 



An hydatid cyst of the liver produces flatness undeviating in area, which 
gradually extends from above downwards, and seldom reaches the pelvic 
brim. Hydatids produce hydatid fremitus on percussion, which is charac- 
teristic. Again, on withdrawal of the fluid, a miscroscopical examination 
will often discover the hooklets of the echinococci. 

Enlargement of the spleen is unsymmetrical ; the tumor is fixed, there is 
no tympanitis, no fluctuation, and the boundaries of the enlarged organ 
can be mapped out on palpation and percussion. Usually the notch at the 
anterior border of the spleen is so distinct that it at once indicates the 
gland. 

Prognosis. — The prognosis depends upon the conditions under which the 
ascites occurs ; if it is dependent upon organic disease of the liver, heart, 
or kidney, the prognosis is unfavorable, but when it is not dependent upon 
structural visceral lesions, e.g., idiopathic and anaemic ascites, the prog- 
nosis is good. The ascitic accumulation may take place rapidly, or weeks 
or months may elapse before the cavity of the abdomen is distended. The 
average duration of hepatic ascites is about six months. So long as the 
cause remains, the fluid will accumulate. Ascites 'may terminate in re- 
covery by the spontaneous or mechanical removal of the fluid, or by the 
removal of its cause, or it may terminate in death from complications, as 
peritonitis, albuminuria or heart-failure, or from pure slow asthenia. 

Treatment. — The first and most important thing in the treatment of 
ascites is to discover the cause, and either to remove or palliate it. In 
most cases the treatment merges into the treatment of the diseased condi- 
tions which produce it. In all cases the diet should be highly nutritious 
and concentrated ; as little fluid as possible should be taken. The contin- 
ued use of powerful diuretics and hydragogue cathartics usually does harm. 
They weaken the patient and often favor rather than retard the 
ascitic accumulation. Elaterium is the most efficient drastic cathartic, 
the potash salts, nitre, squills and juniper are the most efficient diuretics. 
Jaborandi has recently been much employed for the removal of dropsical 
accumulations. In most cases these accumulations can be rapidly removed 
by this drug, but my own experience leads me to the conclusion that it 
hastens rather than retards the fatal issue. Hot-air baths should never be 
employed for the removal of ascitic accumulations. 

Paracentesis abdominis will have to be resorted to sooner or later in these 
cases, but the rule is to postpone it as long as possible. I am, however, 
in favor of tapping before the accumulated fluid has caused pressure 
upon the viscera. I am convinced that whenever fluid accumulation takes 
place in the peritoneal cavity, tapping should be promptly resorted to, 
unless the cause can be removed by mild cathartics or non-stimulating 
diuretics ; and the number of recoveries and the prolongations of life 
which have followed this course in my experience cause me unequivocally 
to recommend it in preference to the prolonged use of those remedial 
measures which increase the discharges from the skin, kidneys and bowels. 
In a large number of cases, improvement of the patient's general health by 
tonics, of which quinine, iron and cod-liver oil are the best, is followed by 



ACTIVE HYPEREMIA OF THE LIVER. 369 

subsidence of the dropsy, and its return is also prevented for a long time 
after its removal by tapping. 



DISEASES OF THE LIVER. 



Diseases of the liver may be classified under the following heads 



L Hyperemia : — 

a. Active or Fluxion. 

b. Passive or Congestion. 
II. Inflammations : — 

a. Interstitial Hep>atitis or 

Cirrhosis. 

b. Circumscribed Hepatitis or 

Abscess. 

c. Diffused Hepatitis or Acute 

Yellow Atrophy. 
Perihepatitis, Local or Gen- 
eral. 

Pylephlebitis, Adhesive and Sup- 
purative. 

VII. Functional 



III. Degenerations : — 

Amyloid or Lardaceous* 
Fatty. 

Pigmentary. 
Atrophy. 

IV. New Growths:— 

Cancer. 
Gummata. 
Hydatids. 
Tubercle. 
V. Jaundice, Hepatogenous and 
Hematogenous. 
VI. Diseases of the Gall Ducts 
and Gall Bladder. 
Derangements. 



ACTIVE HYPEREMIA OF THE LIVER. 

Active hyperemia of the liver is an abnormal determination of blood 
to the organ. It may be acute or chronic. 

Morbid Anatomy. — A liver that is the seat of active hyperemia is more 
or less enlarged in all directions. Its color varies from a light to a dark red. 
It has a firmer feel than normal, although its consistency is really dimin- 
ished. The organ is heavier and smoother than normal, its surface present- 
ing a peculiar shining appearance. 

On section, its substance shows a uniform red color, blood flows freely 
over its cut surface, from the arteries and capillaries which are dilated and 
sometimes tortuous. When the hyperemia is intense, the glandular sub- 
stance of the organ is compressed and there may be evidences of sub-peri- 
toneal effusion. So intense may be the hypersemia that hemorrhagic soften- 
ing and apoplectic extravasation result, and isolated clots or an unbroken 
layer of coagulated blood may be found under its serous covering. 

In chronic hyperemia the liver is often found in a state of partial fatty 
degeneration, somewhat softened, and of a light red or yellow color. In 
rare instances, chronic hyperemia may lead to induration and incipient 
cirrhosis. In the severer types abscesses may be found, and the infiltration 
of a substance resembling albumen has in some cases advanced so far as to 
give distinct colloid degeneration. In syphilitic new-born children, active 
hepatic hyperemia is sometimes found associated with a peculiar plastic 
24 



370 



DISEASES OF THE DIGESTIVE SYSTEM. 



exudation. It is important to remember that the normal hepatic hyper- 
emia temporarily developed after hearty meals or the free use of stimulants 
may be mistaken for active hyperemia. Both acute and chronic hyper- 
emia of the liver may be associated with catarrh of the bile ducts. 

Etiology. — There is a normal functional hyperemia of the liver induced 
by an unusually large meal, or one very rich in hydrocarbons, or by the 
free use of wines : this hyperemia is due to increased blood pressure in the 
vena portae ; it becomes abnormal in those who daily indulge in eating to 
excess, especially if they lead sedentary lives. If the liver-tissue, which 
supports the walls of the capillary vessels, becomes relaxed, there will be an 
abnormal afflux of blood to the organ. This is the case in traumatic 
hyperemia, where a blow over the viscus causes a localized fluxion. Any 
inflammation or growth causing softening of the parenchyma will induce it. 
The action of drugs, spices and alcohol is best explained on this basis. In- 
tense hepatic hyperemia may be caused by miasmatic influences, malaria, 
and other blood-poisons. Under the latter head is included a peculiar 
active hyperemia which occurs in the livers of syphilitic children, and in 
secondary syphilis of adults. High temperature undoubtedly gives rise to 
active hepatic hyperemia, especially when it is associated either with acute 
or chronic malarial infection, Vaso-motor disturbances may undoubtedly 
lead to active hepatic hyperemia. It sometimes occurs during and after 
pregnancy from some unknown cause ; also before the establishment of the 
menses, and during the menopause. Capillary embolism may cause local- 
ized hepatic hypersemia. 

Symptoms. — Active hyperemia of the liver is usually attended by a sense 
of weight and constriction in the right hypochondrium, with some tender- 
ness on pressure under the free border of the ribs. In active malarial 
hyperemia, there is also gastro-intestinal catarrh, nausea, vomiting, diar- 
rhoea, and slight jaundice. There is a bitter taste in the mouth, loss of 
appetite, coated tongue, drowsiness and apathy. Headache is frequent, and 
the patient complains of pain shooting up the right side to the right 
shoulder. This pain is due to pressure on the phrenic nerve, and is more 
intense after meals and when lying on the left side. A sense of dizziness 
comes on when the patient assumes any other position than on the back or 
right side. It is more or less increased by pressure upward against the 
liver. In severe cases of malarial hyperemia, or when it is associated with 
extensive blood changes, such as scurvy, the symptoms are often masked by 
those of the condition with which it occurs. 

Physical Signs. — Inspection in severe cases may show bulging of the 
right hypochondrium, and loss of motion of the lower ribs on the right side. 

On palpation the liver is found enlarged and smooth, and its free 
border is felt below the ribs ; firm pressure against its under surface causes 
pain. 

Percussion. — The area of hepatic dulness is increased in every direction, 
but more vertically than laterally. 

Differential Diagnosis. — A severe active hyperemia may be mistaken for 
cir cum scribed hepatitis with abscess. In circumscribed hepatitis there is 



PASSIVE HYPEREMIA OF THE LIVER. 



371 



acceleration of the pulse, rigors followed by a slight rise of temperature, 
and localized pain. Eecurring chills and sweats indicate the formation of 
pus. In abscess the hepatic enlargement is irregular, while in active 
hyperaemia it is uniform. If the case is seen early, and the enlargement is 
carefully followed, in hyperaemia it will be seen to take place rapidly, while 
in abscess it will be slow. The hepatic enlargement from active hyperemia 
may be distinguished from displacement of the liver downwards, by the 
fact that, although its free border may extend far below the free border of 
the ribs, the normal area of hepatic dulness is not increased. 

Prognosis.— Active hyperaemia generally subsides as rapidly as it occurs. 
The only danger is that the causes which produce it may be continued, 
and lead to some form of hepatic degeneration. 

Treatment. — The main indication in the treatment of this condition is to 
remove its cause. When high living and alcoholic stimulants cause it, re- 
strict the diet and stop the alcohol. When it occurs from prolonged high 
temperature, or from malarial influences, a change of residence is the only 
remedy. An excess of blood in the liver may be temporarily removed by 
saline or mercurial purges, by taraxacum or podophyllum ; their action will 
be increased by the application of one or two leeches about the anus. In 
active malarial hyperemia, the mercurial purges and leeches may be followed 
by full doses of quinine. Turpentine stupes may be applied over a very 
tender liver. When there is gastro-intestinal catarrh with diarrhoea, 
chloride of ammonium and ipecacuanha will be found of service. In those 
who have a predisposition to active hepatic hyperaemia, the daily use of 
mineral waters will be found of service. 



PASSIVE HYPEREMIA OF THE LIVEE. 

Passive or mechanical hepatic hyperaemia (" congestion of the liver") 
consists in an excess of blood, chiefly in the portal veins, with a slowed 
current. 

Morbid Anatomy. — A congested liver, in its early stage, is larger, heavier 
and darker in color than the normal liver, the extent of the increase in size 
corresponding to the degree of the congestion. The capsule may be 
stretched tightly over the enlarged organ, and present a shining appear- 
ance. The consistency of the organ is increased, frequently amounting to 
a stony hardness. 

On section, the cut surface appears mottled, rarely uniformly red in 
color ; the small dark spots seen upon its cut surface are the enlarged and 
thickened veins in the centre of the liver lobules, and as the return of 
blood by these veins is impeded, the surrounding cells undergo atrophy, 
and a granular pigment is deposited about the vena centrales. This change 
in color is made more apparent by a deposit of fat globules in the periphery 
of the lobules, which causes a dirty white ring around the dark central 
spot. Occasionally there are yellowish spots about the central vein due 
either to a catarrh in, or obstruction of the bile ducts, or to distention 



DISEASES OF THE DIGESTIVE SYSTEM. 




of the minute ramifications of the portal vein. In the advanced stage of 

hepatic congestion, 
the liver is diminish- 
ed in size and has a 
peculiar hard feel. 
On section, it presents 
the char acteristic 
"nutmeg" appear- 
ance, which has been 
called the red granu- 
lar liver. The proc- 
esses which were es- 
tablished in the ear- 
lier stage of the con- 
gestion, and the new 
conn e ctive - tissue 
which has been de- 
veloped in the inter- 
lobular spaces, dimin- 
ish the parenchyma 
of the organ. 1 The 
rootlets of the central 
vein become dilated 
and hypertrophied 
and crowd upon the 
liver cells ; thus the 

central spot spreads nearly to the periphery of the lobules. Atrophy of 
the cells grouped around the central vein occurs, and a soft pultaceous 
mass, in which appear new vessels, takes their place. The cells at the 
periphery are in a state of fatty infiltration, and connective-tissue passing 
inward from the interlobular spaces produces the contracted, stony hard 
liver. In connection with these changes in the liver, the mucous mem- 
brane of the stomach is usually the seat of chronic catarrh, and the spleen 
is enlarged. 

Etiology. — The causes of hepatic congestion are mainly included under 
the head of impeded venous return. Heart disease is the most fre- 
quent cause of such obstruction. The damming back of the blood in the 
hepatic veins is the necessary result of tricuspid insufficiency, and of right 
heart failure. When right ventricular hypertrophy fails to compensate for 
valvular lesions in the left heart, or when disease of the lungs, as emphyse- 
ma and chronic pleurisy, obstructs the blood current in the pulmonary artery 
so that the right ventricle is unable to empty itself, engorgement of the 
hepatic veins necessarily follows. The absence of valves in these veins, 
and the fact that they cannot collapse, favor this result. In the same 
way enfeebled heart power, occurring in the course of exhausting diseases, 
causes congestion of the liver. Habitual constipation and a sedentary 

1 Atrophy is chronic congestion with dilatation of the central vessels and their radicles. 



Fig. 71. 
Passive Hepatic Hyperemia. 

Section of liver shoiving a single lobule. 
Central vein of lobule. 

Area of congestion.— Vessels filled with blood, crowding the hepatic 
cells. 

Atrophied liver cells. 

Commencing fatly infiltration of cells in peripheral zone, x 350. 



PASSIVE HYPEBiEMIA OF THE LIVER. 



373 



mode of life 5 either singly or combined, may produce it. The sudden 
suppression of long-continued hemorrhages, as menorrhagia, or bleed- 
ing hemorrhoids, may lead to passive hyperemia of the liver. A large 
mediastinal tumor, such as a thoracic aneurism, may also produce it by 
pressure on the cava. 

Symptoms. — As there is usually some derangement in the circulation of 
the thoracic organs, the early symptoms are very apt to be confounded with 
those of cardiac or pulmonary disease. But soon slight jaundice follows 
the headache, drowsiness and apathy, and it lacks the peculiar greenish 
hue of that which sometimes accompanies the cyanosis of long-standing 
heart disease. Gastric catarrh will usually attend these symptoms, marked 
by loss of appetite, nausea, and vomiting. In the " India Liver" there is 
anaemia, and soon a cachexia is developed. The skin is dry and harsh. 
Later, hemorrhoids appear, and after a paroxysm of dyspnoea and cyanosis 
the hepatic dulness is markedly increased. In severe cases haematemesis 
may occur. If congestion has reached the stage of induration, the gastric 
symptoms become greatly aggravated, and tympanitis, gastric hemorrhage, 
and general dropsy occur. The bowels become constipated, and the faeces 
clay-coiored. The urine is scanty, high-colored, and usually presents traces 
of albumen ; it is loaded with lithates. These patients finally become irrit- 
able, and are subject to fits of palpitation and irregularities of the pulse. 

Physical Signs. — Inspection may show slight bulging of the right hypo- 
chondrium and some restriction in the- movements of the lower portion of 
the right thoracic walls. 

Palpation. — In its early stage, the free border of the liver is readily felt 
below the margin of the ribs ; it is smooth and tender. Later the organ 
is diminished in size, but its free margin can still be felt, and is hard and 
uneven. 

Percussion. — At its commencement the normal hepatic dulness is in- 
creased in every direction, and firm percussion elicits pain. In advanced 
cases the area of hepatic dulness is uniformly diminished. It is always 
important to subject the chest to a thorough physical examination to deter- 
mine the presence or absence of pulmonary or cardiac disease. 

Differential Diagnosis. — Congestion of the liver may be so masked by the 
primary disease which produces it, that it will be overlooked, but it will 
rarely be confounded with any other form of hepatic disease. 

Prognosis. — The prognosis depends upon the condition which causes it. 
If constipation and a sedentary life cause it, the prognosis is favorable. In 
chronic pleurisy and emphysema it can only partially be relieved. When it 
is associated with extreme cardiac disease, recovery is impossible and re- 
lief is only temporary. 

Treatment. — When the symptoms which attend congestion of the liver 
are urgent, a mercurial purge or a brisk saline cathartic with the applica- 
tion of a few leeches about the anus will give relief. If the symptoms aro 
not urgent, a mild laxative followed by a course of mineral waters will 
be beneficial. If the gastric symptoms are severe leeches may be applied 
over the stomach. The diet must be as free from carbo-hydrates as is 



374 



DISEASES OF THE DIGESTIVE SYSTEM. 



compatible with nutrition. Nitro-muriatic acid internally and externally 
is recommended by English and East Indian physicians. Chloride of 
ammonium and iodide of potassium are often advantageous, reducing the 
enlarged organs. In some cases of extensive cardiac disease, mineral 
waters are not ivell borne J and although digitalis will relieve the conges- 
tion, it is apt to interfere with digestion. Each case is peculiar and 
requires its special treatment, which at best is only palliative. 

INTEESTITIAL HEPATITIS. 

(Cirrhosis.) 

Interstitial hepatitis is an inflammation of the connective-tissue of the 
liver. It has been variously named sclerosis of the liver, cirrhosis, the 
" gin-drinker's" liver, the " hob-nailed " liver, granular, and gouty liver. 
Cirrhosis of the liver, the name most commonly used, was first applied by 
Laennec. It means yellow, referring to the color, and not to the consis- 
tence of the organ. 

Morbid Anatomy. — The anatomical changes in interstitial hepatitis begin 
in the connective-tissue covering the smaller twigs of the vena porta?, and 
gradually extend to its larger branches. The hyperplastic process consists 
in the formation of a soft, red, pulpy or gelatinous mass, which makes its 
appearance first in the portal canals. This mass consists of an immense 
number of small round cells, which soon undergo fibrilization and form 
new connective-tissue. The new tissue contracts ; this contraction may 
be limited, or it may involve the whole organ. In the latter case, both 
stages — namely, the stage of enlargement due to the hyperplasia, and the 
stage of diminution in size, the result of connective- tissue contraction- 
may exist in the same liver at the same time. The new tissue, contract- 
ing, presses on the portal capillaries and liver-cells, and gradually en- 
croaches on the intra-lobular structures, causing atrophy and disappearance 
of the cells at the periphery of the lobules, while those at the centre un- 
dergo fatty change, the result of defective nutrition. Sometimes the cells 
at the periphery undergo fatty change before they atrophy. The bile-ducts 
and hepatic capillaries suffer from compression, and the cells around the 
central vein are bile-stained. 

In the first stage of cirrhosis, the liver is slightly enlarged, noticeably in 
the vertical direction ; it is resistant and hard to the feel, the edges are 
rounded and smooth, and the capsule becomes opaque and thickened. Upon 
the capsule are numerous small flattened projections, which are, however, 
not sufficiently prominent to destroy the smoothness. In the first stage the 
liver is uniformly enlarged and hypersemic. In the second stage it is 
smaller than normal, the left lobe usually being but a caudal-like append- 
age to the right, which is nearly globular in shape. The whole organ 
presents a hob-nailed appearance, and is hard, rough, leathery and granu- 
lar. The serous covering assumes a dull gray color, and fibrous bands bind 
the organ to the adjacent parts, especially to the diaphragm. In syphilitic 
cirrhosis these changes are in patches, which are large and well defined. 



INTERSTITIAL HEPATITIS. 



375 



On section the liver- tissue, during the first stage, is extremely hyper- 
semi c. The new cell growth around the branches of the portal vein and be- 
tween the lobules has a pulpy, fleshy look. In the second stage, the liver 
gives a cartilaginous feel to 

A 

iiii 



-\, 





mm 



rn^A 



A 




the knife, and the capsule 
is thickened and resistant. 
The cut surface presents a 
yellow, mottled appearance, 
the mottling being due to 
three changes : first, the 
non-vascular fibrinous 
bands, which are of a slate 
color ; second, the obstruc- 
tion of the bile ducts inter- 
fering with the outflow of 
bile, and the centres of the 
atrophied cells becoming 
pigmented ; third, the cells 
at the periphery of the lobes 
becoming the seat of fatty 
degeneration. The new- 
formed connective-tissue is 
filled with an abundance of 
round cells, formerly called 
nuclei ; they are now known 
as lymphatic corpuscles, and 
are probably emigrated leu- 
cocytes. The smaller 
branches of the portal vein 
are shrunken and twisted, 
and in extreme cases new 
capillaries are developed, 
which communicate with both hepatic and portal vessels. Again, a whole 
lobule may have disappeared and its place be occupied by connective-tissue. 
The bile-ducts have their commencing rootlets destroyed and their mucous 
membrane tumefied. In cases of long-standing cirrhosis, the gall-bladder 
will be found bound to the adjacent parts by adhesions, and its walls are 
thick and tough ; while the spleen is enlarged, softened and congested. 
The gross appearance of the liver in cirrhosis may vary in different cases, 
but the anatomical lesions are the same in all. 

There is a form of this disease which has been called hypertrophic 
cirrhosis, because the liver is markedly increased in size, sometimes reach- 
ing six or seven pounds in weight ; but the fibroid change, the yellow 
staining, the atrophy of liver-cells, and the fatty change at the periphery of 
the lobule, are the same as in the ordinary variety, the only difference being 
a marked increase in the size of the liver. 

As a result of the compression and obliteration of the branches of the 



• j) 

Fig. 72. 

Interstitial Hepatitis. 

Section of liver in advanced cirrhosis, as shown 
nifying power. 

A, A, A. Bands of connective-} 'issue. 

B, B, B. Branches of portal vein. 

C, C\ C. Hepatic ducts. 

B, V. Newly formed connective-tissue. 
E, E, E. Lobules, separated by the advancing cirrhosis. 
F, F. Lobules nearly obliterated, x 40. 



low mag^ 



376 



DISEASES OF THE DIGESTIVE SYSTEM. 




portal and hepatic vein from the new connective-tissue in the advanced 
stage of cirrhosis, a chronic venous congestion occurs in those viscera 
which empty their blood into the portal vein. The spleen, stomach and 

intestines consequently be- 
come the seat of chronic ve- 
nous congestion. The result 
of this is, that with cirrhosis 
of the liver we find an en- 
larged spleen, and a chronic 
gastric and intestinal catarrh. 
If the portal obstruction is 
very great, there will be trans- 
udation of serum from the 
vessels of the peritoneum into 
the peritoneal cavity, causing 
ascites. 

Etiology. — The chief cause 
of cirrhosis is the intemperate 
use of alcohol. Alcohol is 
most rapidly absorbed when 
the stomach is empty. When 
it is taken in a concentrated 
form without food it acts as 
a direct irritant to the hepatic 
circulation. If this irritation 
is long continued interstitial 
hepatitis is the result. Those 
who take alcohol before break- 
fast as well as through the day are almost certain to develop cirrhosis of 
the liver. Those who partake freely and daily of highly seasoned food, 
even though they may not use alcohol, are also liable to develop this 
disease, especially if they reside in hot climates. Syphilis, gout and rheu- 
matism cause it. Gout, especially starting from faulty liver digestion, is 
liable to develop cirrhosis. Malarial hyperaemia, if long continued, may 
lead to it. Extension of inflammation from the capsule of Glisson may 
develop cirrhosis. It may also occur without any assignable cause. 

Symptoms. — The early symptoms of interstitial hepatitis are those of 
hepatic congestion. Following the dull pain and tenderness in the hepatic 
region, the dyspnoea, apathy, headache, nausea and furred tongue, there 
is loss of appetite, especially for meats. The individual has a desire for 
food, but after a few mouth fuls the sense of hunger gives place to loathing ; 
this occurs most frequently at breakfast. Diarrhoea alternates with con- 
stipation, and distressing attacks of retching, especially on waking in the 
morning, are followed by intestinal pain and flatulence. As the dyspeptic 
symptoms increase, slight jaundice appears, but it is never very marked, 
for although the bile secretion is diminished, there is no obstruction to its 



Fig. 73. 



Interstitial Hepatitis. 

■ Same tissue as in last illustration, mare highly magnified. 
A, A, A. Connective-tissue of a portal canal, containing, B, B 
Hepatic ducts ; C, C, Portal veins ; and D, D, Hepatic ar 
term. 

E. Atrophied hepatic cells in periphery of a lobule. 

F. Infiltration of round cells— the commencement of the new con 
nective-tissue growth, x 300. 



INTERSTITIAL HEPATITIS. 



377 



passage into the intestine. Hemorrhoids are early signs of obstructed 
portal circulation and are a very constant accompaniment of cirrhosis, and, 
with the gastric symptoms, are the earliest indications of obstruction to the 
portal circulation. If cirrhosis has been induced by the excessive use of 
alcohol, a craving for alcohol persists. Attacks of vertigo and occasional 
slight elevations of temperature with emaciation and cachexia mark the 
end of its first stage. The dingy hue of the surface, which was early 
present, disappears, and the skin gradually assumes an earthy pallor, rarely 
tinged with yellow. The increase in the hepatic symptoms and the severe 
pain and tenderness over the hepatic region, which are sometimes present, 
are due to intercurrent attacks of perihepatitis. 

At the commencement of the second stage gastritis is established as a 
result of the mechanical obstruction to the capillary circulation of the 
mucous membrane of the stomach, and is marked by acidity, nausea, and 
often by vomiting after taking food, in consequence of which emaciation, 
weakness, and depression of spirits occur ; venous stigmata may now appear 
on the cheeks. The obstruction of the vessels of the gastric mucous mem- 
brane is often so great that hgematemesis occurs, and although the patient 
may experience temporary relief after the first bleeding, the hemorrhage 
will recur, and may be the direct cause of death. Intestinal hemorrhage 
occasionally occurs from the same cause. If there is persistent diarrhoea 
during this stage, it indicates that there is gastro-intestinal catarrh. Tym- 
panitis, as well as intestinal catarrh, usually precedes the occurrence of 
ascites, which is slow and insidious in its advent, and so masked by the 
preceding tympanitic distention that it is often difficult to determine the 
exact time of its occurrence. It will usually be noticed that, before the 
appearance of the ascites, the abdominal veins, especially of the right side, 
are distended, sometimes enormously. 

Ascites is sometimes absent in advanced stages of cirrhosis. When 
this happens, any or all of the following conditions may exist to ac- 
count for its absence : first, during the contraction of the new connective- 
tissue, the branches of the vena portse sometimes remain patent. Second, 
the hemorrhoidal branches of the inferior mesenteric may inosculate with 
the internal iliac. Third, the veins of the colon and duodenum may 
anastomose with the left renal vein. Fourth, the phrenic vein may com- 
municate with some of the more superficial branches of the vena portae. 
Fifth, new vessels may be formed in the adhesions which bind the liver to 
the adjacent parts, and thus relieve the obstructed portal circulation. 
Sixth, the portal and hepatic vessels may anastomose sufficiently within 
the liver to relieve the portal obstruction. Seventh, branches of the vena 
portse, which are distributed on the under surface of the diaphragm, and 
on the inner surface of the abdominal parietes, may anastomose with the 
internal mammary and epigastric veins, and thus assist in returning the 
blood to the right auricle. When the internal mammary in its turn be- 
comes engorged, there is a dark bluish mass surrounding the umbilicus, 
due to distention of the cutaneous veins, and called the "caput Medusce " 



378 



DISEASES OF THE DIGESTIVE SYSTEM. 



When ascites is once developed it progressively increases. By its pressure 
dyspnoea and often pulmonary oedema are developed, and the gastric de- 
rangements are so increased that rapid emaciation quickly follows its 
accumulation. (Edema, beginning in the feet, gradually extends upward. 
Fluid drawn from the abdominal cavity is of a pale amber color, highly 
albuminous, and of a specific gravity varying from 1.010 to 1.020 ; it is not 
turbid, and contains no inflammatory products. Slight jaundice may ap- 
pear with the ascites, but if excessive is due to pressure on the ducts, either 
from connective-tissue indurations or from enlarged lymphatics in the trans- 
verse fissure, wiiich obstruct the outflow from the biie ducts. The mind is 
usually clear to the last, but sometimes the patient will pass into a state 
of complete stupor, which is preceded by delirium and. active cerebral 
symptoms. At first, it seems plausible to ascribe the cerebral symptoms 
to cholsemia, but I have found the jaundice in inverse proportion to the 
cerebral symptoms. Cholsemia may occur in cirrhosis, and then, of course, 
exhibits its peculiar train of symptoms ; but I think the more reasonable 
view is the one that ascribes the delirium, coma, and other cerebral symp- 
toms which come on late in this disease, to alcohol. The stools in cirrhosis 
are characteristic. They are clay-colored in the centre ; surrounding this 
there is a dull pinkish ring, and around this a slaty gray ring tinged with 
mucus. The urine is scanty and very dark colored ; in one-third of the 
cases it contains albumen. Bile pigment is present in the urine when 
jaundice exists. The urine is rich in urates, and a pinkish sediment of 
lithates is very common. 

Physical Signs. — Inspection, in the early stage of cirrhosis, may show a 
slight loss of motion over the lower portion of the right side. In a few in- 
stances the faint outline of the liver margin is seen below the free border of 
the ribs. 

Palpation. — The surface of the liver is smooth, or finely granular; the 
edges are round ; owfirm pressure there is a marked tenderness, and more 
or less resistance. 

Percussion. — The area of hepatic dulness is somewhat increased in the 
early stage (especially over the right lobe) in a vertical direction, and so, 
too, is the area of splenic dulness. 

Inspection, in the advanced stage, shows enlargement of the superficial 
veins of the abdomen, chiefly on the right side, and the caput Medusce is 
often visible. There is usually more or less ascites, and the face and sur- 
face of the body are clay-colored, often tinged with yellow. 

Palpation is best performed when the patient is lying on the left side, 
and if the surface of the liver can be felt, it will be uneven and hob-nailed, 
with sharp, firm edges. 

Percussion gives a diminished area of hepatic dulness, and the left lobe 
of the liver may be so small that the line of hepatic dulness will not extend 
to the left of the median line. Persistent tympanitic percussion is present 
above the line of the fluid, srnd flatness below. The spleen is markedly en- 
larged, and the splenic dulness extends below the free border of the ribs. 



INTERSTITIAL HEPATITIS. 



379 



Differential Diagnosis. — The early stage of cirrhosis may be mistaken for 
fatty or loaxy degeneration of the liver. In fatty liver, the enlargement 
begins without localized pain, and there is no sense of constriction or dys- 
pepsia, so constantly present in the early stage of cirrhosis. In fatty 
liver, the skin is of a light yellow color, is greasy, and has a velvety 
feel ; in cirrhosis, it is of a dingy hue, wrinkled, and rough. There is a 
history of high living, and of a sedentary life, or of some phthisical com- 
plication with fatty liver ; while in cirrhosis, a history of excessive spirit- 
drinking, gout, rheumatism or syphilis is elicited. The liver is doughy and 
painless in fatty degeneration, while it is hard, resistant and tender in cir- 
rhosis. The tendency in fatty liver is to obesity, while emaciation is rarely 
absent in cirrhosis. Ascites is never an attendant of fatty liver. 

Waxy liver is accompanied by a history of syphilis, prolonged suppura- 
tion, or disease of bones ; the face is pale and puffy, the urine is increased 
in quantity and of low specific gravity. Pressure over the liver gives no pain, 
and the surface of the organ is smooth, and its free edges sharp and well 
defined. These symptoms readily distinguish it from cirrhosis. 

The advanced stage of cirrhosis may be confounded with clironic peri- 
tonitis, of a tubercular or cancerous origin, with gastric ulcer, with adhe- 
sive pylephlebitis, clironic or brown atrophy of the liver, multilocular hy- 
datids, gummata and cancer. 

Gastric symptoms are prominent in cirrhosis, and absent in peritonitis. 
The ascitic fluid of cirrhosis is albuminous, while in chronic peritonitis it 
contains inflammatory products. The countenance has a clay-colored or 
jaundiced hue in cirrhosis ; in peritonitis, it is pale and anxious. The liver 
is diminished and the spleen increased in size in cirrhosis. The abdo- 
men is excessively tender in chronic peritonitis, and the fluid accumulates 
more rapidly than in cirrhosis. 

A history of drinking, dyspepsia, hsematemesis and emaciation may sug- 
gest ulcer of the stomach ; but if it is remembered that tympanitis, asci- 
tes, hemorrhoids, clay-colored faeces, dark, scanty urine, a small and hob- 
nailed liver, and an enlarged spleen are present in cirrhosis, and absent in 
ulcer of the stomach, the differential diagnosis is readily made. 

In cancer of the liver, the nodules are very much larger than in cirrho- 
sis. Ascites and enlarged spleen, if present in cancer, occur late, when the 
large size of the liver leaves no doubt in the diagnosis. The liver is exces- 
sively painful and tender on pressure, and there are marked exacerbations 
of the pain. A cancerous cachexia, with an. almost chlorotic hue, exists in 
cancer. These, with the history of the case, and perhaps the presence of 
cancer in other organs, are sufficient for its diagnosis. 

Hepatic phlebitis may give symptoms identical with those of cirrhosis. 
The most important diagnostic point is, that in hepatic phlebitis the as- 
citic fluid accumulates very rapidly, and after paracentesis returns more 
quickly than in cirrhosis. Jaundice occurs early and rapidly deepens, and 
the stools are dark-brown and semi-fluid in phlebitis. The points of dif- 
ferential diagnosis between the other diseases which have been named and 
cirrhosis, will be considered under the head of those diseases. 



380 



DISEASES OF THE DIGESTIVE SYSTEM. 



Prognosis.— -The prognosis will be determined by the stage of the cirrhosis. 
In its early stage its progress may be arrested, but when the stage of contrac- 
tion is reached, the disease is progressive, and the prognosis is exceedingly 
unfavorable. A fatal result occurs in all cases. Its course is a chronic one, 
and though death has occurred in three months from the time the liver be- 
gan to be diminished in size, I have usually found a year and a half to be 
its average duration. Complicating diseases influence the prognosis. Hem- 
orrhage from the intestine and from the hemorrhoidal veins may be so great 
as to exhaust the patient, and render him too feeble to resist the inroads of 
the disease. This class of patients are especially liable to develop the cir- 
rhotic form of Bright's disease. Delirium tremens, pleurisy, and pneumo- 
nia sometimes complicate it. Death may result from exhaustion due to 
faulty nutrition, from the large fluid accumulation, from repeated and pro- 
fuse hemorrhages, and from wasting diarrhoea. Intercurrent pulmonary or 
cardiac disease, peritonitis, or delirium tremens may be the direct cause of 
death. Those cirrhotic patients live the longest who have large dropsical 
accumulations, the dropsy disappearing and recurring. 

Treatment. — Cirrhosis, in its early stages, should be treated in the same 
way as active hepatic hyperemia. In alcohol drinkers, all spirituous 
liquors must be abstained from, and the patients must be placed on a nutri- 
tious, though restricted diet, from which all irritating ingesta are excluded, 
and alkaline waters should be freely taken. If the hepatic congestion is 
intense, leeches to the anus, mercurial purges, and nitro-muriatic acid will 
be found of temporary service. The importance of a restricted diet, and 
the free use of saline waters in this stage of the disease cannot be over- 
estimated. Cod-liver oil is indicated in this- stage. After the stage of 
contraction is reached, the treatment can only be palliative. The most 
important thing to be accomplished now, is to improve nutrition, and to 
relieve urgent and troublesome symptoms. Mineral acids combined with 
vegetable tonics, such as dilute nitric acid and calumbo assist stomach 
digestion ; creosote and sulphite of sodium are of service when acid fermen- 
tation is a distressing symptom. Mineral waters should be discontinued 
during this stage. If constipation exists, the bowels may be regulated with 
rhubarb combined with small doses of ipecacuanha. Cod-liver oil should 
be constantly taken by this class of patients. Care must be taken not to 
suddenly check diarrhoea, or hemorrhages, but if they become exhausting 
opium may be cautiously given. 

Ascites and general dropsy are the most troublesome symptoms in 
this stage of cirrhosis. When it becomes imperative to remove the 
dropsy, it may be attempted through the skin, kidneys and intes- 
tines, or it may be removed by tapping. If the patient is too feeble 
to employ drastic purges and hydragogue cathartics, diuretics and di- 
aphoretics may be resorted to. The condition of the intestinal tract, as 
well as the strength of the patient, will determine whether elaterium, or 
any of the other drastic cathartics can be employed. It must be remem- 
bered that they may excite acute gastric and intestinal catarrh. Diuretics 



HYPERTEOPHIC CIRRHOSIS OF THE LIYER. 



381 



(as squills and digitalis) are more efficient in this than in any other form 
of dropsy. If the kidneys and renal vessels are compressed by the fluid, diu- 
retics will "have little effect. Its removal must not be delayed too long, for 
the strength of the patient may be so diminished that after the removal of 
a large quantity of fluid, fatal collapse may occur. When, however, reme- 
dial measures fail and dyspnoea becomes troublesome, paracentesis abdo- 
minis should always be resorted to. The mechanical removal of the fluid 
may be effected either by the aspirator or trochar. After its removal, the 
hob-nailed surface of the liver may cause peritonitis by the constant irrita- 
tion produced by the respiratory movements. There are few cases where 
tapping has been frequently performed, in which after death a moderate 
amount of chronic peritonitis is not found. The ascites will return sooner 
or later after paracentesis; but when tapping is only required at sufficiently 
long intervals for the patient to recuperate between the tappings, and the 
amount of fluid gradually diminishes or becomes stationary, the case will 
continue for years. 

HYPEETEOPHIC CIREHOSIS OF THE LEVEE. 

Hepatic cirrhosis with hypertrophy of the organ appears in two forms. 
One is known as simple or biliary cirrhosis; the other as fatty hypertrophic 
cirrhosis. 

Morbid Anatomy. — In biliary cirrhosis the bile ducts and radicles become 
distended, and pigment is deposited in the hepatic cells and connective- 
tissue. Degenerative changes affect the parenchymatous elements coin- 
cidently with an abundant development of connective-tissue. The liver 
thus becomes enlarged, hard, and deeply pigmented brown or black. As 
the degenerative changes cause in many parts complete destruction of the 
liver cells, the increase of size in the organ depends largely upon the new 
connective-tissue. Although the organ becomes harder, the fibrous forma- 
tions do not contract as firmly as in simple cirrhosis, and the organ thus 
retains its smooth surface. 

In fatty hypertrophic cirrhosis, called by the French "hypertrophic 
cirrhosis with icterus" the fibrous formations are equally abundant, but 
show even a less tendency to extreme degrees of contraction, while the de- 
generative changes within the parenchyma are distinctly fatty. These fatty 
products are not absorbed, and tend to still further increase the size of the 
organ. Such a liver differs from a simple fatty liver in the presence of 
abundant new connective-tissue between and within the lobules. The 
new growth originates in the portal spaces, and the portal vessels and bile 
ducts become surrounded by compact fibrous tissue from which bands 
radiate along the central and sublobular veins, in such amounts at times as 
to cause their entire obliteration. The biliary passages are affected secon- 
darily and in less degree, the vascular apparatus being the parts particularly 
involved. This forms one of the prominent pathological points of differ- 
ence from biliary cirrhosis. 



382 



DISEASES OF THE DIGESTIVE SYSTEM. 



The hypertrophy, which is often extensive, affects particularly the 
edges of the organ, so that it is like a cube. Sabourin dwells particu- 
larly upon this. There are no granulations upon the surface, and Grlis- 
son's capsule, sometimes thickened from perihepatitis, is smooth and so 
transparent that through it can be seen opaline-looking new connective- 
tissue enclosing yellow fatty parenchyma. Upon section the hepatic 
parenchyma seems made up of fatty nodules, usually circular, smaller 
or larger than the normal hepatic lobules, and almost completely sur- 
rounded by new tissue. 

The latter has sometimes induced absorption of the proper glandular 
elements. With a low power under the microscope there is an appearance 
like subcutaneous adipose tissue, with cirrhotic bands enclosing collections 
of fat cells. These groups of fat cells, which are often simply large oil 
globules, represent the hepatic lobules. The granulo-fatty degeneration 
peculiar to typhoid jaundice is absent. The kidneys are usually the seat of 
simple or similar sclerotic changes. The spleen is enlarged, often more 
than in simple cirrhosis. 

Etiology. — Biliary sclerosis is probably dependent in almost every instance 
upon some form of obstruction in the larger hepatic ducts, from gall stone, 
cicatricial contractions, pressure from tumors, etc. The causes of fatty 
hypertrophic cirrhosis are obscure. It occurs in alcoholic subjects, but is 
by no means confined to them. It seems possible that it may follow biliary 
cirrhosis, or even start as a simple cirrhosis. 

Symptoms. — The clinical distinctions between biliary and fatty r hypertro- 
phic cirrhosis are not clear. In the earlier stages the symptoms are all ob- 
scure and often overlooked. Fullness and oppression in the hypochondrium 
usually are the first to attract attention. Jaundice appears early and is per- 
sistent, being more marked, as a rule, in the biliary form. The enlargement 
of the liver may perhaps be recognized if attention is called to it. When 
the second stage sets in, there will be abdominal pain, nausea, vomiting, 
anorexia, attacks of vertigo, nocturnal delirium or hallucinations, hyperes- 
thesia of the limbs, and then fever. A diagnosis is possible in most cases 
with these symptoms. They are followed by oedema of the face and limbs, 
profuse sweats and often signs of subacute peritonitis. With the increas- 
ing persistent jaundice there may be tendency to hemorrhages. The 
symptoms are very apt to increase and then recede. Usually little flesh is 
lost, and patients may even grow fat. When the abdominal fat is not too 
abundant, physical examination shows a large, smooth, rounded liver, 
seldom very tender on pressure. Splenic enlargement can also be recog- 
nized. Ascites is seldom present ; when developed, it is slight. The whole 
course of the disease is from one to two years, and the second stage may 
last four or five weeks, or be prolonged several months by deceptive intervals 
of apparent recovery. 

Differential Diagnosis. — This must be made from other hepatic diseases 
causing jaundice, by the presence of signs of extensive portal obstruction, 
associated with enlargement of the liver. An alcoholic history, or the 



CIRCUMSCKIBED SUPPUKATIVE HEPATITIS. 



383 



presence of tubercular complications, are important diagnostic points, when 
associated with enlarged liver, in favor of hypertrophic cirrhosis. 
Prognosis. — This is invariably bad. 

Treatment. — The treatment is purely palliative and expectant. None 
of the many theories advanced as to its cause have been accepted. Those 
measures employed in simple cirrhosis may relieve the symptoms, but are 
even more uncertain in their action in this condition. 



CIRCUMSCRIBED SUPPURATIVE HEPATITIS. 



Abscess of the liver is an acute circumscribed hepatitis which results in 
irregular areas of suppuration, the liver-tissue surrounding the points of 
suppuration remaining normal. 

Morbid Anatomy. — In a certain proportion of cases circumscribed hepatitis 
has its origin in an infarction. The emboli which produce these infarc- 
tions are, in most instances, stamped with pysemic infection or are necro- 
tic ; they may vary in number from two or three to a dozen. Immedi- 
ately around the inflamed spots the liver substance is normal or in a state 
of intense congestion, and corresponding to them on the surface of the 
liver are found brownish-red elevated patches from an inch to an inch and 
a half in diameter, and of firm consistence. Their most frequent seat is 
the posterior portion of the right lobe. They may be single or multiple. 
Soon after the development of the infarction purulent inflammation is estab- 
lished. In the centre of the mass the liver cells undergo albuminoid infil- 
tration, become larger, degenerate, and pus is formed. As the process 
advances small cavities containing pus are developed. These may en- 
large into one large abscess or remain separate. If abscesses result from 
other causes than pyaemia, 
the process does not follow f\: y^^ r 
the lobular course, but begins 
by small exudations of lymph 
and pus, which soon coalesce 
and become surrounded by a 
membraneous wall. The cavity 
of the abscess varies in size 
from that of a hazel-nut to 
one capable of containing two 
or three quarts. Their con- 
tents are usually pale yellow 
pus ; but when the suppu- 
rating process has broken 
through the wall of some 
vessel, then the contents are rust colored and have a granular appearance. 
If the process involves the bile-ducts the pus has a greenish or ochre-color. 




Fig. 74. 

Circumscribed Suppurative Hepatitis. 

Sketch showing the cut surface of a portion of the left lobe of the 
liver, the seat ofrnvltiple abscesses. The open months of the di- 
vided hepatic veins are also shown. 



384 



DISEASES OF THE DIGESTIVE SYSTEM. 



A variety of changes take place in these purulent collections ; as they grow 
older, their walls may become smooth, and the encysted pus gradually 
become absorbed, or undergo cheesy or calcareous degeneration. If absorp- 
tion takes place, a cicatrix deeply indented on the exterior of the liver 
marks the place where the abscess approached the surface, and within its 
substance cicatricial tissue indicates its exact seat. In other cases, no lining 
membrane is produced around the purulent collection. As the inflamma- 
tion extends, a necrotic process is established which extends to the surface 
of the liver, and the abscess opens externally. This process may pierce the 
peritoneum, causing a fatal peritonitis ; but this is of rare occurrence, for 
adhesions are formed which bind the diaphragm and adjacent organs to 
the liver ; or the abscesses may open into the pleural cavity, the right 
lung, or the stomach. In rare instances the two large venous trunks, the 
vena portae and inferior cava may be pierced. Frequently the abscess 
ruptures externally, through the adhesions formed between the surface of 
the liver and the abdominal walls. The intestines, the gall-bladder, 
or the pericardium may be perforated by the abscess. Again, the pus 
may burrow in the cellular tissue, and discharge itself at some point at 
the lower part of the trunk. At the autopsy the liver may be found irreg- 
ularly enlarged, often attaining an immense size. The capsule is opaque 
and thickened, and on its surface are elevated flat spots varying in color 
from dark red to yellow. Adhesions generally exist between it and the 
adjacent parts, and a layer of lymph frequently envelops the entire organ. 
The whole liver is hyperaemic. Evidences of perforation, in any of the 
directions which have been mentioned, may be present. 

On section, a dark fluid oozes from the congested surface, and the 
interior of the abscess may exhibit any of the changes above described. 
Near an abscess the coats of the veins, especially the portal, are thickened, 
and their interior is often filled with a shaggy, fibrinous deposit- 
Etiology. — Pyasmic infarction must be regarded as a frequent cause of 
hepatic abscess, especially when associated with injuries to the cranial 
bones. Phlebitis, with the formation of thrombi leading to suppurative 
inflammation, the result of operations on the intestines (as for prolapsus ani, 
hemorrhoids, and strangulated hernia) and any intestinal traumatism, may 
give rise to abscess of the liver. Hot climates and miasmatic influences 
favor, if they do not cause, suppurative hepatitis. In hot climates dysen- 
tery, particularly the epidemic form, is frequently accompanied or followed 
by hepatic abscess, so that dysentery has come to be regarded as one of the 
causes of abscess of the liver. Hepatic abscess sometimes accompanies 
ulceration of the stomach and of the intestine, especially of the colon. 
Ulceration of the gall-bladder and of the appendix vermiformis, perityphlitis, 
pyelitis, ulcerative endocarditis, and cancer of the stomach or of the parts 
near the liver are often associated with hepatic abscess. Worms, calculi, or 
other obstructions of the ductus communis, causing inflammation of the 
hepatic ducts, sometimes lead to ulceration, and this ulcerative process is 
often followed by abscess. The prevailing tendency of modern pathology 



CIECUMSCEIBED SUPPURATIVE HEPATITIS. 



385 



is to ascribe hepatic abscess to an infective embolus, from a preceding 
phlebitis, and the attempt has been made to trace back all the causes above 
named to such a primary cause, though, in many, direct proof is impossi- 
ble. Abscess of the liver may also be the result of inflammation of the bile- 
ducts and of the veins of the liver ; and, finally, it may be developed 
without any recognizable cause. 

Symptoms. — An abscess of the liver of considerable size may exist with- 
out there being local or constitutional symptoms to point to its existence. 
A patient may have fever, gradually become emaciated, and finally die 
from exhaustion, without a single objective symptom of abscess, and yet a 
post-mortem examination will reveal a large central hepatic abscess. Again, 
symptoms of intermittent fever, associated with gastric and intestinal 
catarrh, may be all that, with the greatest care, can be elicited, when, in 
fact, a large abscess is developing in the liver. When abscess is associated 
with dysentery the difficulty is often increased ; for chills and rigors, 
enlargement of the liver, and pain may all be attendants of dysentery with- 
out abscess. Again, in pyaemia, when metastatic abscesses in the liver are 
especially liable to develop, the recurring chills, the sweats, the pyrexia, 
and the jaundice, are all part of the history of the pyaemia, so that in many 
cases we are compelled to rely almost exclusively on the physical signs for 
a diagnosis of abscess of the liver. Such cases of hepatic abscess are fre- 
quently overlooked. 

Usually the development of hepatic abscess is indicated by well-de- 
fined symptoms. A slight feeling of chilliness, sometimes a distinct chill, 
is followed by dull pain and weight in the right hypochondrium, the pain 
often radiating to the tip of the right shoulder ; the chilly sensations recur, 
and resemble those of a slight attack of ague. The pain increases, and 
is aggravated by position and pressure. The tongue is brown and 
furred, there is loss of appetite, slight nausea, and often vomiting, which 
is bilious in character. The bowels are at one time constipated, at an- 
other there is a bilious diarrhoea. 

The respirations are hurried and shortened, either because of slight lo- 
calized pleurisy, which so often accompanies hepatic abscess, or because a 
long inspiration increases the pressure on the liver, and thus causes pain. 
With the dyspnoea there is a short dry cough resembling that of pleurisy ; 
the skin rarely changes color. With the formation of the abscess there is 
a distinct exacerbation of symptoms : hectic, rigors, and recurring night 
sweats occur ; the gastric symptoms become urgent, and there is persistent 
and profuse vomiting. The pain becomes sharp, lancinating and localized, 
and indicates the direction of the future perforation. The temperature 
rises to 103° or 104° F., sometimes reaching 106° F. The pulse is accel- 
erated, generally keeping pace with the temperature. Exhaustion and 
emaciation are rapidly developed, and as the disease advances, typhoid 
symptoms may supervene. If the situation of the abscess is such that 
portal obstruction results, hemorrhoids, ascites and oedema of the extremi- 
ties occur, though peritonitis may be suspected in those cases where there 
25 



386 



DISEASES OF THE DIGESTIVE SYSTEM. 



is ascites. As the abscess advances toward the surface of the liver, attacks 
of perihepatitis are apt to cause severe exacerbations of pain, and the hepatic 
tenderness becomes excessive. Toward the end delirium, jactitation, som- 
nolence, and coma may develop. The urine is scanty, high-colored, and 
contains an abnormal amount of urates, often causing a considerable pink- 
ish deposit. 

Hepatic abscesses may be discharged (as has been stated) in a variety of 
ways. When an external opening is to occur, the skin becomes tense, 
red, shining, and cedematous at some point over the hepatic region ; fluc- 
tuation can be detected, and becomes more and more marked as the ab- 
scess advances toward the surface. In some cases the heart impulse is 
transmitted to the abdominal walls by the intervening tumor. When the 
cavity of the peritoneum is perforated, signs of local or general peritonitis 
are developed, marked by rapidly developed tympanitis, intense and sud- 
den collapse. When an opening occurs into the stomach, severe gastric 
symptoms are developed, accompanied by purulent vomiting and purulent 
stools. A sudden diminution in the size of the hepatic tumor, the sub- 
sidence of the pain and of the urgent symptoms, indicate that the intes- 
tine or biliary passage has suffered perforation. Symptoms of -localized 
pneumonic inflammation in the right lower lobe precede the opening of 
an hepatic abscess into a bronchus. The expectoration suddenly becomes 
purulent and mixed with blood, serum, and shreds of disintegrated lung- 
tissue ; the breath becomes offensive, there is cessation of pain, and sub- 
sidence of the hepatic enlargement. Eecovery in such cases is rare unless 
the abscess is a small one, the patient usually dying of exhaustion from long- 
continued suppuration. When the pleural cavity communicates with the 
abscess, the symptoms of pleuritic effusion and empyema are well defined, 
and when, in this case, an external opening is to occur, the evidences of 
it are the same as those of empyema. Almost immediate death follows per- 
foration of the pericardial sac by an hepatic abscess. Absorption of the 
fluid contents of an hepatic abscess, and the development of cicatricial tis- 
sue, followed by gradual diminution in the size of the liver, are of rare 
occurrence. 

Physical Signs. — Inspection. If the abscess is large, inspection will show 
a bulging of the right hypochondriac region, reaching nearly to the um- 
bilicus. The respiratory movements on the right side are restricted, and 
the respirations are accelerated. If the abscess is to open externally, there 
is a flattened, defined bulging near the free border of the ribs, between 
the intercostal spaces. 

Palpation. — The liver is enlarged and has an uneven feel, especially 
when the abscesses are multiple and superficial. The pain, localized in 
the case of a single abscess, is increased and diffused in multiple abscesses 
by pressure. Fluctuation is a valuable sign, but cannot always be de- 
tected. When it can be, a ring of abnormal hardness surrounds the spot. 
Palpation should be made from before backward ; if a single large abscess 
exists, its outline may be well defined. 



CIRCUMSCRIBED SUPPURATIVE HEPx\.TITIS. 



387 



Percussion. — The area of hepatic dulness is always more or less in- 
creased. If the abscesses are multiple, it may be increased in all direc- 
tions ; bat if there is only one large abscess, the area of dulness will 
correspond to the direction of enlargement, which may be upward or 
downward ; by its direction we are able to determine the probable mode 
of the termination of the abscess. 

Differential Diagnosis. — The readiness with which the diagnosis of ab- 
scess of the liver may be made will depend upon its size and situation ; 
small abscesses can only be suspected. Abscess of the liver may be mis- 
taken for hydatids of the liver, cancer, localized pleurisy, intercostal neu- 
ralgia, abscess of the abdominal ivalls, enlarged gall-bladder, perihepatitis, 
suppurative pylephlebitis, and active hyperemia of the liver. 

Hydatids occur most frequently in those living in northern climates, 
and abscesses most in those who live, or have lived, in hot climates. Hyda- 
tid tumors run a chronic course, and are slow in growth ; while abscess 
is usually a rapid and acute disease. Accompanying hydatids there is no 
pain, rigors, hectic, or sweats ; but these are important symptoms in abscess. 
Gastric disturbances and a rapidly developing cachexia are prominent in 
abscess, and absent in hydatids. In some cases of hydatid tumor the hyda- 
tid "thrill" or fremitus can be detected ; it is never present in abscess. 
With the exploring trochar the liquid in the one will be found to be pus, in 
the other a clear saline fluid containing hooklets of the echinococci. 

Cancer of the liver is generally associated with cancer of the stomach, 
breast, or some other organ, primary cancer of the liver being very rare. 
In cancer, the hepatic enlargement is slower than in abscess, and there is 
usually a more or less marked cancerous cachexia. Suppurative fever, chills, 
hectic, and sweating are present in abscess, and absent in cancer. The temper- 
ature in cancer is normal or sub-normal, and jaundice, if present, is persist- 
ent. Ascites is common in cancer, and rarely present in abscess. In can- 
cer, palpation discovers scattered nodular masses, which rarely fluctuate ; 
while in abscess a large fluctuating tumor can usually be mad* out. The 
exploring needle withdraws pus from an abscess, while blood follows the 
puncture of a cancer nodule. 

Pleurisy on the right side can usually be readily distinguished from ab- 
scess of the liver by the physical signs alone. The grazing friction sound 
accompanies loss of vocal fremitus ; the dulness on percussion, the feeble 
respiratory murmur, and the crepitant friction sound decide the question. 

Intercostal neuralgia occurs most frequently in women with a neuralgic 
history. The pain is located in the region of the sixth, seventh, and eighth 
intercostal spaces, and the three points of tenderness are almost diagnostic. 
When the pain of abscess becomes as excruciating as that of neuralgia, in- 
spection, palpation, and percussion will all reveal well-marked enlargement 
of the liver. Gastric disturbances, chills and profuse sweats are prominent 
signs of abscess, and are absent in intercostal neuralgia. 

Inabscess of the abdominal walls, there is no history of pyaemia, dysentery, 
or internal ulceration, which so often precede an hepatic abscess. In he- 



388 



DISEASES OF THE DIGESTIVE SYSTEM. 



patic abscess the line of dulness is well marked, and corresponds in outline to 
the hepatic area ; while in abscess of the abdominal walls the line of dulness is 
ill defined, and does not follow the hepatic outline. A tense, shining, oedem- 
atous skin, and superficial tenderness and hardness appear early in abscess 
of the abdominal walls. The signs of pus formation are early in abscess 01 
the abdominal wall, and very late in abscess of the liver, if they appear at 
all. The respiratory movements cause an upward and downward motion 
in the tumor of an hepatic abscess ; while an abscess of the abdominal wall 
will remain stationary during the respiratory acts. 

An enlarged gall-bladder will usually be accompanied by a history of bil- 
iary colic. The presence of a pear-shaped, movable, fluctuating tumor, oc- 
cupying the normal position of the gall-bladder, a history of jaundice, and 
the absence of constitutional symptoms indicate enlarged gall-bladder ; 
while the tumor in abscess of the liver is broader, less movable, less globu- 
lar in shape, and is attended by chills and sweats. 

Prognosis. — The majority of abscesses of the liver terminate fatally. Py- 
semic abscesses are generally multiple ; their average duration is three 
months ; I have known death to occur within three weeks after the com- 
mencement, and I have known them to be prolonged over a period of two 
years. In abscess from other causes than pyaemia, the prognosis is favora- 
ble whenever there are no indications of an opening into the pericardium, 
peritoneum, or pleural cavity. When an hepatic abscess complicates a severe 
attack of dysentery, the prognosis is unfavorable. Their duration is shorter, 
and the prognosis is better when they open externally ; their next most 
favorable termination is when they open into a bronchus, or into the intes- 
tinal canal. Pyaemia and dysentery often cause death when the accompany- 
ing abscess is too recent to have induced it. Exhaustion from suppuration 
may cause death, especially when accompanied by intestinal catarrh. Peri- 
tonitis, pericarditis, pneumonia, and empyema sometimes cause the fatal 
result. 

Treatment. — When multiple abscesses occur, antiseptics have been pro- 
posed, but there is no evidence that they arrest the progress, or diminish 
the severity of the suppurative process. When suppurative hepatitis can 
be recognized early, it should be treated according to the rules which have 
been given for the management of acute hepatic hyperaemia. Local blood- 
letting by leeches may be employed when the symptoms are localized and 
well defined ; and mercurial purges may be given at the onset, in combina- 
tion with large doses of quinine, but they should be discontinued when sup- 
puration is established. We rarely have an opportunity to carry out the 
preventive treatment, for the abscess is formed before the patient seeks 
medical advice. When pus has formed, and the locality of the abscess can 
be determined, aspiration should be performed. If the withdrawal of the 
pus is followed by decided signs of improvement, the aspiration may be 
repeated at intervals indicated by the amount and effects of the purulent 
accumulation. Few cases, however, will be permanently benefited by aspira- 
tion. I question very much if those cases reported cured by one or two 



DIFFUSE PAKENCHYMATOUS HEPATITIS. 



389 



aspirations were true hepatic abscesses. The dysentery and the gastro- 
intestinal catarrh, which are so often attendants of hepatic abscess, are 
best treated with large doses of ipecacuanha ; a fuller description of this 
method of treatment will be found under the head of dysentery. 

The question of operative interference is one which it is often difficult 
to decide. Strong opinions have been given for and against it. On the 
one hand, it is claimed that if a free opening is not made, death may result 
from exhaustion produced by large purulent accumulations, or the abscess 
may open into the peritoneal cavity, pericardial sac, or pleura, and thus 
cause death. The process is a progressive one, and each day more and more 
of hepatic tissue will be involved, and thus diminish the chances of recov- 
ery. On the other hand, those who oppose opening the abscess say that 
peritonitis and the entrance of air may result from it, that the ribs are more 
liable to become eroded, and the surrounding tissue to become gangrenous, 
when an opening is made. Some regard it as highly dangerous to pass an 
instrument into the liver, claiming that it may excite a suppurative process 
in healthy liver-tissue. All these objections are removed if antiseptic 
methods are employed. If no adhesions have formed between the liver and 
the abdominal walls, they should be established by caustics, and then the 
sac may be opened ; if it is very large, all of the pus should not be allowed to 
escape at once. It is always safest to open the sac by means of caustics, 
using the knife to divide the superficial tissues. The abscess should be 
opened as soon as possible. When hepatic abscesses open into the bronchi, 
colon, or gall-bladder, absolute rest must be insisted upon. In all cases, 
during convalescence, absolute rest and a careful regimen must be main- 
tained for months. The diet throughout the whole course of the disease 
should be the most nutritious, and stimulants should be freely given. 
The importance of sustaining the patient in every possible way is ap- 
parent. 

DIFFUSE PARENCHYMATOUS HEPATITIS. 

This disease, also called acute yellow atrophy and malignant jaundice, 
has been regarded as a ee passive degeneration," the metamorphosis being 
more rapid than in any other gland structure in the body. Some think it 
due to bilious liquefieation or polycholia, and that it is a general disease — 
like typhoid fever or cerebro-spinal meningitis — with a local lesion. The 
more recent views are that acute yellow atrophy is a diffuse inflammation 
of the whole hepatic structure, where the inflammatory changes are so 
rapid as to lead to disintegration and complete destruction of the liver 
cells and subsequent atrophy. Whether it is an exudative process, or one in 
which there first occurs albuminoid infiltration of the hepatic cells, and 
then molecular change, is still a disputed question, but the more reason- 
able view is that it comes from albuminoid infiltration, irregular cloudy 
swelling of the cells, and subsequent softening of the hepatic tissue. 

Morbid Anatomy. — It is seldom that one sees a liver that is the seat of 



390 



DISEASES OF THE DIGESTIVE SYSTEM. 




diffuse hepatitis until after the process is completed, but the few that have 
been studied present the evidences of having been the seat of an intense 
congestive and exudative process. The liver lobules have a dark gray 
muddy ring at the periphery, due to granular degeneration or albuminoid 
swelling of the peripheral cells, while the liver structure immediately sur- 
rounding the central vein is normal. The latter is, however, soon involved, 
and in place of liver cells there are fat and pigment granules, with traces of 

leucin and tyrosin. All outline of lobular 
structure disappears, the capillaries are 
intensely engorged, and the bile-ducts 
become more or less completely closed, 
owing to the compression which they 
suffer from peripheral exudation. Thus 
the bile formed between the central vein 
and the exterior of the lobule has no 
mode of escape, except through the cen- 
tral vein. The liver is diminished in size, 
sometimes to two-thirds of its normal size; 
in the early stage the organ is supposed 
to be very slightly enlarged. The diminu- 
tion is most marked in the right lobe. 
It is so soft that it folds upon itself, and 
takes any shape and position from the 
pressure of the adjacent organs. At the 
post-mortem, the body will be emaciated, 
the skin very much discolored, and ecchymotic spots will often be found 
scattered over the surface. 

The capsule is loose, freely movable, very much wrinkled, and opaque or 
yellowish in appearance. The parenchyma is soft, flabby, and brittle, and 
varies in color from a bright yellow to a yellow-red. 

On section, when the disease is far advanced, the color of the cut sur- 
face is of a rhubarb red, the outlines of the lobules are lost, and only a 
detritus of granular matter is left. The blood is darker and thicker than 
normal and coagulates imperfectly. It may contain leucin and traces 
of urea. If the organ be set aside for a while it becomes covered with crys- 
tals of leucin and tyrosin. 

The heart is jaundiced, fatty and pultaceous. 

The spleen is enlarged and softened, and leucin is found in it. The gall- 
bladder is empty, or contains a small amount of pale bile or mucus. 

The kidneys are slightly enlarged, and in most cases are in a state of 
acute fatty degeneration. Hemorrhages from the surface of the mucous 
membrane of the stomach and intestines are common. Occasionally there 
is softening of the central portion of the cerebral substance, and staining 
of the meninges. The serous cavities contain fluid, often bloody, and in 
rare instances nearly every organ in the body is blood stained and has 
leucin and tyrosin in its tissues. 



Fig. 75. 

Cells, etc., from an hepatic lobule in Acute 
Yellow Atrophy. 

A, A. Hepatic cells filled with granular detritus, 
with obscuration of nuclei and cell walls. 

B. A group of atrophied cells. 

C. Cells with fatty infiltration. 

D, E. Pigment granules, with blood and ty- 
rosin crystals, x 300. 



DIFFUSE PARENCHYMATOUS HEPATITIS. 



391 



Etiology. — Acute yellow atrophy is a rare form of disease. Its causes are 
regarded by some as constitutional, by others as due to a peculiar miasm. 
Two-thirds of the cases occur in pregnant females, between the ages of 
twenty and thirty. The supposed predisposing causes are sex, pregnancy, 
chronic alcoholism, syphilis, malaria, sexual excess, and a prolonged course 
of mercurials. But with our present knowledge, it is difficult to say 
whether these are really predisposing causes, or that the acute yellow 
atrophy is an intercurrent accident. Among the exciting causes may be 
named mental emotion, great grief, or fear. It is doubtful if obstruction 
of the bile-ducts alone can excite acute yellow atrophy ; some are inclined 
to regard malaria as an exciting cause, rather than a predisposing one. 
While its etiology is still so obscure, the history of its development leads to 
the conclusion that a malarial poisoning is present in a large proportion of 
cases. 

Symptoms. — The symptoms of the early stage of acute yellow atrophy 
usually pass unnoticed, for they are not in themselves distinctive. When 
the disease is slow in its advent, loss of appetite, occasional vomiting, a 
furred tongue, slight headache, and a sense of fulness in the right hypo- 
chondrium may be the only symptoms for the first week. Jaundice may 
precede it for a week or two. In cases where its advent is sudden, it will 
be ushered in by constant vomiting and great prostration. In either case 
during its early stage the temperature will be raised only a degree or two, 
and the pulse but slightly accelerated. A condition of despondency is often 
present, there are wandering pains simulating rheumatism, and a sense of 
great depression. Delirium and convulsions may be the only ushering-in 
symptoms. After from three to five days, the characteristic symptoms of 
the disease are developed ; of these jaundice is the earliest and most con- 
stant, it is progressive and never very intense, first affecting the upper half 
of the body. The rise in temperature and increased pulse-rate which 
marked its premonitory stage disappear, and now even a retarded pulse 
and sub-normal temperature may exist. In a few instances, after the first 
twenty-four hours, the temperature ranges from 100° to 101° F. during the 
whole course of the disease. The vomited material consists of mucus 
tinged with bile ; later it assumes the nature of black vomit, similar to that 
in yellow fever, the color being due to gastric capillary hemorrhage. There 
is intense pain in the epigastric and right hypochondriac regions, which is 
increased by firm pressure over the liver. In the stage of coma, the hepatic 
tenderness is so great that pressing the liver up against the diaphragm may 
rouse the patient. At first the cerebral symptoms are those of mental de- 
pression and slight headache, which rapidly increases in severity ; this, 
later, gives place to wild delirium, jactitation, and convulsions. Twitch- 
ings of the voluntary muscles of the head and neck (trismus) mark the 
convulsive stage of the disease. These spasms usually follow the vomiting, 
but in cases where the disease runs a rapid course, typhoid symptoms 
make their appearance, sordes collect on the teeth, while low muttering 
delirium, subsultus, muscular tremors, and partial stupor precede the 



392 



DISEASES OF THE DIGESTIVE SYSTEM. 



convulsions. The convulsions are epileptiform, and are sometimes ushered 
in by a peculiar shrill cry. 

During the period of nervous excitement, the pulse undergoes remark 
able changes. It may rapidly rise to 120, 130, or even 140 beats in a 
minute, falling in moments of calm to 80 or 90, the temperature remain- 
ing unchanged. The breathing during the convulsions is interrupted 
or stertorous, and a peculiar groaning noise is heard with each inspira- 
tion ; the expirations are prolonged and puffing. Whether the convulsions 
have been preceded by typhoid symptoms or not, the patient gradually be- 
comes more and more tranquil, passes into stupor, and finally into deep 
coma, from which he cannot be aroused. The discharges from the 
bowels and bladder are either passed involuntarily or retained. The 
pupils are normal or slightly dilated, and respond to light slowly. The 
breathing becomes sighing, the pulse reaches 140 to 150, and grows shorter 
and shorter until death occurs. The skin during the progress of the disease 
has become more or less deeply jaundiced, ecchymotic and petechial spots 
sometimes appear on the surface, and there may be hemorrhages from the 
stomach, nose, intestine, uterus, and kidneys. In pregnant females abor- 
tion is likely to occur before death. The fceces are firm, clay-colored, and 
often blood-stained. The urine is acid and dark in color, is not quite 
up to the normal amount, and often contains albumen and blood ; urea 
and uric acid have totally disappeared, the sulphates and phosphates are 
diminished in quantity, and leucin and tyrosin are found in their place. 
The duration of the disease varies from one to three weeks. 

Physical Signs. — Palpation elicits extreme tenderness over the epigas- 
trium and right hypochondrium. 

Percussion. — The area of hepatic dulness rapidly diminishes from day 
to day, and as the liver decreases in size it is displaced backward, so that 
there is no well-defined area of hepatic dulness in front. As the liver 
diminishes in size the spleen enlarges. 

Differential Diagnosis. — Diffuse parenchymatous hepatitis may be mis- 
taken for yellow fever, pymmia, typhoid fever, and the lilious remittent 
variety of pernicious fever. 

In acute yellow atrophy, the liver is diminishing in size from day to 
day, while in yellow fever it is steadily increasing. The spleen is increased 
in size in acute yellow atrophy, and is unchanged in yellow fever. The 
urine in yellow atrophy is acid throughout, and contains leucin and tyro- 
sin ; while as soon as jaundice appears in yellow fever the urine becomes 
alkaline. Yellow fever is ushered in by a distinct chill, while yellow 
atrophy of the liver rarely begins with a chill. The pulse, in severe forms 
of yellow fever, is gaseous in character and is rarely over 110, while in 
acute atrophy the pulse may reach 140 or 150 per minute. The stools are 
dark and fluid in yellow fever, and firm and clay-colored in acute atrophy. 

Pycemia is ushered in by distinct chills. The chills in pyaemia are 
followed by irregular rigors and exhausting sweats, which do not occur in 
acute atrophy. In pyaemia there is diarrhoea, and in acute yellow atrophy 



DIFFUSE PARENCHYMATOUS HEPATITIS. 



393 



the stools are firm and elay-colored. In pyaemia there is a peculiar sweet 
sickish breath, which is absent in acute atrophy. Evidences of multiple 
abscesses, especially in the lungs, soon follow the sweats of pyaemia ; these 
do not occur in acute atrophy. The presence of leucin and tyrosin and 
the absence of urea, with the other urinary symptoms of acute atrophy, 
are in marked contrast with the normal urine of pyaemia. Physical 
(hepatic) signs are negative in pyaemia, while a daily diminishing area of 
hejDatic dulness is usually present in acute yellow atrophy. 

Typhoid fever has nearly the same premonitory symptoms as acute 
yellow atrophy, but the steady rise in temperature with the typical morn- 
ing and evening exacerbations and remissions during the first week, are in 
marked contrast with the continual low temperature of acute atrophy. 
The delirium is wandering in typhoid, and wild in acute yellow atrophy. 
The characteristic " rose rash " appears about the seventh day of typhoid 
fever. Diarrhoea is the rule in typhoid fever, while constipation and clav- 
colored faeces are the rule in acute atrophy. In typhoid, the urine is 
simply diminished in amount, and the urea is increased, while in acute 
yellow atrophy the urea is greatly diminished in quantity, and often com- 
pletely absent, and the other (mentioned) urinary changes are present. In 
typhoid fever the liver is slightly enlarged, while in acute yellow atrophy it 
is markedly diminished in size. 

The "MUous remittent" form of pernicious fever very closely re- 
sembles in its symptoms acute atrophy of the liver. The severe sudden 
chill, rapid rise in temperature to 105° or 107°, the sweating, and the re- 
mission in pernicious fever are all, however, absent in acute atrophy. Free 
pigment exists in the blood in bilious fever, and is absent in atrophy. 
Jaundice is a late symptom of pernicious fever, but occurs early in acute 
atrophy. The liver is markedly enlarged in pernicious fever, and as 
markedly diminished in size in acute yellow atrophy. Poisoning from 
phosphorus can only be diagnosticated from acute yellow atrophy when we 
know the drug has been taken. 

Prognosis. — This is exceedingly unfavorable, and those cases where a cure 
has been reported are in the doubtful list. The average duration is one 
week, the extreme limits being twelve hours and four weeks. Cholaemia 
ami uraemia, by inducing the cerebral symptoms which have been referred 
to, may be the direct cause of death. Peritonitis and hemorrhages from 
the stomach and bowels are also frequent causes of death. 

Treatment. — All plans of treatment have thus far failed either to arrest 
the progress, or to diminish the fatal tendency of this disease. It has 
been preferred, in the early stages, to administer drastic purges, and apply 
leeches over the region of the liver and about the anus, and in the robust 
and plethoric to practice venesection ; there is, however, no evidence that 
these measures have any controlling influence over the disease. Pregnant 
females should be placed in pleasant apartments, with cheerful surround- 
ings. vVhen the pain over the liver is intense, leeches and hot fomenta- 
tions over the hepatic region, with morphine hypodermically, will afford 



394 



DISEASES OF THE DIGESTIVE SYSTEM. 



relief. When the cerebral symptoms develop, chloric ether in drachm 
doses every hour will often quiet the wildest delirium. Hemorrhages from 
the mucous surfaces can usually be checked by astringents and cold. Bis- 
muth or strychnia will sometimes relieve the vomiting. Bi-carbonate of 
soda in ten-grain doses every hour has been given with apparent benefit. 



PERIHEPATITIS. 

Perihepatitis is an inflammation of the capsule of the liver. It is im- 
portant to remember that the liver has two envelopes, the outer, the serous 
covering which is part of the peritoneum, and an inner, its true fibrous 
covering, the capsule of Glisson. 

Morbid Anatomy. — A liver which has been the seat of perihepatitis is 
diminished in size, except when it is complicated by those diseases of the 
organ which give rise to enlargement. The capsule is thickened, the thick- 
ening varying from a few lines to half an inch ; it is more or less firmly 
adherent to the colon, stomach, diaphragm, and abdominal walls. In 
syphilitic perihepatitis, Grlisson's capsule is hard and leathery and has a 
granular appearance. Sometimes the capsule is so thickened and con- 
tracted in the transverse fissure of the liver as to obstruct the portal vein 
and hepatic duct. The liver substance usually remains normal, being only 
slightly compressed on the surface of the organ, corresponding to the fur- 
rows between the larger lobules. In " perihepatitis syphilitica " prolonga- 
tions of new connective-tissue will penetrate the parenchyma, and the out- 
lines of the lobules will be indistinct. This condition is called induration. 
Slight atrophy of the parenchyma may occur at points corresponding to 
the circumscribed capsular thickening. The coats of the hepatic veins 
may be thickened and the bile-ducts dilated. The gall-bladder is some- 
tiuies displaced by the contraction of the new tissue, and the ductus 
communis may be partially occluded by fibrous bands. Perihepatitis is 
usually accompanied by pleurisy in the lower part of the right pleural 
cavity. 

Etiology. — Exposure to cold, when the liver is in a state of active hy- 
peremia, is the most frequent cause of perihepatitis. Blows over the 
hepatic region often excite it, and it may come from an extension of in- 
flammation from the peritoneum or from the right pleura. In all in- 
flammatory forms of hepatic disease and during the development of new 
growths, perihepatitis is of frequent occurrence. Syphilis is a very com- 
mon cause. 

Symptoms. — It is often ushered in by a chill, followed by a slight rise 
in temperature and a corresponding increase in the pulse rate. The pulse is 
tense and wiry in character ; pain in the hepatic region is its most constant 
symptom, and is increased by pressure, by a full inspiration, by coughing, 
and by lying on the right side. Jaundice is rare, but when the new tissue 



PERIHEPATITIS. 



395 



compresses the common duct it may be developed. A dry, hacking cough 
is rarely absent. New tissue developments in the transverse fissure may 
cause sufficient obstruction to the portal vein to produce ascites. From 
obstructions of the common duct, under similar circumstances, gall-stones 
may form and be found in the faeces. 

Physical Signs. — On palpation the liver will be found intensely tender, 
slight pressure causing severe pain. It may be diminished in size, its 
edges lobulated, rounded, smooth and harsh. 

Percussion. — The area of hepatic dulness is somewhat smaller than 
normal. 

Auscultation. — In the early stage there is sometimes heard over the liver 
a rubbing sound, like the friction sound in pleurisy. 

Differential Diagnosis. — Perihepatitis may be confounded with intercos- 
tal neuralgia of the right side, with pleurisy, and with abscess of the 
liver. 

In intercostal neuralgia there is usually a neuralgic history and three 
diagnostic points of tenderness -.—first, at the exit of the nerve from the 
spinal canal ; second, midway between the sternum and the spine ; third, 
just at the edge of the sternum. The pain is usually confined to the sixth, 
seventh and eighth intercostal spaces. In perihepatitis there is generally 
equal tenderness over the whole hepatic region, and pressure up under the 
ribs increases the pain. Elevation of temperature, increase in the pulse- 
rate, and the history of a chill are all absent in intercostal neuralgia. 

In pleurisy, the pain is located under the right nipple. The pain is 
lower down in perihepatitis, and pressure up under the ribs will cause a 
marked increase in its severity. The dyspnoea is more urgent in pleurisy 
and the cough has a teasing, hacking character. With the advent of plas- 
tic exudation in pleurisy, there is diminished vocal fremitus, dulness on 
percussion, feeble respiratory murmur, and a " sticky 93 crepitating friction- 
sound. 

Perihepatitis often accompanies abscess of the liver, and then the dif- 
ferential diagnosis is difficult. In abscess there are hectic, rigors, and re- 
curring sweats ; while in perihepatitis there is but one chill, and that at the 
commencement. The temperature in abscess is 103° and 105°, while it is 
lower, rarely above 101° F., in perihepatitis. Urgent gastric symptoms, 
profuse and persistent bilious vomiting, are marked in abscess of the 
liver, and absent in perihepatitis. In abscess there is a rapidly developing 
cachexia, which does not exist in perihepatitis. In abscess, distinct fluctua- 
tion on palpation is often present, while it never occurs in perihepatitis. 
Percussion in abscess shows an area of hepatic dulness either uniformly 
increased, or increased in one direction, while the area of hepatic dulness 
is never increased in perihepatitis. 

Prognosis.— The prognosis in perihepatitis is good ; it is influenced, how- 
ever, by the disease which it accompanies. The chief danger is that 
repeated attacks will lead to "induration" or compression of the portal 
vein, and subsequent atrophy of the liver. In the latter case, all the 



396 



DISEASES OF THE DIGESTIVE SYSTEM. 



symptoms of cirrhosis will follow. When obstruction to the ductus 
communis is sufficient to cause jaundice, the prognosis is unfavorable. 

Treatment. — Eest in the recumbent posture is essential to the successful 
treatment of this disease. The severe pain which usually attends it can 
be relieved by hypodermic injections of morphia and the application of 
leeches over the hepatic region. Warm anodyne poultices should be ap- 
plied after the leeches. In those cases where there is active hepatic hy- 
persemia, a mercurial or saline purge is indicated, unless general peritonitis 
exist. In all cases the diet should be non-stimulating and nutritious, and 
an individual who has once had perihepatitis should abstain from all forms 
of alcoholic stimulants. 

PYLEPHLEBITIS. 

Pylephlebitis is an inflammation of the portal vein, accompanied by 
coagulation of its contents. Under this term are now included all cases 
of "portal thrombosis,*' whether the thrombosis is preceded, followed, or 
unattended by an inflammatory process. It is of two varieties, adhesive 
and suppurative. In adhesive pylephlebitis there is more or less extensive 
obliteration of the veins ; in suppurative, the thrombus which forms in 
the vein becomes a centre of purulent accumulation. When the unquali- 
fied term pylephlebitis is used, the adhesive variety is always indicated. 

Morbid Anatomy. — In adhesive pylephlebitis the coats of the portal veins 
become thickened and their calibre is diminished, fibrin collects upon the 
constricted portion, and thus thrombi are formed. Sometimes the coagu- 
lum forms before any recognizable change in the coats of the vein has 
occurred. When this happens, the process may commence in a small branch 
and extend to the main trunk, or a single spot in a large branch may be 
the point where blood first coagulates. In either case, obliteration of the 
vein is the result. The wall of the vein is the seat of hyperplasia, 
adhesion of its two surfaces occurs, and as a result the vein is obliterated 
and a fibro-cellular cord alone remains. As a rule the liver is smaller in 
size than normal, and may exhibit on its surface cicatricial contraction, 
showing the lines of the obliterated vein. 

On section, coagula may be found in all stages of formation. 

The spleen is usually found much enlarged. The abdominal cavity is 
often filled with fluid, and the superficial abdominal veins on the right 
side are enlarged and tortuous. The gall-bladder is usually found full of 
greenish bile. 

Etiology. — Certain blood conditions predispose to adhesive pylephlebitis, 
and chief among these are acute septic and malarial poisons. The most 
common and direct cause is narroioing of the trunk of the portal vein, from 
contraction of cicatricial tissue in the transverse fissure of the liver, or from 
pressure of enlarged lymphatic glands, tumors of the pancreas, omentum, 
or stomach : — hence cirrhosis plays the most important part. Blows, in- 
juries to the walls of the vein, and inflammation of the tissue immediately 



PYLEPHLEBITIS, 



397 



about it, act as direct causes. The secondary causes are an extension of 
inflammation from inflamed hemorrhoidal tumors, from the umbilical phle- 
bitis of the new-born, from severe local inflammation of the intes- 
tine, from extension of inflammation from the mesentery to the mesenteric 
vein, from a peculiar form of phlebitis called •'•'gouty," and from a chronic 
inflammation excited by pressure of gall-stones. 

Symptoms. — When the main trunk of the portal yein or its larger branches 
are not involved, the disease cannot be recognized. But when they are exten- 
sively involved, fluid rapidly accumulates in the peritoneal cavity, and after 
withdrawal it quickly reaceumulates. This is an important point in the 
diagnosis. The veins of the abdomen, and often those of the thorax, be- 
come enlarged, tortuous and prominent ; at the same time hemorrhoids, 
which often attain immense size and become very painful, are developed. 
The spleen enlarges so rapidly in some cases that the extent of the enlarge- 
ment can be determined each day. Profuse and exhausting vomiting, with 
haematemesis, is common, and diarrhoea, with frequent discharges of fluid 
blood from the bowels, marks the advanced stage. Gastro-intestinal hem- 
orrhages and epistaxis may lead to fatal syncope. In the majority of cases 
its course is rapid ; — if it is slow in its development, it gives rise to precisely 
the same symptoms as those of the latter stage of cirrhosis of the liver. Jaun- 
dice is never a prominent symptom. If it does occur, it is usually due to 
a complicating catarrh of the bile-ducts. 

Physical Signs. — Inspection and palpation will give the evidences of fluid 
in the abdominal cavity, and the superficial veins will be markedly enlarged 
and cord-like. 

Percussion. — The normal area of the hepatic dulness is diminished, un- 
less waxy degeneration or some other disease of the liver precedes its devel- 
opment. The spleen is enlarged in all cases. 

Differential Diagnosis. — Cirrhosisis the only disease which would be liable 
to be confounded with pylephlebitis. In the advanced stage, it is impossi- 
ble to make a differential diagnosis. The previous history of the patient is 
important : — in cirrhosis it is one of chronic alcoholismus, gout, rheuma- 
tism, or syphilis, none of which can be regarded as causes of pylephlebitis. 
Cirrhosis is much slower in its development than pylephlebitis. The ab- 
dominal dropsy accumulates rapidly in pylephlebitis, while in cirrhosis it 
accumulates slowly, and does not return quickly after paracentesis. The 
stools in cirrhosis are firm and clay-colored. The urine contains abundant 
urates in cirrhosis ; these are absent in pylephlebitis. Persistent tympani- 
tis precedes the ascites of cirrhosis, and is absent in pylephlebitis. 

Prognosis. — The prognosis is unfavorable. Death may result from as- 
phyxia, from gastric and intestinal hemorrhage, and from exhausting 
diarrhoea. 

Treatment. — Medication avails little in this disease ; the treatment is al- 
together palliative. The diarrhoea and hemorrhage should be checked with 
vegetable astringents. If dyspnoea becomes urgent, on account of the large 
accumulation of the fluid in the abdominal cavity, paracentesis should be 



398 



DISEASES OF THE DIGESTIVE SYSTEM. 



performed. The food should be highly nutritious, and taken in small 
quantities, at short intervals. 



SUPPURATIVE PYLEPHLEBITIS. 

Suppurative inflammation of the portal vein is always a secondary disease, 
and leads to the formation of small hepatic abscesses. 

Morbid Anatomy— The wall of the vein is the seat of the inflammatory 
process ; it becomes thickened, and its cavity is filled with a puriform 
fluid, coagulated blood, or a stratified thrombus. The primary seat of the 
process may be the trunk of the vein before it enters the liver. It may 
extend to the smaller branches, and from them to the liver substance. If 
coagula occupy the venous twigs as well as the trunk of the vein, it is com- 
mon for the puriform infiltration to take place only in them, while a firm 
clot obstructs the main channel. When the veins near the surface of the 
liver are the seat of suppurative pylephlebitis, extension of the process from 
the sheath of the vessels to the adjacent parenchyma gives rise to small ab- 
scesses. The liver becomes enlarged and softened, and circumscribed col- 
lections of pus are visible underneath its capsule. 

On section, the calibre of the vena portge is seen enlarged and gaping ; 
the wall is thickened. Its contents vary : sometimes it only contains pus; 
at others, fibrinous matter and small coagula of blood are mixed in the 
purulent fluid. Abscesses are found along the course of the larger portal 
veins, and the smaller branches often terminate in larger collections of pus. 
If pieces of thrombi have been swept into the blood current, infarctions are 
found in all stages, from reddish-brown clots to purulent masses. The 
spleen is usually found enlarged, and of a dark purplish color. 

Etiology.— The chief causes are ulceration and inflammatory processes in 
the abdominal cavity. Typhlitis, perityphlitis and ulceration of the vermi- 
form appendix sometimes induce it. Diseases of the rectum, as recto-ure- 
thral fistulae and suppurating hemorrhoidal tumors, chronic peritonitis, ab- 
scess of the spleen, suppurating mesenteric glands, diseases of the mesen- 
tery which have pus as their product, and diseases of the bile ducts, such 
as inflammation, ulceration and perforation, especially when caused by im- 
pacted gall-stones, often excite suppuration in the portal vein. Severe 
blows over the region of the liver have been followed by pylephlebitis. 
Suppurative gastritis may be followed by it. 

Symptoms. — The symptoms of. this disease are usually well marked. Pain 
is the first and most constant symptom. The location of the pain varies in 
different cases ; it is generally most intense about the umbilicus and right 
hypochondriac region, just to the right of and below the xiphoid cartilage. 
Frequently it is felt below the spleen, and again it seems to come from, or 
extend to, the region about the caecum. The pain is burning in character, 
and accompanied by slight tympanitis and tenderness. With the pain the 
temperature is elevated, the pulse- rate increased, and soon a more or less 



SUPPURATIVE PYLEPHLEBITIS. 



399 



prolonged rigor occurs, during which the temperature will rise to 101°, 
102° F., or even higher. After this comes a profuse and exhausting sweat. 
The rigors and sweats continue for two or three days, and may occur so 
regularly in the morning or evening as to suggest the presence of some form 
of malarial fever ; usually, however, the chills are irregular. Slight jaun- 
dice, gradually deepening, but never very intense, is soon present, and 
sometimes assumes a greenish tint. The pulse is gradually increased in 
frequency, reaching in some cases 130 per minute. The spleen increases 
in size daily, and is quite tender to pressure. The appearance of the patient 
is that of one suffering from some grave form of disease. He becomes 
greatfy emaciated, and there is more or less profuse diarrhoea, often contain- 
ing blood. Hsematemesis and bilious vomiting are frequently present, and 
as the disease advances the fever assumes a hectic type, with signs of gen- 
eral peritonitis, accompanied by painful tympanitis and obstinate vomiting. 
Ascites, if present, is slight. Petechias appear upon the surface, and aph- 
thae develop in the mouth. Typhoid symptoms usually come on toward 
the close, with low, muttering delirium, subsultus, somnolence, and fatal 
coma. The mind may be clear to the last, the patient dying in an ex- 
tremely emaciated condition. In this disease there sometimes occur dis- 
tinct remissions at the end of the first- week, but this must not mislead one, 
for exhausting rigors and sweats will soon follow and lead to a fatal result. 
The urine is scanty, non-albuminous, and usually contains bile pig- 
ment. 

Physical Signs. — By palpation and percussion both liver and spleen are 
found uniformly enlarged, and very tender, but the spleen is relatively 
much more enlarged than the liver. 

Differential Diagnosis. — Suppurative inflammation of the portal vein may 
be mistaken for adhesive pylephlebitis, for malarial fever, abscess of the 
liver, and catarrh of the bile-ducts. 

In suppurative pylephlebitis severe pain, rigors and sweats usher in 
the disease, and recur irregularly throughout its course ; these never mark 
the advent of the adhesive variety. A large amount of fluid accumulates 
rapidly in the abdominal cavity in adhesive pylephlebitis, and it rarely, if 
ever, occurs in suppurative. Jaundice is the rule in suppurative pylephle- 
bitis, and the exception in adhesive. The liver is smaller than normal in 
adhesive, and larger than normal, and tender, in suppurative. The spleen 
is enlarged in both diseases, but it is excessively tender in the suppurative 
form. 

In malarial fever the rigors and sweats follow a definite order, while 
in suppurative pylephlebitis they occur irregularly. There is no pain in 
malaria, while in suppurative pylephlebitis it is diffused over the hepatic, 
umbilical and splenic regions. 

Diarrhoea rarely occurs in abscess of the liver, and if present it is of 
short duration, often alternating with constipation, when the stools are 
firm and clay-colored ; while profuse diarrhoea exists from the commence- 
ment in suppurative pylephlebitis. Jaundice is rare in hepatic abscess, 



400 



DISEASES OF THE DIGESTIVE SYSTEM. 



and of common occurrence in suppurative pylephlebitis. Fluctuation is 
often present in abscess of the liver, and never in suppurative pylephle- 
bitis. 

In catarrh of the bile-ducts slight fever soon gives place to a normal 
temperature and a slow pulse, while there is a high temperature and rapid 
pulse throughout the course of suppurative pylephlebitis. 

Prognosis. — Nearly all the cases of suppurative pylephlebitis are fatal. 
Its duration varies from one or two weeks to one or two months, the aver- 
age being about one month. Death may occur from diarrhoea, from hem- 
orrhage, from exhaustion, and from the intense gastric catarrh which may 
complicate the disease. 

Treatment. — We are powerless to arrest this disease ; and its treatment is 
altogether palliative. Morphia hypodermatically is the only reliable means 
of relieving the pain which is so distressing. Diarrhoea is a part of its 
natural history, and all the resisting power of the patient is required to 
withstand the exhaustion and cachexia which it produces. Although 
quinine has no controlling power over the disease, it may be used as an 
antipyretic and stimulant, and should be freely administered in connection 
with stimulants and a most nutritious diet. 



AMYLOID DEGEKEKATTOtf. 

The most common degenerations of the liver are the amyloid and the 
fatty. 

Amyloid, waxy or lardaceous degeneration of the liver, is never a pri- 
mary disease. It is one of the painless enlargements of the liver. 

Morbid Anatomy. — The degenerative process begins in the walls of the 
capillaries and small arteries, very rarely in the veins. Various theories 
have been advanced concerning the nature of this degeneration ; some 
claim that it depends upon blood changes, and refer to the connection 
between waxy change and syphilis in support of their views. Others main- 
tain that, the alkalinity of the blood being diminished, the normal relation- 
ship between its other constituents is disturbed, and as a consequence 
amyloid material or " dealhalized fibrin " is deposited ; that the process 
is not one of simple infiltration. In detail the changes are as follows : 
—the capillaries are stretched and consequently have their diameter 
increased ; their walls then become thickened by infiltration or deposit, so 
that their channel is narrowed or wholly occluded. The material depos- 
ited is a substance resembling albumen in its reaction ; it is nitrogenous, 
homogeneous, and translucent, with a dull, shining surface. Its reaction 
is characteristic, a watery solution of iodine changing it to a deep red- 
brown color, which gradually passes off ; if before it entirely disappears a 
drop of concentrated sulphuric acid is poured over it, a violet or deep blue- 
black color results. The change in the capillary walls is rapidly followed 
by a similar one in the walls of the arterioles all the coats of the smaller 



AMYLOID DEGENERATION. 



401 



arteries are involved simultaneously, the most marked change, however, be- 
ing in their muscular coat. The amyloid change in the liver always begins 
in the radicles, midway between the centre and the periphery of the 
hepatic lobules. An extension of the infiltration to the adjacent liver- 
cells causes them to enlarge, become irregular in outline, and coalesce in 
masses ; finally a whole lobule becomes involved. This enlargement, the 
increased lateral pressure, and the diminution of the lumen of the vessels, 
cause a decrease in the blood supply, and this leads to atrophy of the liver- 
cells. The liver is uniformly enlarged, sometimes to such an extent as to 
nearly fill the abdominal cavity. It is stony hard, non-elastic, heavier 
than normal, its specific gravity is increased, and its edges are sharp and 
well defined. The capsule is tense, shining, and has a gray " waxy" look. 
In some rare cases enlarged lymphatics are found in its transverse fissure, 
and then jaundice may be present. 

On section, the liver cuts with a " creaking " sound, like bacon (hence 
its name lardaceous), and 
the cut surface has a 
6S cheese yellow," or dull 
gray, glistening appearance. 
The whole or a part of the 
liver may be involved. If 
the whole liver has under- 
gone amyloid degeneration, 
the cut surface presents a 
homogeneous appearance, 
and either the outline of 
the lobules is lost or they 
are seen to be enlarged and 
irregular ; sometimes a 
" yellow rim " can be traced 
at their periphery, due to 
fatty change. The micro- 
scope shows the lobules to be 
increased in size ; the liver 
cells at the periphery of 
the lobules are infiltrated 
with small spherules of fat ; 
midway between the sur- 
face and centre of the lobule there is a zone of amyloid matter, and in 
some instances there is a pigment deposit in the zone just about the vena 
centralis. We have, then ; first, the fatty zone at the periphery of the 
lobules ; secondly, the waxy intermediate zone ; and, thirdly, the pig- 
ment zone around the central vein. The liver cells lose their polygonal 
outline, 1 and become irregularly oval or circular in shape. Their cell-walls 

1 Quite recently CorniJ, in examining many specimens, found no change in the hepatic cells. 
26 




Fig. 76. 
Amyloid Degeneration. 

Section of a Lobule of the Liver in amyloid degeneration. 

A. Central rein of the lobule. 

B. Normal hepatic cells. 

C. Pigmented cells. 

D. Commencement of the amyloid change. 

E. Waxy zone— the hepatic cells completely changed. At F, 

cells are shown containing fat. x 350. 



4G$ DISEASES OF THE DIGESTIVE SYSTEM. 



cannot be traced, bat merge into the neighboring mass of amyloid 
material. The contents of the cell are atrophied, nuclei are not visible, 
though occasionally a nucleus of one cell stands out enlarged and shin- 
ing. A semi-transparent homo- 
geneous mass fills the cell, caus- 
ing it to present the appearance of 
"waxy scales.'' Fatty degenera- 
tion frequently coexists with amy- 
loid change. The liver will then 
partake of the characters of both 
waxy and fatty change. Cirrhosis 
or simple atrophy may precede or 
be associated with waxy degenera- 
tion, and syphilitic nodules and 
cicatrices from " perihepatitis sy- 
philitica " may exist in a liver 
which had subsequently under- 
gone waxy degeneration. The kid- 
neys undergo amyloid degenera- 
tion. The spleen is enlarged, firm 
and waxy ; the lymjihatics gener- 
ally, and the g astro -intestinal mu- 
cous membrane may also become 
the seat of the amyloid change. 
Etiology. — Seventy-five per cent, of the cases of waxy liver occur in males 
between twenty and fifty years of age. Syphilis is its chief cause. Pro- 
longed suppuration and chronic diseases of bone are also prominent causes. 
Caries, necrosis, especially when the larger joints are involved, rickets, dys- 
entery, chronic intestinal ulceration, and sometimes chronic pyelitis are 
reckoned among the morbid conditions which predispose to it. A scrofu- 
lous diathesis, prolonged exposure to malaria, and a cancerous cachexia are 
among the rarer conditions under which amyloid degeneration is devel- 
oped. 

Symptoms. — Its advent is never well defined, occurring as it does with 
diseases which are prone to cause ansemia and wasting of the body ; its sub- 
jective symptoms are at first very obscure. There is no pyrexia accompany- 
ing it. The patient has a sense of weight, fulness, and constriction in the 
right hypochondrium, never amounting to pain, the sensation being rather 
one of discomfort. Jaundice and ascites are not part of the natural his- 
tory of amyloid liver. When jaundice is present, it is due either to an 
intercurrent catarrh of the bile-ducts, or to pressure from the enlarged 
lymphatics in the transverse fissure. Ascitic accumulations result from 
complicating peritonitis or from the pressure of enlarged glands in the trans- 
verse fissure. Late in the disease, diarrhoea and vomiting are induced by 
the slightest irregularities in diet, on account of the implication of the gas- 
trointestinal tract in the amyloid change. On an examination of the 
blood of one who has suffered from waxy degeneration of the liver, the 




Fig. 77. 



Diagram showing the three Intralobular Zones. 

V. Small branch of Portal Vein. 
A. Hepatic Artery. 
D. Bile Duct. 

The three vessels are surrounded by fibrous connective- 
tissue, a prolongation of Glisson's capsule, and alto- 
gether constitute the elements of the Portal Canal. 



AMYLOID BEGENEKATIOtf. 



403 



proportion of white blood globules will be found increased. The skin has 
a pale, "waxy" look, and oftentimes exhales a peculiar odor. Early in 
the disease the faeces are firm, and pale in color, because of absence of bile ; 
later, when the so-called "waxy diarrhoea" sets in, there are pale mucous 
stools, sometimes having a dysenteric odor. The urine is increased in 
amount, is of a pale lemon-yellow color, low specific gravity, averaging 
about 1.010, and contains albumen. The amount of the albumen increases 
as the disease progresses ; epithelial and large hyaline casts are present. 
Anasarca may occur in the advanced stage of the disease, with general 
dropsy. 

Physical Signs. — Inspection in the advanced stage of the disease shows 
bulging of the hepatic and splenic regions. The sharp edge of the liver 
will be found projecting below the free border of the ribs, with a firm, hard, 
resistant feel and a smooth surface. The spleen is increased sometimes to 
three times its normal size, and is resistant. 

Percussion. — The areas of hepatic and splenic dulness are increased 
equally in all directions. 

Differential Diagnosis. — Waxy liver may be confounded with the first 
stage of cirrhosis, which has already been referred to, and also with 
fatty liver, the diagnosis of which is considered in the history of that 
disease. 

Prognosis. — The prognosis is unfavorable ; the disease is progressive and 
fatal, and we can only hope to arrest its progress when it occurs with syph- 
ilis. Its exact duration cannot be estimated, since its beginning is so ob- 
scure. It is usually slow in its development, and extends over a period of 
many months and sometimes years. Among its most frequent complica- 
tions are diarrhoea, purulent peritonitis, perihepatitis, fatty and waxy 
kidney, dysentery, pulmonary oedema, pneumonia, and pulmonary gan- 
grene. Death may result from exhaustion due to faulty nutrition or diar- 
rhoea, from general dropsy, and from uraemia or other complicating 
diseases. 

Treatment. — The first indication for treatment is to be found in its causa- 
tion. If it is developed in connection with disease of the bones, the diseased 
bones should be removed, and prolonged suppuration arrested. If syphilis 
exist, antisyphilitic measures are indicated. In phthisis, empyema, and 
other similar diseases, attention must be directed to the primary disease. 
Alkalies have been administered, on the ground that the amyloid material 
is "dealkalized fibrin," and that with the suppurative process a large quan- 
tity of alkalies pass rapidly out of the system. When once the amyloid 
process is well established, the diet should consist largely of meat ; sugars 
and starch should be avoided. Alcoholic stimulants may be taken in mod- 
eration. The climate, clothing, and general hygienic surroundings of the 
patient are important. Tonics, and iron combined with some preparation 
of iodine are indicated in all cases. Bat when a history of syphilis is clearly 
elicited, then iodide of potassium may be given in large doses, with the 
hope of arresting the progress of the disease. Alkalies, chiefly potassic salts, 



404 



DISEASES OF THE DIGESTIVE SYSTEM. 



are in great repute among the advocates of the " alkaline treatment/' and 
they can be given without fear of injury in nearly every case. It is claimed 
by some that ammonium chloride produces the most beneficial effects, but 
my own experience does not sustain the strong statements that have been 
made regarding it. The mineral waters are too exhausting for this class of 
patients, and, although they may give temporary relief, should not be used 
in its treatment. External applications, such as iodine ointments, and 
nitro-muriatic acid baths, have been used, but without any markedly 
favorable results. If ursemic symptoms develop, measures for their re- 
lief should be promptly instituted. Drastic purges, however, must not 
be employed, for the condition of the gastro-intestinal tract contra-indi- 
cates their use. 



CHRONIC ATROPHY OF THE LIVER. 

The term "atrophy" includes all those forms of hepatic disease in which 
there is a diminution in the size of the liver, due to decrease in either the 
number or the size of the hepatic cells. Strictly speaking there are six 
varieties of hepatic atrophy, viz. : — acute yellow atrophy, induration 
atrophy, from repeated attacks of perihepatitis, cirrhosis, atrophy from 
long continued hypercemia, atrophy from adhesive pylephlebitis, and chronic 
atrophy. All these varieties have already been considered under their 
proper head, except the one termed chronic atrophy. The liver in chronic 
atrophy may have a brown or red color ; hence the term chronic brown or r&i 
atrophy. The pathological processes which lead to it are similar to tho 3 
which take place in atrophy of any gland tissue. 

Morbid Anatomy. — Chronic atrophy may be partial or general. The 
liver is smaller than normal, and its diminution in size is uniform. Some- 
times its weight is decreased to twenty-four ounces. It is flabby and 
tenacious, its edges are thickened, its capsule is smooth, of normal thick- 
ness, and free from adhesions. Sometimes it is shrivelled, but never 
" hob-nailed " or lobulated. In partial atrophy, there are often large de- 
pressions on the surface, the result of the pressure of neighboring organs, 
or of tight lacing, or the wearing of belts tightly about the waist. A large 
quantity of thin blood flows from its cut surface, which has a uniform 
brown-red or mottled appearance. The sections of the larger portal vessels 
gape. The outline of the lobules is obliterated. The portal vein and 
its branches are enlarged, the walls assume a yellow- red color, the fibrous 
sheath, derived from Glisson's capsule, is thickened, and its finest ramifica- 
tions end in blind pouches or club-shaped extremities near the periphery of 
the lobule. The capillaries are usually filled with pigment granules. 
Sometimes the hepatic vein is involved, but never to the same degree as 
the portal. The bile ducts are either empty or contain a small amount of 
pale, turbid fluid, having traces of albumen. By the microscope the gran- 
ular contents and nuclei of the hepatic cells will be found to have dis- 



CHRONIC ATROPHY OF THE LIVER. 



405 



appeared. The cell walls will 
pigment granules, traces of bile 
coloring matter, or little fatty 
spherules will be seen occupy- 
ing their place. When the 
atrophy is partial, these morbid 
changes will be found to exist 
underneath the depressions on 
the surface, where pressure has 
been long continued. The 
spleen is usually enlarged, but 
only slightly. The gastroin- 
testinal mucous membrane is 
the seat of catarrh, and some- 
times there are punctate hem- 
orrhages beneath its mucous 
surface. 

Etiology. — The causes of par- 
tial chronic red atrophy are tight lacing and pressure from peritoneal 
effusions and from abdominal tumors. It may also be caused by extensive 
adhesions to adjacent organs. General atrophy may be due to the con- 
traction of the new connectiye-tissue developed in the substance and on the 
surface of the organ, and to chronic malarial infection. 

Symptoms. — The symptoms closely resemble those of cirrhosis of the 
liver. There is loss of appetite, furred tongue, a sense of weight in the 
right hypochondrium, accompanied by the train of symptoms which attend 
chronic gastritis. There is profuse and exhausting diarrhoea alternating 
with constipation, hemorrhoidal tumors, hsematemesis, intestinal hemor- 
rhages, tympanitis, ascites and emaciation, — all which may be present in 
interstitial hepatitis. 

Physical Signs. — Palpation. If the surface of the liver can be reached, 
it will be found smooth and resistant. 

Percussion. — The area of hepatic dulness will be diminished in every 
direction. 

Differential Diagnosis. — The differential diagnosis between chronic red 
atrophy and cirrhosis of the liver is always difficult. In cirrhosis there 
will be the history of spirit drinking, of gout or rheumatism ; none of 
which will form a part of the history of chronic atrophy. In cirrhosis, 
slight jaundice is common toward the end of the disease ; it never exists 
in uncomplicated red atrophy. Venous stigmata, which are so often 
met with on the cheeks in cirrhosis of the liver, are absent in chronic 
atrophy. Diarrhoea is not so common or persistent in cirrhosis as in 
atrophy. The urine in cirrhosis is high colored and contains albumen, bile 
pigment, and lithates; while in atrophy it is pale, and bile pigment is 
rarely present. In cirrhosis the liver is hob-nailed and rough on palpa- 
tion, while in atrophy it is smooth on its surface. 

Prognosis. — Recovery from chronic red atrophy never occurs. Death 



be indented and shrivelled, and often 




Fig. 78. 



Chronic Atroph}-. 
Section of portion of a Lobule. 

A. Hepatic cells, shrivelled and pigmented ',' with disap- 

pearance of nvclei. 

B. Cells containing fat spherules. 

C. Pigmented capillaries, x 300. 



406 



DISEASES OF THE DIGESTIVE SYSTEM. 



may result from exhaustion due to the diarrhoea, from haematemesis or in- 
testinal hemorrhages, and from general dropsy. 

Treatment. — Little can be accomplished in the treatment of this disease 
except to alleviate suffering and prolong life ; it is incurable. When the 
ascites causes dyspnoea it must be removed by mechanical means. 



FATTY LIVER. 



Fatty degeneration of the liyer occurs either as a fatty infiltration or 
as a metamorphosis of the albuminous elements of liver-tissue into fat. It 
is one of the painless enlargements of the liver. 

Temporary fatty infiltration of the liver is a physiological state which 
occurs after the ingestion of food rich in hydrocarbons. 

Morbid Anatomy. — In fatty infiltration, the liver is increased in size and 
has a peculiar flattened appearance. Its surface is smooth and presents a 
pale brown or light yellow color, according to the degree of infiltration ; 
its borders are smooth and rounded, and it has a doughy, flabby feel, and 
pits on pressure. Its capsule is tense, shining, and transparent ; enlarged 
tortuous vessels are frequently seen traversing it. 

On section the organ cuts readily, and the warmed knife blade is coated 
with oil globules ; little blood flows from the cut surface. In the early 
stage it presents a reticulated, mottled appearance, of a dull yellow color. 
This appearance is due to the rim of fat globules around the periphery of 
the acini, while the parts immediately about the central vein are intensely 

congested and pigmented. In 
the latter stage, the whole 
surface presents a homogene- 
ous bright ( ' butter yellow " 
color, and fat cells are found 
: j3 occupying the centre of the 
^t^'r ^ U ^ e - Amyloid degeneration 
o^Hlb and fatty infiltration may be 
found in the same organ. 
With the microscope the lobules 
will be found enlarged, and 
the cells at their periphery are 
rounded, larger than normal, 
and filled with fat globules. 
These fat globules vary in size, 
sometimes a single oil drop 
occupies the entire cell space, 
the clouded nucleus and gland- 
ular contents being pressed up 
against the cell wall. At first 
the capillaries near the central 
vein are distended, and the 
cells about the vein are infiltrated with fat to a slight extent:; later on 




Fig 

Fatty Infiltration. 
Section of a Portal Canal and portion of three Lobules. 
A, A, A. Connective-tissue of Portal Canal. 

B. Branch of Portal Vein. 

C. Hepatic Artery. 

D. Hepatic Duct. 

E. Periphery of a Lobule, in which ' small fat globules 

are seen in the liver-cells. 

F. Same as B, with increased amount of infiltration. 

G. Periphery of a third Lobule, in which the lesion is 

still further advanced, x 280. 



FATTY LIVEK. 



407 



the capillaries are compressed and the cell filled with pigment granules. 
Pigment deposit and fatty infiltration are not often found in the same 
cell. When the cell-wall remains intact, and the accumulation of fat is very 
great, the outline of the cell is uneven. The proportion of fat has ranged 
as high as seventy-eight per cent, when the liver was freed of water, and 
consisted of olein and margarin, with slight traces of cholesterin and 
sugar. 

Etiology. — Fatty Infiltration.— As has been stated, an exaggeration of the 
normal physiological processes will lead to a pathological accumulation of fat 
in the liver. Thus we find it in those eating largely and exercising little, 
especially if the food taken is rich in hydrocarbons, and if alcoholic stimu- 
lants are freely used at the same time. The obese and the gourmand are 
always subject to this disease. Females are more liable than males to fatty 
infiltration of the liver. Fatty infiltration occurs most frequently at the 
middle period of life, when the time of active physical exertion is past. A 
warm and moist climate predisposes to it, especially when one or more of 
the above-named causes are in operation. Pulmonary phthisis is often ac- 
companied by fatty infiltration of the liver, the deficient respiratory power 
causing imperfect oxidation. Extensive crippling of the lung from any 
cause may lead to it. In the new-born the liver sometimes contains an 
abnormal quantity of fat, and there is undoubtedly an hereditary predispo- 
ition to it in some families. 

Fatty Metamorphosis, or true fatty degeneration, may occur at circum- 
scribed spots in the liver, about cancer-nodules, pathological new forma- 
tions, and in advanced stages of cirrhosis, chronic atrophy, and amyloid 
degeneration. It may be uniform throughout 
the whole liver, as a result of poisoning from 
phosphorus, antimony, arsenic, ether, and 
chloroform, or from blood-changes in typhoid, 
yellow, and .puerperal fevers, in small pox, 
scarlatina, pyaemia, and any disease where an 
extremely high temperature is sustained for a 
considerable period. There is a similar form 
of degeneration, due to the altered state of 
the blood, in old age. 

Symptoms. — The symptoms of fatty liver, 
with few exceptions, are decidedly negative. 
The fatty accumulation, though not enough 
to cause sufficient obstruction to the portal 
circulation, to lead to ascites or splenic en- 
largement, is sufficient to give rise to gastric 
symptoms, such as dyspepsia, flatulence, and 
loss of appetite. There being no inter- 
ference with the formation and outflow of 
the bile, neither jaundice nor changes in the 
color of the faeces occur. As the disease progresses the enlargement of the 
liver may cause a sense of fulness in the right hypochondrium, never, 




Fig. 80. 

Fatty degeneration. 

Section showing part of a Lobule in a 
case of poisoning by phosphorus. 

A. Hepatic cells showing the granular 

change of true fatty degeneration. 
x 350. 

B. Capillaries. 



408 



DISEASES OF THE DIGESTIVE SYSTEM. 



however, attended with pain. The slightest indiscretion causes an attack 
of gastric catarrh and diarrhoea, which persists long after the removal of 
the cause. The patient is anaemic and moody, and there is a general loss 
of muscular power, with a disposition to sleep. The blood is hydraemic. 
The skin is sometimes shining, always "velvety" to the feel, and often 
pasty and smooth, like that of a wax figure. The integument all over the 
body feels smooth, velvety, and flabby. Dyspnoea results as much from the 
weakness and anaemia, as from pressure of the enlarged liver. When symp- 
toms of acholia, due to the altered state of the blood, are attended by absence 
of bile in the intestinal tract, rapid anaemia, exhaustion, delirium and col- 
lapse occur, and extensive fatty metamorphosis is then usually associated 
with some other hepatic degeneration. The faeces are usually normal in color 
and the bowels are irregular and constipated ; in the highest grades of fatty 
metamorphosis they are pale and clay-colored, and attacks of diarrhoea are 
frequent. The urine is pale, non-albuminous, and of a low specific gravity. 

Physical Signs. — Palpation. The rounded smooth edges of a uniformly 
enlarged liver are readily felt below the border of the ribs ; the organ has 
a doughy, soft feel. When fatty degeneration occurs with waxy or colloid 
disease, the liver is diminished or is of normal size and smooth. 

Percussion. — The area of hepatic dulness is increased in all directions, 
the increase being mainly downward and forward. 

Differential Diagnosis. — Fatty and waxy degeneration are frequently 
mistaken for each other. In waxy liver a history of syphilis, prolonged 
suppuration, or disease of bones will be elicited ; in fatty liver there is a 
history of alcoholism, prolonged wasting disease, or one of high living and 
sedentary habits. In waxy liver, the skin is pale, dry, and has a peculiar 
odor resembling that of indigo ; in fatty liver the skin shines with fat, 
and has a velvety feel. The blood is hydraemic in fatty liver, and is leu- 
kaemic in waxy liver. The urinary symptoms in both are distinct : in 
waxy liver the urine is often increased in amount, is albuminous, and con- 
tains casts ; in fatty liver it is normal. In waxy liver the faeces are early 
deficient in bile and pale in color ; in fatty liver they are normal until 
an advanced stage of the disease is reached. A waxy liver is hard ; a fatty 
liver is soft and flabby. A waxy liver may become much larger than a 
fatty liver, and its edges are sharply defined ; while in fatty liver they are 
smooth and rounded. With a waxy liver the spleen is enlarged, but with 
fatty liver it is normal in size. 

Prognosis. — Fatty infiltration of the liver is not a grave form of disease. 
There is danger only when fatty degeneration of liver-tissue occurs. 
Death may result from fatty heart, pulmonary oedema, acholia, apo- 
plexy, the exhausting diarrhoea, and from the complications already re- 
ferred to. 

Treatment. — When the diet, mode of life, or climate is the main element 
in its causation, the indications for treatment are simple. A restricted 
diet, with no fat or sugar, and with regular daily exercise in the open air 
will, in most cases, increase the patient's strength and lessen the size of 
the liver. Care must be taken not to stop alcoholic stimulants too suddenly, 



PIGMENT DEGENERATION. 



409 



for fatty heart may co-exist. They must be decreased gradually. In all 
cases, a residence in an elevated temperate region, free from marshes, is im- 
portant. The vegetable bitters combined with alkalies will aid in restor- 
ing the appetite when it is lost. Iron should be administered in the form 
of the carbonates and lactates. Ehubarb and aloes will best relieve the 
constipation, and vegetable astringents control the diarrhoea. In syphilis, 
iodide of potassium is of service. In the fatty liver of phthisis, nothing can 
be expected from treatment so long as the phthisis is progressive. 



PIGMENT DEGENEEATIOK 

The pigment or melanotic liver is that form of hepatic degeneration in 
which there is an abnormal deposit in the liver of pigment derived from 
the coloring matter of the blood. In pigmentation there must be prima- 
rily a fault in the circulation or in the blood-vessels ; usually it is the re- 
sult of^slowing of the blood current. The red corpuscles either pass 
through the walls entire, or liberate the haemoglobin, which then transudes 
the capillary vessels. The blood from .^~v~ 
the spleen, loaded with pigment, J0:i? 1 1 >5^k 

passes into the portal vein, is carried 

through the interlobular veins, then ^^f^%7ff7^ - 

into the veins just within the periph- v \\ V ^ J' % 

ery of the lobule. Haemoglobin re- "K^? ', '* 

maining in the portal capillaries soon <^ ^^' e ^>^ N ^'"^i^^^ 7 

breaks up into haematoidin and, ac- f (^\7V;. -1^7/*? ^&\7 %Y r ~ 

cording to some, into melanin, though ^^^tJ^f&;^>: 

we are inclined to-day to regard me- ' ^^^^^^^S^^i0^0f^ 

lanin as altered haematoidin. This - : : l : 

haematoidin is first yellowish, later it ^\7^^r^ ( ^^ ^Sty^ 



consists either of brownish-black 
granules or crystals of an intensely 

black color. Both haematoidin and Fig.si. 

melanin remain unaltered when once „„ fi/in nf J^T*™' » > nt™ 

section of an Hepatic Lobule from a case of per- 
formed. Pigmentation of the liver . nidous fever. 

° i A. Central vein of the lobule. 

IS Confined to the VaSCUlar System. Longitudinal section of a small hepatic duct. 

. ^ C. Vessels contain'uig small pigment granules in 

JiiXtenSlVe Capillary Stagnation With great numbers. The pigmentation in this case 

, , » • . was pretty general throughout the intralobular- 

a large amount of pigment matter oc- capillaries, x 250. 
eluding the vessels gives rise to atrophy of the cellular structure. 

Morbid Anatomy. — The liver is at first enlarged from congestion and 
the capsule is smooth and tense ; afterward the organ becomes smaller 
than normal and atrophies, its color being much deeper than in the ear- 
lier stage and its edges sharply defined. 

On section, in the first stage, dark blood flows from the congested paren- 
chyma. If the cut surface presents a mottled appearance there is a steel- 
gray or black ring around, and slightly encroaching on, each lobule, shad- 
ing off toward the central vein. In congestion of the liver pigmentation 



410 



DISEASES OF THE DIGESTIVE SYSTEM. 




commences about the central vein, and gradually diminishes toward the 
periphery of the lobule. If the surface is uniform it presents a color which 
resembles "graphite/' a blackened gray color having a slight lustre, and 
the pigment deposit is seen to have reached the central vein. Occasionally 
spots of extravasation are found scattered throughout the organ. On sec- 
tion of an atrophied " pigment liver " the whole cut surface is black, and all 
trace of the lobules is frequently lost. A microscopical examination shows 
the capillaries, not only portal but hepatic, filled with granules or crystals, 
either throughout their entire extent or in isolated patches. The hepatic 

cells contain no pigment, but are filled 
with oily or amyloid material, or some- 
times with dark-colored bile. Leucin 
has often been found in the parenchy- 
ma of a pigmented liver. In an 
"atrophied" liver, the lobules and 
cells are shrunken, and the capillary 
system is a mass of pigment. The 
I spleen is softened and usually enlarged, 
never smaller than normal, and is 
more extensively pigmented than the 
liver. In some cases of pigment liver, 
there are evidences of hemorrhages 
into the various serous cavities. In 
connection with pigment degeneration 
of the liver, pigmentation may occur 
in all the organs of the body. 

Etiology. — Malarial infection is the 
only known cause of melanotic liver, 
but whether a large amount or peculiar 
kind of malarial poison is necessary for its development has not as yet 
been determined. 

Symptoms. — Frequently those who have had extensive pigment deposits 
in all the organs of the body, have given during life no symptoms to indi- 
cate their presence. The first effect of extensive pigmentation of the liver is 
an abnormal secretion of bile. The liver is enlarged and tender to press- 
ure. The skin in the milder forms is ash-colored, and in severer forms it 
is of a dark-bronze hue. There may be slight jaundice. There is gastro- 
intestinal catarrh with nausea, loss of appetite, flatulence, painful tympa- 
nitis, vomiting, and diarrhoea which may pass into dysentery. In severe 
cases, hemorrhage from the gastro-intestinal mucous membrane and from 
the kidney occurs, attended by exacerbations and remissions correspond- 
ing to febrile exacerbations and remissions. There is rapid emaciation 
and extreme exhaustion with giddiness, headache, and ringing in the ears. 
Occasionally the vertigo comes on so suddenly that the patient falls to the 
ground without the least warning. Active delirium is often followed by 
profound coma. The urine and faeces are passed involuntarily during the 
period of stupor. Coma is the most frequent termination of the cerebral 



Fig. 82. 

Pigment Degeneration. 

Section of the same tissue as preceding cut, show- 
ing the centime of a lobule move highly magnified. 
A. Central vein of the lobule. 

B, B. Strongly pigmented capillaries. 

C, C. Hepatic cells infiltrated with fat. x 450. 



CANCER OF THE LITER. 



411 



variety of pigment liver. In severe cases which terminate in recovery there 
is often temporary loss of memory. 

Physical Signs. — Inspection shows the ashy-gray, jaundiced, or brown 
colored skin. 

Palpation. — The surface of the liver is smooth, and in the first stage the 
organ is larger, softer, and more tender than normal. In the second stage 
it is small and hard. 

Percussion, — In the early stage the area of hepatic dulness is increased; 
in the later stage it is uniformly diminished. 

Differential Diagnosis. — The liability of confounding pigment degenera- 
tion with other diseases of the liver is not so great as is the difficulty of 
recognizing its existence. If. in intense malarial infection, cerebral or 
urinary symptoms come on suddenly with hemorrhages from the mucous 
surfaces, a bronzed hue of the skin, and the physical changes in the size of 
the liver already referred to, pigmentation of the liver may be suspected ; 
and if, in addition to these, pigment matter is found in the blood, the 
diagnosis will be established. 

Prognosis. — The prognosis is favorable if the patient, can be removed 
from the source of malarial infection. The elements which render the 
prognosis unfavorable are severe cerebral and renal symptoms combined 
with signs of extensive portal obstruction. Death may occur from exhaus- 
tion due to the diarrhoea, dysentery, or intestinal hemorrhage. 

Treatment. — The preventive treatment corresponds to the preventive 
treatment of malarial fever. When the disease is once established, the 
chief indication is to administer large doses of quinine. The symptoms in 
all varieties of the disease remit as soon as the individual is brought fully 
under the influence of this drug. Purges act unfavorably. If the cere- 
bral symptoms are urgent, ammonia may be combined with quinine. 
Preparations of iron and a change of residence to a non-malarial district 
are essential to its successful management. The diet should be of the most 
nutritious character and non-stimulating. 

CANCER OF THE LIVER. 

Cancer of the liver may be either primary or secondary. It is secondary 
to cancer of the stomach in one-half of the cases. It has been estimated 
that one out of every one hundred persons has cancer of the liver. The 
varieties of cancer met with in the liver are scirrhus, medullary, melanotic, 
and colloid cancer. Infiltrated cancer without any change whatever in the 
form of the organ has been found. 

Scirrhus is usually primary, while medullary is almost always second- 
ary. Scirrhus makes its appearance first as rounded masses. These masses 
increase rapidly and soon attain their full size, which varies from that of a pea 
to that of an orange ; they then remain stationary for a time until the fibrous 
tissue contracts. The number of these nodules varies inversely with their 
size. Scirrhus developments usually commence in the interlobular spaces 
and gradually extend toward the centre of the lobule. As the liver-cells 



412 



DISEASES OF THE DIGESTIVE SYSTEM. 



*ire being crowded upon, the portal capillaries disappear, while the hepatic 
vessels enlarge and ramify in the cancerous mass as a new and peculiar 
vascular net-work. The neighboring lymphatic glands may also become 
infiltrated with cancer, and often exert sufficient pressure upon the bile- 
ducts to obstruct the outflow of the bile. The cancerous growth sometimes 
involves the walls of the portal yein, and, extending in the direction of the 
capillary terminations, fills up their channel. The bile-ducts also may be 
obstructed, distended, or ruptured. With these changes, the centre of the 
cancer-nodule becomes harder and harder ; or by shutting off its own 
nutrition, the interior of the nodule becomes fatty, while the periphery is 
soft and vascular. The obliteration of the capillaries at the exterior of the 
mass shuts off the nutrition of the adjacent liver-cells, and this induces 
fatty degeneration. The theory of the development of medullary cancer 
(the inijilantation theory, as it is called) is that cancer-cells pass through 
the lymphatics, or blood-vessels, and reaching the interlobular spaces 
become the starting points of the cancer development. This theory has 
received much attention, and experiments seem to warrant our adopting it 
as one method, at least, in which cancer may develop. 

Medullary cancer is simply a modification of scirrhus. Rapidity of de- 
velopment is the distinguishing pathological difference, — the line between 
the two forms often being arbitrarily drawn, for scirrhus may pass into 
medullary, and vice versa. 

Melanotic cancer of the liver is also of rapid growth. The nodules, 
though very numerous, are small in size. The cancer-cells have a deposit 
at their centre of yellow, brown or blackish pigment, the " granite " look- 
ing spot shading off toward the periphery. Its course is the same as in 
other varieties of hepatic cancer. 

Colloid cancer is of rare occurrence in the liver, appearing only as a 
degenerated form of scirrhus or medullary cancer. If either of these forms 
undergoes mucoid or colloid degeneration, a gelatinous, gray, tenacious 
fluid takes the place of the cancer-juice, while the fibrous framework be- 
comes more distinctly alveolar. Melanotic sarcoma has been found ; it 
often pursues as malignant a course as true carcinoma. 

Morbid Anatomy. — In nodular scirrhus cancer the liver is irregularly 
increased in size, the right lobe being usually most affected. With medul- 
lary cancer it is often so much enlarged as to fill the abdominal cavity. In 
color it is darker than normal, and it is increased in weight, sometimes 
reaching twenty pounds. Upon its surface are nodules, hard, elastic, 
rarely fluctuating, and umbilicated at their centres. Occasionally, there 
are no nodules on the surface, the cancerous developments being confined 
to the interior of the organ. The capsule of the liver is thickened and 
sometimes the seat of cancerous development. Adhesions connecting it 
to the adjacent parts are the result cf intercurrent local peritonitis. 

On section, if the degeneration is advanced, the liver cuts hard, and 
creaks like cartilage under the knife. The cut surface is seen studded with 
nodules, the diameters of which vary from one-eighth of an inch to four 
inches. Between the nodules the liver-tissue is sometimes congested, and 



CANCER OF THE LIVER. 



413 



of a dark red color, or it is atrophied. The nodules increase in density from 
their centre outward, or have a central cavity filled with fatty granules. 
On pressing them, more or less cancer-juice exudes according to the density 
of the tumor. The color of the tumor varies from a glistening dirty white 
to a deep red, according as the vascular net-work is meagre or abundant. 
If there has been obstruction to the bile ducts the parenchyma will be of a 
"bright yellow color. Evidences of extravasation from distended vessels may 
be found throughout the liver-tissue and often in the interior of the can- 
cerous growth. 

Under the microscope, a cancer nodule will be found to consist of a fibrous 
framework or "stroma "in which are cancer-cells and cancer-juice. In 




Fig. 83. 
Cancer of the Liver. 
Section showing part of a cancerous nodule with the contiguous hepatic tissue. 

A. Connective-tissue of a portal canal in ivhich the nodule was developed. 

B. Hepatic duct in longitudinal section. 

C. Hepatic artery. 

D. Stroma of cancer. 

E. Alveoli of the same filed with " cancer cells. 

F. Empty alveoli. __, 

G. Peiiphery of an hepatic lobule I ordering on the cancer, infiltrated at EH. 
I. Infiltration of connective-tissue with same, x 300. 

scirrhus the fibrous stroma is greatly in excess of the other elements. The 
cancer-juice contains a large amount of fine granular matter, nucleated 
cells and distinct free nuclei. The cells are of large size and irregular, 
and the nuclei and nucleoli are often multiple and very distinct. The 
walls of the capillary vessels in the tumor are thin, and their calibre large. 
A ring of liver cells at the margin of the cancer-nodule exhibits well- 
marked degeneration. 



414 



DISEASES OF THE DIGESTIVE SYSTEM. 



Medullary Cancer. — The gross appearances of the liver are the same 
as in seirrhus, except that the nodules are fewer and larger. They are 
very soft and fluctuating, and frequently the more advanced tumors 
have ruptured through the peritoneal envelope of the liver. In this 
variety the cancer nodules are often lobulated. Those which occupy the 
surface of the liver project as large irregular tumors. 

On section large nodular masses of curdy-white homogeneous matter re- 
sembling foetal brain-substance are found scattered throughout the liver- 
tissue. Between the cancer nodules the liver substance is more or less in- 
tensely congested. Dark red hemorrhagic spots are seen scattered over its 
cut surface. 

On a microscopic examination a small amount of fibrous stroma is found 
containing a very large number of cells. The cells are much larger than 
in seirrhus, though the same in kind, and they are the seat of more fatty 
degeneration. 

Melanotic Cancer. — In common with the morbid appearance of all can- 
cerous developments, we find, besides, that the liver is nodular and very 
dark. 

On section the surface presents a peculiar mottled appearance resembling 
granite, and there are numerous small nodules studding the whole gland. 
On pressure a dark fluid flows from the cancerous mass, varying in color 
from a gray-brown to a deep black. 

A microscopical examination shows a stroma varying in amount and 
color. Sometimes it is colorless, sometimes very dark. The degree of 
vascularity has wide ranges ; the cells at certain spots in the liver often dis- 
appear and only a peculiar pigment color remains. 

Colloid Degeneration. — The surface of the liver in this form of cancer 
differs from the other varieties in that it is smooth with large lobulations. 

Under the microscope the cancerous mass is made up of large and spherical 
alveoli with thin walls. The alveoli contain mucoid or colloid matter, 
with fatty material and a few epithelial cells. 

Etiology. — The causation of primary hepatic cancer is unknown ; in 
most instances there exists an hereditary predisposition. It is a disease of 
middle life, occurring oftenest between the ages of forty and sixty-five. 
Medullary cancer of the liver, especially when secondary, is sometimes met 
with in early life, even as early as the fourth year. It occurs equally among 
males and females. Some have dated its development from some great 
mental emotion or strain, others from the receipt of a blow upon the right 
hypochondrium. Cancer of the liver is often secondary to cancer of the 
stomach, mamma, ovary, uterus, pancreas, brain, or portal vein. Clinical 
exparience indicates that extirpation of external cancerous masses is very 
apt to be followed by cancer of the liver. 

Symptoms. — The early symptoms of hepatic cancer are obscure. The 
more superficial its development, the more marked are the symptoms and 
the easier the diagnosis. It will be noticed that the individual is gradually 
losing flesh and strength, he complains of a sense of weight and fullness in 
the right hypochondrium, he is anaemic, and the surface assumes a doughy 



CANCER OF THE LIVER. 



415 



hue ; with these there may be pain localized over the hepatic region, or 
shooting up toward the right shoulder, and sometimes to the back. The 
pain soon becomes lancinating in character, and is localized at some point 
over the liver which is tender to pressure. There is loss of appetite, flatu- 
lence, nausea, vomiting, and constipation alternating with diarrhoea. The 
vomiting is often profuse and persistent. There is progressive emaciation, 
and theskin assumes an earthy pallor. Jaundice is present in one-half of 
the cases, and is due either to compression of the bile ducts or to intercur- 
rent catarrh of the ducts, and when once developed it is permanent. Asci- 
tes occurs more frequently than jaundice ; the accumulation at first is in- 
considerable in amount and increases slowly. It is due to compression of 
the portal vein by the cancerous tumor or by enlarged glands in the trans- 
verse fissure, or to chronic peritonitis. (Edema of the feet comes on late. 
The temperature is normal or sub-normal. Dyspnoea may become an 
urgent symptom in the advanced stage of hepatic cancer. The cervical 
and inguinal glands may be enlarged. Hemorrhages from the stomach, 
intestines, mouth, and vagina, with petechial and ecchymotic spots, are 
sometimes accompaniments of hepatic cancer. It is to be remembered that 
hepatic cancer may run its entire course without pain, without jaundice^ 
and without ascites. In medullary cancer, loss of flesh and the peculiar 
cancer countenance may not appear until the end of the case. The faeces 
are normal at first, later they are firm and clay-colored. The fluid stools 
of cancer diarrhoea contain no bile. The urine is scanty and high-colored. 
Deposits of lithates and of bile pigment are rarely absent. 

Physical Signs. — Inspection. There may be a perceptible bulging in the 
right hypochondrium and the outlines 
of large nodules may be visible. 

Palpation discloses an enlarged and 
irregularly shaped liver, tender to 
pressure. Hard, smooth nodules are 
felt over its surface, which rarely 
fluctuate. If the nodules are urn- 
bilicated it establishes the diagnosis 
of cancer. In colloid cancer of the 
liver, and when the cancerous devel- 
opment is central, no nodules will be 
felt. 

Percussion. — The area of hepatic 
dulness is irregularly increased and 
marked by an irregular line of flatness 
below the free border of the ribs. 

Auscultation. — A friction sound, 
caused by the rubbing of the rough- 
ened peritoneal surfaces, is sometimes 
heard. 

Differential Diagnosis;, — Cancer oi 
the liver may be mistaken tor hydatid 




Fig. 84. 

Diagram shotting enlargements of the Liver as 
determined by percussion. 

A, A. Line of diaphragm. 

B, B. Lower border of costal cartilages. 

C. Dotted line enlargement upward. 

D. Shaded area indicating successive and in- 

creasing enlargements, 

E. Lower edge of Liver in Cancer, Leukcemia 

and Adenoma. 



416 



DISEASES OF THE DIGESTIVE SYSTEM. 



of the liver, abscess of the liver, waxy degeneration with gummata, cancer 
of the stomach, and an enlarged gall-bladder. 

In hydatids there are no gastric or severe constitutional symptoms. 
Cancer of the liver is rapid in its development, rarely exceeding one year 
in duration, while hydatids are of slow growth, lasting from four to eight 
years. Gastro-intestinal hemorrhages are common in cancer, and do not 
occur in hydatids. Pain is a prominent symptom in cancer; hydatid 
tumors are painless. In cancer the nodules are hard, tender, and firm ; 
hydatid tumors are large, soft, smooth and elastic, and can be freely manip- 
ulated without pain. The peculiar hydatid fremitus is sometimes obtained 
by percussing a hydatid tumor. In hydatids (with an exploring trochar) a 
saline fluid containing the hooklets of the echinococci may be withdrawn, 
which will decide the diagnosis. 

In waxy degeneration of the liver, there is a history of syphilis, pro- 
longed suppuration, or disease of bone ; and in cancer an hereditary cancerous 
history, or the evidences of carcinoma elsewhere. The progress of waxy liver 
is slow ; that of cancer is rapid. A waxy liver is painless, while pain in 
cancer is constant. In waxy liver the spleen is markedly enlarged ; in cancer 
it is normal in size, unless it is the seat of cancer infiltration. Jaundice and 
ascites are rare in waxy degeneration, and frequent in cancer. 

In cancer of the stomach gastric symptoms are urgent and appear 
much earlier than in cancer of the liver. In cancer of the stomach there 
is usually coffee-ground vomiting and cancer-cells in the ejected matter. 
In cancer of the stomach the pain and gastric symptoms are aggravated 
after ingestion of food, while in hepatic cancer the pain and gastric symp- 
toms are constant. In cancer of the liver in thin subjects, immovable 
nodulated tumors may be felt by pressing up under the ribs ; while in 
gastric cancer a single tumor which is movable, and changes its posi- 
tion as the stomach is full or empty, is usually felt. In hepatic cancer 
there is absolute dulness over the tumor; while in cancer of the stomach 
the percussion note has a peculiar tympanitic quality. 

Cancer of the right kidney, impaction of fmces, and various alterations 
in the size of the healthy liver will not long confuse one if the symptoms 
and physical signs are carefully analyzed. 

Prognosis. — Cancer of the liver is a fatal disease. The average duration 
is about one year. Medullary cancer runs its course in from two weeks to 
four months. The duration of all varieties will be influenced by the pres- 
ence or absence of complications. Death may result from exhaustion, 
from the cancerous cachexia, dropsy, diarrhoea, dysentery and hemorrhages, 
or from peritonitis, pneumonia or pulmonary oedema. 

Treatment. — All varieties of cancer of the liver are incurable, hence the 
absurdity of all the so-called curative measures. The diet should, be nu- 
tritious, and care should be exercised not to overfeed this class of patients. 
Easily assimilated preparations of iron are often of service. Diarrhoea, if 
present, may be checked by such remedies as gallic acid, lead, and opium. 
The operation of paracentesis should be delayed as long as possible. In 
the advanced stage of the disease alcoholic stimulants are often necessary 



GRTMMY TUMOR OF THE LIVER. 



417 



and beneficial. In the great majority of cases the principal office of the 
physician is to relieve pain, and morphia is our most reliable remedy for 
this purpose ; it should be given in sufficient quantities to keep the patient 
comfortable . 

GUMMY TUMOR OF THE LIVEE. 

This form of new growth is perhaps the most characteristic lesion of con- 
stitutional syphilis. Some writers group these tumors under the head of 
syphilitic disease of the liver. Those forms of perihepatitis, cirrhosis, and 
amyloid degeneration which are of evident syphilitic origin, I have inferred 
to describe in connection with the other corresponding forms, giving at the 
same time the few differences due to the syphilitic causation. 

Morbid Anatomy. — The syphilitic nodules, gummy tumors, or " gum- 
mata " appear first as small masses of reddish-gray, pulpy, vascular tissue, 
scattered throughout the liver. Their point of origin I believe to be the 
wall of the capillaries, — the cells and nuclei of the " syphiloma" being due 
to the growth of the nuclei of the capillaries. The mass is composed of 
highly organized granulation- tissue, and is usually spherical in shape. The 
liver may be enlarged, or may retain its normal size, according to the ex- 
tent of the waxy change which usually accompanies the development of 
the gummata. Diminution of its size is due to perihepatitis causing re- 
traction. Under these circumstances the organ is lobulated, and deep, 
whitish furrows indent it, the result of cicatricial contractions. Fibroid 
nodules occasionally lie in these cicatrices. The bulgings are soft and smooth 
to the touch. The capsule is firm and opaque, and the seat of fibroid thick- 
ening, and is frequently bound to surrounding parts by adhesions. 

On section there will be found scattered through the liver rounded 
masses varying in size from a pea to an orange, yellowish- white in color, 
either surrounded by congested parenchyma, or as isolated spots in the 
midst of an infiltrated homogeneous grayish -red mass. They may be en- 
capsulated, a layer of translucent fibrous-tissue surrounding them and 
shading off imperceptibly into the surrounding liver-tissue. Brown spots 
in the tumors correspond to obstructed bile-ducts. The liver parenchyma, 
between the nodules, undergoes various changes : at one time it is con- 
gested and hypertrophied, at another it is atrophied and undergoes fatty 
degeneration. In well-marked cases there are two zones, an outer, red and 
fleshy, and an inner, dry, grayish and firm. Again, nothing may remain 
of a previous gumma but a shrivelled cicatrix. 

A microscopical examination of a fully developed gummy tumor reveals 
three processes :— first, at the periphery, there is a vascular mass of gran- 
ulation-tissue, embedded in which are cells bearing a striking resem- 
blance to white blood globules, and some larger nucleated ones. Sec- 
ondly, just beneath this zone is found a fibro-nucleated mass, the fibril- 
lations being very dense and cicatricial. Thirdly, in the centre of the mass 
are found fat-granules and broken-down cells, with occasional traces of 
cholesterin, and sometimes faint evidences of fibrillar tissue. Cheesy and 
calcareous masses are also sometimes found in the centre of the gumma. 
27 



418 



DISEASES OE THE DIGESTIVE SYSTEM. 



Etiology. — As has been stated, gummata are the most characteristic of 
the lesions of internal syphilis. They are met with under no other condi- 
tions. 

Symptoms. — The subjective symptoms of hepatic gummata are few and 
inconstant. At a post-mortem, a liver may be found studded with gummy 
tumors, when no symptoms referable to the liver were present during life. 
There is generally a history of increasing debility, and a feeling of press- 
ure, tightness, and dull pain in the region of the liver. Sometimes the pain 
is severe and localized, at other times it is dull and diffused over the whole 
hepatic region. The pain in one case is constant, in another intermittent. 
If jaundice exists, it is due to the pressure either of the gummata or of an 
enlarged lymphatic. The temperature is normal, and the pulse-rate is but 
slightly increased. Ascites may result from pressure on the portal vein, or 
from chronic peritonitis, which often complicates its development. Both 
jaundice and ascites are not present until the liver has become very much 
enlarged. The symptoms which are present in the advanced stage of this 
disease, such as diarrhoea, loss of appetite, vomiting, hemorrhoids, gastric 
and intestinal hemorrhage, are due rather to the accompanying hepatic de- 
generation than to the gummata. 

Physical Signs. — Palpation may show the liver to be enlarged or normal 
in size ; a moderate increase in size is the rule. The organ has smooth 
lobules upon its surface between which run deep fissures. The lobulations 
are soft and elastic, never fluctuating. 

Percussion. — The area of dulness is increased and its outline is irregular 
below the free border of the ribs. The area of spleen-dulness in the ma- 
jority of cases is slightly increased. 

Differential Diagnosis. — Gummata of the liver may be mistaken for can- 
cer, and if the liver is diminished in size, for syphilitic cirrhosis. The 
differential diagnosis of both has been considered. 

Prognosis. — Gummata of the liver rarely directly destroy life. The prog- 
nosis is unfavorable when ascites, gastro-intestinal hemorrhage, persist- 
ent diarrhoea, or a marked cachexia exists. Complicating diseases also influ- 
ence the prognosis ; amyloid degeneration of the spleen and kidneys is a bad 
complication. The most frequent intercurrent lung diseases are pleurisy, 
pneumonia, pulmonary oedema, and chronic bronchitis. Death occurs from 
exhaustion due to the syphilitic marasmus, from diarrhoea, dysentery, and 
dropsy. Pneumonia and pulmonary oedema often cause it, and sometimes 
cholgemia, with its peculiar symptoms, ends in coma and death. 

Treatment. — The treatment of this affection resolves itself into the treat- 
ment of syphilis. As it is a tertiary symptom, our main reliance is on large 
doses of the iodide of potassium combined with mercurial inunctions. With 
these iron and cod-liver oil should be constantly taken, and the patient 
should be placed under the best hygiene. The diet should be nutritious 
and non-stimulating. Opium combined with nitric acid will always con- 
trol the diarrhoea if it becomes exhausting. 



HYDATIDS OF THE LIVEE. 



419 



HYDATIDS OF THE LIVEE. 



Hydatid tumors are cysts due to the development in the liver of the em- 
bryos of the tmnia echinococcus ; these embryos are called " echinococci," 
their development " hydatids" ; they are usually single, and for more than 
two or three to be present in the same liver is a phenomenal event. 

Morbid Anatomy. — An ovum of taenia echinococcus, either during masti- 
cation or from the action of the digestive juices, has the envelope containing 
the echinococcus removed, and then by its booklets it bores its way from 
the stomach or intestine into the liver. It there becomes encysted: the 
cyst consists of an external laminated cuticular layer and an internal par- 
enchymatous lining. Erom the internal layer numerous little heads bud 
forth in the form of vesicles, and these, the "daughter vesicles," in turn 
bear a second crop, the "grand-daugh- 
ter cells," the mother-sac meanwhile 
enlarging, partly from the increase in the 
number of the vesicles, and partly from 
its own secretion, which is clear and wa- 
tery. As these successive generations of 
vesicles appear, broods of immature tae- 
nia ("scolices") in the form of a gray- 
ish granular layer, are developed first 
upon the internal surface of the mother 
sac and then upon that of the other 
cysts, in the order of age. While the 
younger vesicles cling to the parent- 
walls, the larger and older ones become 
detached, and float in the interior of 
the continually enlarging parent-sac. 
Proliferation of connective-tissue upon the exterior of the sac resulting 
from the inflammatory process excited by the pressure of a foreign body, 
develops a fibrous capsule closely connected with the adjacent liver par- 
enchyma ; this is supplied with blood by the hepatic and portal capilla- 
ries. 

During its enlargement the hydatid tumor loses its spherical shape and 
becomes indented. As it increases in size, the fibrous capsule becomes 
thickened, rough and cartilaginous ; sometimes it undergoes ossification. 
The echinococci may be destroyed by the bile which enters the cysts when 
the bile-ducts are opened, or by the inflammation which is established be- 
tween the connective tissue capsule and the wall of the true sac, causing 
a grayish oily material of variable consistence to be developed. The clear 
fluid in the cavity of the hydatid becomes cloudy, then opaque, while all 
traces of the vesicles disappear, and at last only a few hooklets of the echi- 
nococci remain. This is a process of fatty degeneration. Sometimes 
the formation of vesicles i& so rapid that their number is beyond all pro- 
portion to the fluid, and then they die and collapse, undergoing no degen- 




Sketch from an Hydatid Tumor showing the bud- 
ding vesicles. 



420 



DISEASES OF THE DIGESTIVE SYSTEM. 



erative process ; again, when neither of these terminations is reached, the 
hydatid tumor may continue to increase in size until finally it bursts into 
the adjacent cavities. 

The most frequent rupture is into the right pleural cavity. The hyda- 
tid tumor, by its pressure upon the diaphragm, causes it to become thin, 
and to rise upward, sometimes as high as the second rib. Finally the 
diaphragm ruptures and the sac is discharged into the pleural cavity, or 
when the pleural surfaces become adherent the tumor ruptures into the 
lung-tissue or bronchi. These tumors sometimes rupture into the perito- 
neal cavity, and peritonitis results, or the stomach or intestinal canal may 
communicate by a small aperture with the hydatid sac. A communication 
is sometimes established between the bile-ducts and the hydatid tumor, and 
the ducts become filled with the contents of the hydatid mass ; the ductus 
communis may become obstructed by a large hydatid vesicle. Another 
mode of termination is by an intense inflammatory action, causing sup- 
puration of the liver-tissue in the vicinity of a ruptured hydatid tumor, 
which consequently is filled with coagulated blood and pus ; more rarely 
a gangrenous process may be established in it. 

The liver is irregularly enlarged and displaced. The increase in size 
varies with that of the projecting cysts, which are sometimes large enough 
to fill the abdominal, and a portion of the thoracic, cavity. The bulging 
is globular if the cyst is simple and is situated in the right lobe of the 
liver. The tumor is elastic and often fluctuating. A uniform enlarge- 
ment of the liver results from a centrally located hydatid, The capsule 
covering the cyst is thickened, and adhesions often bind the liver to the 
surrounding parts. 

On section, the liver-tissue in the vicinity of the tumor is found com- 
pressed and atrophied, or congested and hypertrophied. The mother-sac is 
commonly the size of afcetal head. The true cyst wall is a gelatinous, whitish, 
semi-transparent membrane, containing the hydatid fluid, floating in which 
are vesicles from the size of a millet-seed to that of an egg, and varying 
in number from hundreds to thousands. On the inner walls of the larger 
ones, and on that of the parent-sac, are younger vesicles about the size of a 
pin's head. On the inner side of the sac are also found patches of white 
granular matter. The cysts may be found filled with atrophied and shriv- 
elled vesicles embedded in a debris consisting of fat-granules, cholesterin, 
hsemaglobin, and bile. Its consistency varies : sometimes it is liquid and 
watery, then semi-fluid, gelatinous, or like a thick paste ; at other times 
only a few booklets remain in this gray, putty-like mass. The cyst may 
contain blood or pus. 

A microscopical examination shows the sac of the hydatid to be a gela- 
tinous mass made up of concentric hyaline lamellae. The scolices are from 
1-75 to 1-225 of an inch in length ; the head is furnished with four suckers 
and a proboscis, about which are sicMe-shapecl hooklets in number from 
twenty-five to fifty. The body is striped longitudinally and transversely, 
and has a groove between it and the head, which latter, being usually re- 
tracted into the body, causes the animal to look somewhat like an in- 



HYDATIDS OF THE LIVER. 



421 



IS 




Hydatids of the Liver. 

A. Read of echinococcus from an hydatid tumor. — B. 

Discs— C. Rooklets.—D. Pedicle. 
E. Fragment of capsule of hydatid tumor, shmving 

itsiamellat.—F. Germs. x 200. 



dented rubber ball, the hooks fringing the depression. The fluid 
clear or slightly opalescent, it has a 
specific gravity of 1010 to 1015, is 
usually neutral in reaction, and is 
non-albuminous. It is chiefly water 
containing chloride of sodium. 

Etiology. — The essential cause of 
the development of hydatids is the 
entrance into the stomach, or intes- 
tines, of the tasnia echinococcus. If 
they remain in the intestine they be- 
come tape-worms ; when they pass 
into the liver they develop hydatids. 
Hydatids are chiefly met with be- 
tween the ages of thirty and fifty. 
They are rare in childhood and old 
age. They are most common among the poor and filthy, and in cold 
climates. It is estimated that one out of every six of the inhabitants of 
Iceland has hydatids of the liver. Dogs, sheep, pigs, cats, and rats are 
subject to tapeworms, and as the ova of these parasites are discharged in 
the excrements of these animals, they can only gain entrance into the 
human stomach through polluted drinking-water, or the most filthy prac- 
tices. 

Symptoms. — If an hydatid tumor is deeply seated and of small size, it gives 
rise to no symptoms and cannot be recognized. A large hydatid tumor 
will cause sufficient functional disturbance by its pressure to be easily 
recognized. The patient may first see or feel a tumor in the region of the 
liver, and have a sense of weight and dragging in the right hypochon- 
drium. Symptoms of pressure of the tumor on adjacent organs are the 
first, and often the only ones which attract attention. Dyspnoea, a dry 
hacking cough, and bronchial catarrh may result from the upward press- 
ure of the tumor. When the heart is displaced by the tumor, there is 
palpitation ; and when the stomach is encroached upon there is vomiting, 
dyspeptic symptoms and emaciation. When the portal vein or vena cava 
is pressed upon by the hydatid tumor, ascites, jaundice and hemorrhoids 
may result. When the hydatid compresses the bile-duct, or when there is 
intercurrent catarrh of the ducts, or when they have become obstructed by 
the hydatid vesicles, jaundice sets in and absence of bile in the fasces is 
noted. A large vesicle may, in passing the duct, give every symptom 
of gall-stone colic, and thus be confounded with it. 

When the pleura is perforated, the symptoms of acute pleurisy are devel- 
oped, and in most cases the cavity is rapidly filled with pus containing 
hydatid vesicles. Peritonitis may result from spontaneous or traumatic 
rupture of an hydatid cyst. The opening into the stomach or intestines 
being usually very small, it is rarely attended either by peritonitis or sec- 
ondary abscess ; when a cyst is evacuated in this way the case usually ter- 
minates in recovery. When shreds of hydatid vesicles and echinococci are 



422 



DISEASES OF THE DIGESTIVE SYSTEM. 



found in the urine, it indicates that the rupture has taken place into the 
urinary passages. When the hydatid tumor is to discharge itself through 
the abdominal parietes, redness of the skin, tenderness, pain, and fluctua- 
tion will precede its discharge. If, in a patient who is known to have 
hydatids of the liver, there is pain, elevation of pulse and temperature, 
extreme sensitiveness over the hepatic region with a peculiar friction sound 
on auscultation, it may be suspected, that inflammation in and around the 
sac has occurred. In such case abscess may be excluded by the absence of 
rigors and sweats. 

Finally, the growth of an hydatid of the liver is in rare cases attended 
with pain caused by its pressure. The faeces are normal unless jaundice 
exists, in which case they are firm and clay-colored. The urine is generally 
normal, but if pus or albumen is found in it, pyelitis exists as a result of 
the pressure of the tumor on the renal vein. 

Physical Signs. — Inspection may show a distinct bulging in the right 
hypochondrium, w r hich has the appearance of a globular elevation over the 
right or left lobe of the liver. The ribs often project, and respiratory 
movements on the right side are interfered with. 

Palpation discovers an enlarged liver, elastic to the touch when the 
tumor is deeply seated ; when it is superficial, fluctuation may be detected. 
The tumor is smooth, but if two, three or more cysts exist, the liver will 
have a lobulated outline below the free border of the ribs. 

Percussion. — The normal area of hepatic dulness is increased in some 
one direction. When the tumor is superficial, the hydatid thrill or "fre- 
mitus " is elicited by firm percussion. This sign, peculiar to hydatids of 
the liver, is elicited in the following manner : place three fingers, slightly 
separated, firmly over the most prominent part of the tumor ; give a sharp 
blow upon the middle one, and a vibration or fremitus will be communicated 
to the other two. 

Differential Diagnosis. — Hydatids of the liver may be mistaken for cancer, 

abscess, abdominal aneurism, enlarged gall-Madder, pleurisy, rarely multi- 
locular hydatids, and a cyst of the right kidney. In abdominal aneurism 
there will be severe and constant pain in the back ; the tumor is soft, 
doughy, and compressible, has an " expansive " pulsation and is immov- 
able, while an hydatid tumor moves up and down with the respiratory 
movements and fluctuates. A "bruit" synchronous with the heart and 
often double will be heard over an aneurism, while neither of these is 
ever present in hydatids. The femoral pulse will be altered in an abdom- 
inal aneurism, but normal in hydatids of the liver, 

When a pendulous hydatid cyst is attached to the liver by a pedicle, we 
may readily mistake it for an enlarged gall-bladder. An enlarged gall- 
bladder is usually preceded by jaundice, biliary colic, or symptoms oi 
catarrh of the ducts, while an hydatid has no such previous history. On 
palpation it will be found that an hydatid does not correspond exactly to 
the position of the gall-bladder. The gall-bladder is pear-shaped and evades 
manipulation or pressure, while an hydatid tumor is globular and readily 
manipulated. 



HYDATIDS OF THE LIVER. 



423 



When hydatids extend into the pleural cavity so as to be mistaken for 
pleurisy, the heart will be displaced much more than ever occurs in pleu- 
risy. Percussion in pleurisy marks out a line of dulness which is trans- 
verse when the patient is erect, and which changes with his position, while 
in hydatids the upper limit of dulness is irregular and stationary, being 
lower near the median line of the body than toward the axilla. This is 
m important point. In hydatids the lower edge of the liver is below 
the free border of the ribs and rises and falls with the respiration ; in 
pleurisy the liver occupies nearly its normal position and is station- 
ary. 

In a cyst of the right kidney, there is the history of a growth from below 
upward, while in hydatids the tamor grows from above downward. In 
cystic kidney the colon lies in front of the tumor, while in hydatids of the 
liver the colon is behind the tumor. An hydatid of the liver rises and falls 
with respiration, while a cyst of the kidney is motionless. In hydatids of 
the liver, an exploring needle will withdraw a non-albuminous, salty fluid, 
containing hooklets of the echinococci, while from a cyst of the kidney it 
will withdraw an albuminous fluid with chlorides and perhaps pus. 

Prognosis. — Hydatids are dangerous in proportion to their size and the 
direction of their growth ; if they cease to enlarge, they may be regarded as 
harmless. Their average duration is about four years. They have been 
known to exist twenty-five years. If they rupture into the pleura, lung, 
peritoneum, pericardium, or through the abdominal walls, the prognosis is 
unfavorable. When the discharge takes place into the intestines, stomach, 
or bronchi, the prognosis is favorable. Death occurs from exhaustion caused 
by the pressure of a very large hydatid, rarely from that caused by ascites 
through pressure on the vena cava. Suppuration of the cyst, or an abscess 
developed secondarily to phlebitis may induce fatal exhaustion. Any one 
of the pulmonary complications referred to may cause death. A fatal result 
has, in some few cases, followed hemorrhage from the sac through an ex- 
ternal opening. Peritonitis, pericarditis, and uraemia are infrequent causes 
of death, and when the pulmonary artery is plugged, when the vena cava 
is opened, or when a large vesicle is lodged in a bronchus, asphyxia is the 
immediate cause of death. 

Treatment. — Prophylactic measures consist in preventing the drinking- 
water from being contaminated by the evacuations of animals, and in not al- 
lowing dogs to feed upon the offal of sheep. Chloride of sodium and iodide 
of potassium have been proposed as internal remedies to destroy the echino- 
cocci. The chief solid ingredient of hydatid fluid is chloride of sodium, 
but no trace of iodide of potassium has ever been found in the fluid after 
the administration has been continued for months. 

If the tumor is of large size, and is still increasing in size, operative inter" 
ference is necessary. Select the point where the hydatid tumor is most 
prominent, and puncture with a fine aspirating needle. The dangers which 
have been feared in this procedure are peritonitis, and the entrance of air 
into the peritoneal cavity. Peritonitis maybe avoided by pressing the parts 
about the puncture firmly against the tumor as the aspirating needle is 



424 



N DISEASES OF THE DIGESTIVE SYSTEM. 



withdrawn, so that no fluid can escape into the peritoneal cavity. All dan- 
ger of the entrance of air is obviated if a small aspirating needle is used ; all 
of the fluid should not be withdrawn from the cyst at the first aspiration. 
It is important to enjoin absolute rest after the operation for two or three 
days ; febrile symptoms and pain will follow the withdrawal of the fluid, 
and the tumor will decrease in size ; usually a second puncture will be re- 
quired. It is not essential to wait for adhesions to form between the tumor 
and abdominal wall, though it is much safer if they exist. 

Where sinrple puncture is not sufficient to destroy the echinococci, iodine 
or bile may be injected into the cavity of the sac. When the fluid with- 
drawn is pus, or when the symptoms are indicative of a suppurating cavity, 
it is best to establish adhesions by caustics. Vienna paste is to be preferred 
for this purpose, and the same precautions are to be exercised as in the 
opening of an hepatic abscess. Puncture of the cyst by insulated needles, — 
electrolysis, — has been claimed to be very successful in those cases where it 
has been resorted to, but it seems to me that it is the puncture, rather than 
the electric influence, which produced the favorable result claimed for it. 
Never hesitate to aspirate an hydatid tumor when it is well developed and 
elevated above the level of the abdominal walls ; the nearer the cyst is to 
the surface, the better the result of the aspiration. 

MULTILOCtTLAR HYDATIDS. 

Multilocular hydatids in their 2^athology are similar to the ordinary hyd- 
atid, except that in the one case a cyst is formed, and in the other it is 
wanting. 

Morbid Anatomy. — The liver is enlarged, the right lobe being out of all 
proportion to the rest of the organ ; it is hard, and sometimes has a carti- 
laginous feel. There are large nodules on its surface, the tumors often 
being as large as a child's head. The capsule is thickened and opaque over 
the tumor, and adhesions may be formed with surrounding parts. 

On section a tumor is usually found embedded in the right lobe, varying 
in size from that of an orange to a cocoanut, with a reticulated surface. 
The stroma is connective-tissue, dull-yellow in color, and the spaces are 
rounded, oval, or caudate, from the size of a pin's head to that of a pea, 
usually communicating with one another by small apertures, and contain- 
ing a clear or semi-transparent gelatinous substance. The stroma gener- 
ally contains some hepatic parenchyma, which, at the periphery of the 
mass, is dark-colored from pigment deposit, and nearer the centre is in a 
state of partial or complete fatty degeneration. In the centre of the mass 
is usually found a large spot of suppuration, varying in size, or a cavity 
filled with a light-brown fluid or a greenish fetid pus. This cavity is well 
defined, having a wall whose lining membrane is sacculated at points, with 
openings into neighboring cavities. This membrane frequently has clus- 
ters of hydatid vesicles upon it. The surface cavities are much smaller 
than the central one, and are strung along like "strings of pearls," com- 
pressing and occluding the branches of all the vessels of the liver at the 



MULTILOCULAR HYDATIDS. 



425 



point whence the growth develops. The rest of the liver is congested or 
hyper trop hied. 

Microscopically, the gelatinous contents in one of the alveoli are found to 
be made up of the laminated structure of the vesicle and containing echi- 
nococci with their circlets of booklets ; it is rare, however, to find perfect 
"scolices." The cyst-wall may exhibit calcareous, fatty, or pigmentary 
degeneration. Between the cysts small globules, consisting of calcare- 
ous matter, are sometimes found, and also granular and crystalline haema- 
toidin. The spleen is usually enlarged. 

Etiology. — The etiology of multilocular hydatids is the same as that of 
a single hydatid tumor. When the ova of the taenia reach the liver, the ques- 
tion arises: what is it that causes the peculiar alveolar or colloid arrange- 
ment of the vesicles ? This has been variously explained : some claim that 
when the embryo enters either the lymphatics, blood-vessels, or bile-ducts, 
the growth extends along the channels of either system, since it cannot ex- 
tend concentrically because of the exterior pressure. I am inclined to 
agree with those who think that when a cyst-wall is developed around the 
embryo and no connective-tissue encapsulates the cyst, it can- grow in all 
directions. Their development is yet obscure. 

Symptoms. — The insidious approach and slow progression which mark 
the course of single hydatid tumors are present here. The effects of pressure 
may be shown by vomiting and dyspepsia when the stomach is encroached 
upon ; constipation and difficulty in defecating when the intestines are 
pressed upon ; and ascites, oedema, hemorrhoids, and enlarged spleen, 
when the portal trunk or vena cava is compressed. There are no subjective 
signs. When suppuration occurs there will be a slight rise in temperature, 
increased frequency in the pulse, and other symptoms which attend the 
formation of pus in the liver. Gastro-intestinai hemorrhages, and hemor- 
rhages from mucous surfaces rarely occur. When the bile-ducts are in- 
volved, jaundice is the first, or an early symptom ; the jaundice gradually 
deepens and is persistent. The fasces are clay-colored. 

Physical Signs. — Palpation shows the liver early enlarged, having slight 
elevations, with a smooth feel. Later it is hard, resistant, nodular, and 
uneven. The tumors are confined to the right lobe, or, at least, are best 
marked there. 

Percussion. — The area of hepatic dulness, in the region of the right lobe 
especially, is increased, and the spleen is enlarged with multilocular hyda- 
tids. There is neither fluctuation nor the " hydatid thrill." 

Differential Diagnosis. — When the bile-ducts are involved a diagnosis may 
be made by exclusion ; in other cases the affection is liable to be con- 
founded with cancer, cirrhosis, and nodular (syphilitic) waxy liver. 

In cancer of the liver there is a history of a gradually developing ca- 
chexia and lancinating, almost constant, pain, with evidences of cancer else- 
where, or an hereditary tendency ; while in multilocular hydatids there are 
no constitutional symptoms and no pain, the hepatic region merely being 
tender. The duration of cancer is rarely more than a year, while the de- 
velopment of multilocular hydatids is protracted to two or three years. A 



426 



DISEASES OF THE DIGESTIVE SYSTEM. 



cancer nodule, on palpation, is usually umbilicated and soft at the centre ; 
while a multilocular hydatid is smooth and elastic. An exploring trochar 
will remove all doubt. 

In cirrhosis of the liyer there is a history either of alcohol drinking, 
rheumatism, gout, or syphilis ; in multilocular hydatids no such history 
necessarily exists. In cirrhosis the liver is smaller than normal and hob- 
nailed ; in multilocular hydatids it is enlarged and the nodules are of a 
larger size. Ascites is common in cirrhosis ; while it is rare in hydatids. 

In a nodular waxy liver there is a well-marked history of syphilis ; there 
is a complicating diarrhoea, albuminuria, and the characteristic waxy 
cachexia, which are absent in multilocular hydatids. 

An hydatid tumor can only be diagnosticated from multilocular hydatids 
by the exploring trochar. The fluid in multilocular hydatids contains pus 
in varying quantities, a few booklets of the echinococci, and numerous 
small vesicles ; while that from an ordinary hydatid is nearly pure water, 
containing the hooklets and 2, few vesicles. In many instances the hydatid 
thrill is present in a single hydatid tumor, but never present in multilocu- 
lar hydatids. 

Prognosis. — In those cases in which the jaundice is intense, the disease 
may run its course in six months ; in other cases, the course is as pro- 
longed as in single hydatids. Peritonitis is a frequent complication, and 
amyloid degeneration of the liver may also occur with it. Death results 
from the exhaustion due to the suppuration or from the complicating peri- 
tonitis. 

Treatment. — There is no medicinal treatment which can in any way affect 
the course of this disease ; and operative interference has thus far proved 
unsuccessful. This class of patients must be sustained during the exhaus- 
tion of the supervening suppuration. The pain, if severe, may be relieved 
by hypodermatics of morphia. 

TUBERCULOSIS OF THE LIVER. 

Tubercle of the liver is always secondary to tubercle elsewhere. It is 
probably more common than is usually supposed, from the fact that 
hepatic tubercle is always microscopic. 

Morbid Anatomy. — The liver is slightly but uniformly enlarged in size. 
On close inspection the surface is seen to be irregularly elevated and de- 
pressed, and looks and feels, in this respect, like the surface of an orange. 

On section the liver cuts hard, the parenchyma being tense and tough. 
The tissue is pale and yellow, resembling a fatty liver. The bile-ducts at 
points are expanded, the walls being thinned. They contain a turbid 
fluid mainly composed of mucus and bile. There are also small cavities 
filled with pus and bile. When the tubercle has undergone retrograde 
metamorphosis, small gray masses the size of a pin's head are seen, "yel- 
low tubercle," or larger yellow masses the size of a pea ; these changes 
are usually best marked just beneath the capsule. 

A microscopic examination shows miliary tubercles scattered between the 



JAUNDICE. 



427 



lobules. When, as a result of obliteration of blood-vessels, tubercles under- 
go fatty degeneration, the so-called " yellow tubercle" is the product. 

Etiology.— Hepatic tubercle occurs as part of acute miliary tuberculosis, 
and is secondary to tubercle in the lungs, peritoneum, spleen, and lym- 
phatics. 

Symptoms.— There are no symptoms indicative of hepatic tuberculosis, 
independent of those of general tuberculosis. 1 



JAUNDICE. 



Jaundice is a yellow discoloration of the skin, due to the presence of bile 
or blood pigment. There are two varieties, hepatogenous or obstructive 
jaundice, and hematogenous or non-obstructive. 

Hepatogenous jaundice is the more common variety, and is caused by 
the absorption of bile, its passage into the ductus communis or intestine 
being prevented by some mechanical obstruction. 

Hematogenous jaundice results, probably, from a change in the blood, 
whereby its coloring matter is set free in excess. 

Morbid Anatomy of hepatogenous jaundice. In a normal state, the liver- 
cells are constantly manufacturing bile, which flows along the bile-ducts 
into the ductus communis. The cause of its outward flow is the vis a tergo, — 
the secretion of the bile in the hepatic cells, — for there are no muscular 
fibres except in the larger bile-ducts ; the respiratory movements also assist 
slightly in its outward flow. When from any causes the bile cannot enter 
the common duct or the duodenum, the small ducts and then the hepatic 
cells become overfull and distended. In consequence of this increased 
pressure, bile passes through the wall of the smaller ducts into the blood- 
vessels and lymph channels. If the normal tension of the capillary system 
in the liver is diminished, then the passage of bile through the walls of the 
vessels is favored and jaundice results. Bile pigment with serum exudes 
and stains the tissues, even the bones, the teeth and pathological new forma- 
tions. In both hepatogenous and hematogenous jaundice, the staining occurs 
in the same way. 

Hematogenous Jaundice. — In health the bile pigment is formed within 
the liver, by transformation of the coloring matter of the blood, and after 
it has been poured into the intestine, it is partly absorbed by the blood and 
appears, after another change, as one of the coloring matters of the urine. 
Under abnormal conditions, and as the result of processes that are not fully 
understood, coloring matter is either set free in excess or is not excreted 
with the bile, and is then deposited in the tissues producing jaundice. As 
this variety of jaundice is thought to have its origin in morbid conditions 
of the blood, it is called hematogenous. 

The anatomical lesions which are associated with hematogenous jaundice 
have already been considered in connection with the history of the different 
hepatic affections in which it occurs. 



1 Lymphatic formations, simple cysts, dermoid cysts, erectile cavernous tumors, and benign fibrous 
growths occur in the liver, but are only of pathological interest. 



428 



DISEASES OF THE DIGESTIVE SYSTEM. 



Etiology. — The causes of hepatogenous jaundice may be included under 
three heads : 

I. Those which obstruct the larger hepatic ducts. 
II. Those which obstruct the hepatic radicles. 
III. Those which diminish capillary tension. 

Those obstructions of the larger hepatic duct which haye their seat within 
the duct are : 

(1) Inflammations of, or inflammatory exudations from, the lining mem- 
brane of the duct, that which accompanies duodenal catarrh being the most 
frequent. (2) Biliary calculi. (3) Inspissated bile and mucus. (4) Hydatid 
vesicles. (5) Distomata. (6) Foreign bodies from the intestinal canal, such 
as stones of fruits and round worms. (7) Congenital occlusion, or plugging 
of the duct. (8) Cicatrices from ulcers on the mucous membrane of the 
duct. (9) Carcinomatous growths from the lining membrane of the ducts. 

The causes which obstruct the duct by external pressure, are : 

(1) Contraction from perihepatitis, or from inflammation of the hepatico- 
duodenal ligament. (2) Tumors of the pyloric extremity of the stomach, 
of the head of the pancreas, and of the kidney. (3) Pressure from a preg- 
nant uterus, from ovarian and fibroid tumors, from omental tumors, and 
from large impaction of faeces. (4) Enlarged lymphatic glands in the trans- 
verse fissure from waxy, cancerous, or tubercular change, abdominal aneu- 
rism, and the new tissue in hypertrophic cirrhosis of the liver. 

Slight hepatogenous jaundice may be caused by compression or oblitera- 
tion of the hepatic radicles, such as occurs in cirrhosis and the other atro- 
phies of the liver, in active and passive hyperemia, in hydatid tumors and 
multilocular hydatids, in cancerous and syphilitic tumors, in abscess of the 
liver, in adhesive pylephlebitis, and perhaps in acute yellow atrophy. 

Finally, the bile may be prevented from entering the intestine in its normal 
amount when capillary tension is diminished. This may occur in severe 
right diaphragmatic pleurisy, in perihepatitis, in thrombosis of the trunk 
or of the larger branches of the vena portae, and in exhausting hemorrhage 
from the radicles of the portal vein. 

The causes of hematogenous jaundice are fevers, especially yellow, typhus, 
typhoid, and the malarial fevers. It is often an attendant of pyaemia, puer- 
peral fever, septicaemia, and suppurative pylephlebitis. The poison of 
snake-bites, phosphorus, mercury, copper, antimony, and the excessive 
use of ether and chloroform may cause it. Pneumonia, probably by its 
action on respiration, and ulcerative endocarditis induce it ; it may follow 
a fright, a fit of anger, great anxiety, or cerebral concussion. A long con- 
tinued hepatogenous jaundice may lead to a hematogenous jaundice ; and 
it is yet undecided whether the icterus in yellow atrophy belongs to the 
first or second named group. 

Differential Diagnosis. — Hematogenous jaundice accompanies acute in- 
fectious fevers and other conditions of blood poison, while hepatogenous 
jaundice can be traced to some mechanical interference with the outflow 
of the bile. The yellow staining is slight in hematogenous jaundice ; 
while the discolorization in hepatogenous jaundice is more intense and may 



CATARKH OF THE BILE-DUCTS. 



429 



appear suddenly without constitutional disturbances. A feeble and irreg- 
ular heart-action, a small pulse, and a tendency to hemorrhages attend 
hematogenous jaundice; while an unimpaired heart-action, a slow pulse, and 
a low temperature mark the development of hepatogenous jaundice. There 
is great itching of the surface in hepatogenous jaundice which is absent in 
the hematogenous variety. The faeces are dark in hematogenous jaundice, 
and white or clay-colored in hepatogenous. The urine is albuminous, con- 
tains a small amount of bile pigment, and deposits a sediment of uric acid 
in the hematogenous variety, while it is rarely albuminous in hepatogenous 
jaundice and contains bile-pigment in considerable amount, the quantity 
varying with the intensity of the jaundice. 

DISEASES OF THE GALL-BLADDER AND GALL-DUCTS 
will be considered under the following heads : 

I. Catarrhal Inflammation of the III. Cancer of the Gail-Bladder. 

Biliary Passages. IV. Enlargement of the Gall-Blad- 
II. Exudative Inflammation of the der. 

Biliary Passages (croupous V. Gall Stones. 
or diphtheritic). 

CATAKRH OF THE BILE-DUCTS. 

Morbid Anatomy. — Catarrhal inflammation of the mucous membrane of 
the larger bile-ducts, the ductus communis, and the gall-bladder is similar 
to that of other mucous surfaces. There is hyperemia followed by an ab- 
normal secretion of mucus and muco-pus which more or less obstructs the 
outflow of bile. The catarrhal process usually begins in the duodenum 
and extends inward, and in severe cases may be so rapid that pus will be 
the product of the inflammation, in which case the deeper tissues are in- 
volved and numerous little ulcers may form, and when the duct is perfo- 
rated by them, cavities of varying sizes, resembling small abscesses, result. 
When the catarrh becomes chronic the deeper tissues are infiltrated, caus- 
ing thickening and induration of the ducts from the consequent obstruction 
to the exit of the bile. Dilatations occur at points along the bile ducts ; 
these dilatations often become very large and occasionally form cysts ; at 
other times the alternate dilatations and constrictions give the appearance 
of a string of beads. The lymphatics often become involved, and their en- 
largement gives a nodular appearance to the mucous membrane. Ulcera- 
tive processes are more frequent in chronic catarrh of the bile passages 
than in acute. The liver is uniformly enlarged and its margins are firm 
and sharp. 

On section, its substance presents a mottled appearance, resembling a 
nutmeg, and varies in color from a deep yellow to an olive green. The 
color is deeper at the centre of a lobule and shades off toward its periphery. 
The gall-ducts commonly have their mucous membrane pale and covered 
with a thick, purulent mucus ; and plugs of mucus and epithelial debris 



480 



DISEASES OF THE DIGESTIVE SYSTEM. 



are found in them, most frequently near or at the opening of the duct into 
the duodenum. The gall-bladder is enlarged, and the cystic and common 
ducts often attain immense size ; in one case this diameter reached an inch 
and a half. 

In chronic catarrh the liver is normal or diminished in size, and is soft, 
flabby and shrivelled. 

On section it is greenish-black in color, the hepatic ducts are dilated, 
forming cysts, and little points of ulceration are formed on the mucous 
surface of the duct, often extending into the adjacent parenchyma which 
is atrophied. The ramifications of the vena portse are compressed by the 
ducts, and thickened bile may cause these ducts to present the appearance 
of a dark brown tube. The gall-bladder is enlarged in size, and sometimes 
there are spots of ulceration upon its walls which may also undergo cal- 
careous changes. 

Etiology. — The most frequent cause of biliary catarrh is extension of a 
gastro-duodenal catarrh. Most of the structural diseases of the liver may 
lead to or be attended by catarrhal inflammation of the bile ducts. Thoracic 
disease where the venous return is impeded (as in cardiac valvular lesions 
and emphysema) may cause catarrh of the biliary passages. General blood 
diseases, syphilis and pyaemia prominently, and mineral poisons, phos- 
phorus, and perhaps arsenic, cause it. A gouty diathesis causes or pre- 
disposes to a catarrh of the biliary passages, just as it does to catarrhal 
inflammations of the mucous membranes elsewhere in the body — bronchitis, 
for instance. Foreign bodies, as calculi and parasites, in the bile passages 
may cause biliary catarrh. Exposure to cold and an altered condition of 
the bile may induce it. 

Symptoms. — The subjective symptoms of biliary catarrh are at first obscure. 
It is usually preceded by the symptoms of gastro-duodenal catarrh, and 
hence for a few days there will be loss of appetite, furred tongue, flatulence, 
nausea and vomiting. There is also some pain and tenderness in the epi- 
gastrium, and in most cases the temperature will be slightly raised, and the 
pulse accelerated. The bowels are constipated, unless it is accompanied 
by extensive intestinal catarrh, when diarrhoea will be present. The f ascal 
discharges are of a light clay color and contain no bile. The urine is of a 
dark green color, and contains bile pigment. The liver is enlarged and 
tender, especially over the region of the gall-bladder. The absence of 
bile from the intestine favors gaseous distention of the bowel. The 
sclerotic becomes yellow, and gradually the entire surface assumes a yellow 
hue. The temperature falls to normal and the pulse is slowed. As the 
jaundice deepens, there is a noticeable loss of strength, the patient becomes 
apathetic and disposed to sleep during the day. There is headache, vertigo, 
and great depression of spirits ; itching of the surface becomes exceedingly 
troublesome. 

All these, symptoms remit, the appetite returns, and the faeces and urine 
return to their normal color ; or the catarrh becomes chronic and continues 
for months, the jaundice deepening, exhaustion and emaciation becoming 
extreme. Then gastric and intestinal hemorrhages frequently occur, and 



CATARRH OP THE BILE DECTS. 



431 



ascites may be followed by general anasarca ; corna closes the scene. The 
last stage of chronic catarrh is accompanied by evidences of atrophy of the 
liver. 

Physical Signs. — Inspection reveals a jaundiced condition of the skin 
and conjunctiva?, and perhaps a bulging in the right hypochondrium. ■ 

Palpation discovers an enlarged, smooth and tender liver. The gall- 
bladder is enlarged, and sometimes there is a pear-shaped fluctuating tumor 
at its anterior margin. The gall-bladder is tender on firm pressure. Late 
in chronic catarrh the liver is diminished in size. 

Percussion shows a uniform increase in the area of hepatic dulness, 
which, however, in chronic disease may be normal or diminished. 

Differential Diagnosis. — This condition may be mistaken for suppurative 
pylephlebitis and exudative inflammations of the ducts. The former has 
already been considered, the latter will be considered under exudative in- 
flammations. 

Prognosis. — This is good ; catarrh of the bile ducts is not a dangerous 
disease. The jaundice usually continues from three to five weeks, but 
sometimes it continues for months. The prognosis is rendered unfavorable 
when oft-repeated biliary catarrhs lead to permanent closure of the ducts 
and atrophy of the liver. Catarrh of the bile-ducts may be complicated 
by peritonitis, pleurisy, pneumonia, dysentery, suppurative hepatitis, or 
acholia. Death then results from exhaustion, from faulty nutrition, or 
dropsy, from intercurrent diseases, rupture of the ducts, or with brain 
symptoms — i: acholia. '' 

Treatment. — It should be remembered that the jaundice is only a symp- 
tom, and requires no treatment. The treatment of this catarrh is mostly 
symptomatic ; it is usually self-limiting and will subside without remedial 
measures. If the hepatic pain is severe, leeches followed by an anodyne 
poultice over the points of greatest tenderness will usually relieve it. When 
the bowels are constipated, " blue-pill," or a saline purgative is first de- 
manded, after which old cider or tamarinds will regulate the bowels for the 
remainder of the attack : nitro-muriatic acid acts favorably in most cases. 
If there is diarrhoea, ipecacuanha or Dover's powder will readily control it. 
When the urinary secretion is much diminished the salts of potash in com- 
bination with diaphoretics may be administered. The diet throughout 
should contain no carbo-hydrates ; the food should consist principally of 
lean or prepared meats, vegetables, and skimmed^milk. 

When there is a gouty diathesis, colchicum and iodide of potassium are 
often of service. In a syphilitic diathesis, chloride of ammonium and the 
bi-chloride of mercury are indicated. Emetics rather aggravate the gastric 
intestinal catarrh than cause the expulsion of a hypothetical plug in the 
common duct, and should not be administered. Finally, if the hepatic 
parenchyma become involved, a tonic and diuretic plan, similar to that 
adopted in cirrhosis, may be adopted. The use of mineral waters must be 
determined by tne influence which they exert on each patient ; in some 
cases increased appetite results, while in others they seem to hasten the 
wasting process. 



432 



DISEASES OF THE DIGESTIVE SYSTEM. 



EXUDATIVE INFLAMMATION OF BILIARY PASSAGES. 

Under the head of exudative inflammation of the biliary passages I in- 
clude both a croupous niad & diphtheritic process. Both are rare and seldom 
recognizable during life. 

Morbid Anatomy.— The commencement of croupous inflammation is the 
same as catarrh ; but the inflammatory product is fibrinous. 

In diphtheritic inflammation, the deeper tissues of the walls of the gall- 
bladder and bile-ducts are involved, and large gray sloughs, more firmly 
adherent than in croupous inflammation, are formed upon their walls. The 
liver is usually enlarged. 

On section the ducts within the liver are seen clogged with inspissated 
bile, and occasionally there are abscesses. When constriction and occlu- 
sion of the ducts exist, they become dilated behind the narrowed portion, 
and resemble cysts, containing a pale yellow fluid with loose coagula floating 
in it. The gall-bladder is sometimes filled with a gray- white liquid, neutral, 
albuminous, and sometimes containing leucin ; at other times the liquid is 
purulent, or thick and dark like tar. On the mucous membrane of the 
gall-bladder and common duct is a yellowish- white fibrinous layer, varying 
in thickness and tenacity, having all the anatomical characteristics of a 
diphtheritic exudation. The walls of the gall-bladder and larger ducts are 
thickened and sometimes ulcerated. The ulceration may lead to perfora- 
tion and fistulous openings. Adhesions sometimes bind the gall-bladder 
to the surrounding parts. If the diphtheritic process extends to the venous 
coats pylephlebitis may result ; sometimes the bile-ducts open into branches 
of the vena portae. 

Etiology. — These inflammations occur with typhus and typhoid fevers, 
cholera, diphtheria, pyaemia, septicaemia, bilious fever, and from the 
irritation produced by biliary calculi. 

Symptoms. — The first symptom of exudative inflammation of the biliary 
passages is a sense of constriction in the right hypochondrium. This is soon 
followed by pain, increased by pressure in the region of the gall-bladder, 
and vomiting. There are active febrile symptoms, but these are usually 
not marked. If ulceration of the ducts or implication of the branches 
of the portal vein occurs, then chills, sweats, and the other symptoms of 
pyaemic abscesses of the liver result, or the symptoms of pylephlebitis are 
developed. When an opening into the peritoneal cavity occurs, rapidly 
fatal peritonitis is the result. If there is no obstruction to the outflow of 
bile, neither jaundice nor alteration in the color of the stools will be 
present. 

Physical Signs. — Inspection may show a slight elevation of the free border 
of the ribs. 

Palpation discovers a pear-shaped, tender, movable tumor at the nor- 
mal site of the gall-bladder. Slight pressure over it gives pain. 

Percussion. — The area of liver dulness is normal or slightly increased ; 
over the enlarged gall-bladder the percussion note is dull and somewhat 
tympanitic in character. 



CANCER OF THE GALL-BLADDER. 



433 



Differential Diagnosis. — Exudative inflammation of the bile-ducts may be 
mistaken for simple biliary catarrh. The points which will aid in a di- 
agnosis are the occurrence of intense pain, active febrile symptoms, and a 
careful study of the etiology of each case. 

Prognosis. — This is determined by the disease which it accompanies. 
It usually terminates in death. 

Treatment. — Absolute rest is important. To relieve the pain leeches may 
be applied oyer the tumor, followed by poultices and, later, by counter- 
irritation. The diet and saline purgatives should be the same as in sim- 
ple catarrh, unless the primary disease contraindicates their use. If symp- 
toms of pus formation are present, quinine may be given in large doses 
and tonics are indicated. If the tumor becomes large, so that there is 
danger of its rupture, it may be aspirated, the same rules being observed 
as in hydatids and abscess. 

CANCER OF THE GALL-BLADDER. 

Cancer of the gall-bladder is usually associated with cancer of the liver 
substance, and is often the primary seat of the development of scirrhus 
or medullary cancer of the liver. 

Morbid Anatomy. — The gall-bladder is enlarged, nodular and adher- 
ent to the surrounding parts ; sometimes there are spots of ulceration on 
its surface, and there may be fistula? from the gall-bladder to the intestine. 
On section its wall is found thickened, and the cavity sometimes filled with 
a cancerous mass in which are embedded numerous concretions. 

Etiology. — This is the same as that of cancer of the liver. It is often 
secondary to cancer of the stomach. Concretions are so often found that 
some have ascribed its development to gall-stones. 

Symptoms.— The subjective symptoms are few : none are constant except 
the gastric derangement and the paroxys*ms of lancinating pain ; vomiting 
is common and severe, because of the pressure of the tumor on the py- 
lorus. Jaundice may be present when the common duct is involved. 
While the tumors often increase very rapidly, the cancerous cachexia and 
emaciation are slow in their development. In some cases the symptoms 
undergo marked exacerbations and remissions. Swelling of the glands in 
the inguinal and axillary regions may occur. 

Physical Signs. — Palpation will discover over the site of the gall-bladder 
a hard, nodular and immovable tumor. It is tender, and sometimes fluctu- 
ates at the centre. 

Percussion shows an increase in the area of hepatic dulness below the free 
border of the ribs. 

ENLARGED GALL-BLADDER. 

Dropsy of the gall-bladder is a term used to include those cases where- 
on account of some obstruction, bile is prevented from entering the nat- 
ural reservoir, and an increased secretion from its mucous surface leads to 
its distention. 

28 



434 



DISEASES OF THE . DIGESTIVE SYSTEM. 



Morbid Anatomy. — The gall-bladder is found enlarged, sometimes reach- 
ing the size of a cocoa-nut. The walls are thickened, at some parts more 
than at others, and occasionally sacculations render its outlines uneven. 
The cystic wall is often tense, and now and then plates of calcareous matter 
are found upon it. On opening it there may be a discharge of gas from its 
interior, but more commonly a curdy white fluid fills its cavity. This fluid 
contains whitish flakes of albuminous matter resembling synovial fluid ; 
it may contain bile, and then it is dark and viscid. On close examination 
the mucous surface resembles a serous membrane, and the muscular fibres 
of its wall are attenuated and wide apart. Later on, the fluid contents of 
the cavity may disappear, and only a mass of pultaceous matter remains. 
When the obstruction has been near the opening into the duodenum, the 
ductus communis and the cystic duct are dilated and their walls thick- 
ened. 

Etiology. — Hydrops cystidis felloe, as it is sometimes called, may be caused 
by a catarrhal, croupous, or diphtheritic inflammation of the cystic duct, 
which obstructs the passage of bile into the intestine. Plugging of the 
common or cystic duct, or of the neck of the gall-bladder, by a calculus, 
may cause dropsy of the gall-bladder. Multilocular hydatids or hydatid 
cysts may plug the cystic duct and induce it. Pressure by tumors outside 
of the duct, as enlarged glands in chronic peritonitis, aneurisms, impacted 
faeces, and cancerous growths of the adjacent parts, occasionally leads to it. 

Symptoms. — When the cystic duct alone is pressed upon or in some way 
plugged, there are few subjective symptoms. The patient may notice a 
bulging in the hepatic region, which steadily increases, and is accompanied 
by pain, nausea, vomiting, loss of appetite, and constipation. But the color 
of the skin, urine, and faeces exhibits no change. If a calculus is the cause 
of the obstruction, there is usually a history of " bilious colic," and if 
abdominal tumors press upon the cystic duct there will be the physical 
evidences of their existence. 

Physical Signs. — Inspection may reveal a globular tumor near the rectus 
muscle, at the free border of the ribs. Palpation discovers at the normal 
site of the gall-bladder a pear-shaped, extremely movable tumor, which is 
elastic and rarely fluctuating. When the ductus communis is obstructed, 
jaundice is a prominent symptom, and the other symptoms which have been 
described under " catarrh of the bile-ducts " are present. Occasionally the 
tumor suddenly disappears, the stools become dark, and the skin regains 
its normal color. This denotes that the obstruction, which is then com- 
monly a calculus, has been temporarily removed. When external openings 
are formed, or rupture into the peritoneal cavity occurs, there are, in the 
latter case, evidences of a rapidly developed peritonitis, and, in the former, 
a remission of symptoms with a biliary fistula discharging externally. 

Differential Diagnosis. — Dropsy of the gall-bladder may be mistaken for 
abscess, hydatids, and medullary cancer of the liver. In medullary cancer, 
there is, in nine-tenths of the cases, an hereditary predisposition or a his- 
tory of cancer of the stomach or heart ; while in dropsy of the gall-bladder 
we get a history of previous biliary catarrh, or of the passage of gall-stone? 



GALL-STOKES. 



435 



In cancer, the constitutional symptoms and cachexia are marked, while 
persistent gastric symptoms, ascites and hemorrhages from mucous surfaces 
are absent in enlarged gall-bladder. Cancer growths are slow, and precede 
jaundice if it exists, while a gall-bladder enlarges rapidly, and follows jaun- 
dice. Palpation, in cancer, discovers a nodular, uneven, immovable mass be- 
low the free border of the ribs. An enlarged gall-bladder gives rise to a 
smooth, pear-shaped, elastic, or fluctuating tumor, which is movable and 
projects below the free border of the ribs in the direction of the gall-bladder. 

Prognosis. — This varies with the cause. When inflammatory products or 
gall-stones induce the dilatation, it is better than when it is due to external 
pressure ; it is always attended with more or less danger. 

Treatment. — The treatment, when it is the result of catarrhal inflamma- 
tion of the ducts, has already been considered. When it is due to the pres- 
ence of gall-stones, the treatment appropriate to such conditions is indica- 
ted. If the enlargement is very great and shows no indications of becoming 
stationary or diminishing in size, aspiration should be practised. 



GALL-STONES. 



When bile is retained in the gall-bladder for a long time it decomposes, 
and the cholate of soda and other bile salts, with cholesterin, globules of 
bile-resin, and granules are precipitated. These materials combine to form 
concretions, which are called biliary calculi. Catarrh of the gall-bladder 
always accompanies this retention and decomposition of bile. 

Morbid Anatomy. — The number of gall- 
stones varies : single calculi are rare ; eight 
thousand were found in one case. Their 
usual number is about thirty. Their size 
varies from that of a pin's head to that of 
a goose egg. In shape they are originally 
spherical, ovoid, or pear-shaped ; but when 
there are many and they lie in contact 
with one another for a long time, they 
have numerous facets developed on their 
surface; six, or even twelve are some- 
times found on a single calculus. Warty 
or "mulberry" calculi are occasionally 
met with ; solid or hollow casts of the 
larger bile ducts, and those which resemble 
rhomboidal crystals, and the star-like cal- 
culi with blunt points are rare forms of 
gall-stones. These calculi are commonly 
of a light-brown or greenish-yellow color ; 
they may be white, green, blue, red, or 
black. The specific gravity of fresh calculi 
is about 1.02, and it may reach 1,09, so that 
they will not float in water. In most cases a fresh biliary calculus can be 




Fig. 87. 

Sketch of a gall-bladder filled with biliary 
calculi. This bladder contained 260 
gall-stones. At B are single calculi 
showing facets. 



436 



DISEASES OF THE DIGESTIVE SYSTEM. 



margarin and traces of iron. A 




Fig. 88. 



crushed between the fingers. Gall-stones may form in the smallest radicle 
of the hepatic duct. 

On section a biliary calculus will rarely be found homogeneous through- 
out. Its substance, if it breaks down like clay, consists of cholesterin and 
lime. If it has a saponaceous fracture, it consists of bile-resin and choles- 
terin. The ingredients of biliary calculi are cholesterin, the coloring 
matter of the bile, bile-resin, lime salts, mucus, epithelium, biliary acids, 

gall-stone usually has a nucleus, an 
external crust, and an intermediate 
portion. The nucleus may be 
formed of crystals of cholesterin, 
cholate of lime, mucus, a distoma, 
blood-clot, round worm or foreign 
body. Most nuclei are formed of 
casts of the hepatic ducts. Some- 
times small calculi form the nu- 
clei of larger ones, and in very rare 
instances multiple nuclei are ob- 
served. The external crust varies 

Section of a large Gall-stone, showing successive layers, in thickness at different points, and 

A ' ^em%ScTsfze Inte ^ diate portion '~ a Nu ' is distinguished from the interme- 
diate portion by its color ; it is 
commonly composed of cholesterin, and its color is due to a mixture of 
cholesterin and biliary pigment ; carbonate of lime gives a rough, whitish 
crust. The intermediate structure usually consists of crystalline radia- 
tions of cholesterin, which substance forms about eighty per cent, of all 
gall-stones. In this radiation can be seen evi- 
dences of a lamellar deposit, and sometimes, 
when there is no radiation, the layers are concen- 
tric, like those of an onion. Again, light layers 
of cholesterin alternate with deeper ones of pig- 
ment ; gall-stones are rarely found to undergo a 
process of erosion or disintegration. 

The gall-bladder may be normal, or enlarged 
and sacculated, and is often adherent to the in- 
testine, abdominal wall, and adjacent organs. Its 
walls are thickened, and there are evidences of a 
local or general catarrh ; late in the disease there 
may be fibroid contraction and calcareous degen- 
eration in the cystic walls. Ulceration of the walls is frequently found in 
a bladder distended with calculi. When a gall-stone becomes impacted 
near the entrance of the ductus communis into the duodenum, the duct 
may become enormously dilated, and have its walls thickened, hyper- 
trophied, or calcareously degenerated. 

When the ulcerative process extends through the walls of the gall-blad- 
der or of the larger ducts, we may have openings externally through the 
abdominal walls, usually about the umbilicus, called "biliary fistulae. 5 ' 




Crystals 
stones, 
plates, 
x 200. 



Pig. 89. 

of cholesterin from gall- 
mowing the characteristic 
with one comer wanting. 



GALL-STOKES. 



437 



These fistulous openings may lead from the gall-bladder or ductus com- 
munis to the duodenum, stomach, colon, right ureter, trunk of vena portae, 
pleura, or vagina. When calculi are found in the smaller ducts, they may 
excite abscess of the liver, local fatty degeneration, inflammation of the 
ducts or pylephlebitis. Either by rupture into the cavity, or by extension 
of inflammation, peritonitis may be caused by the presence of gall-stones. 
They may also excite ulceration and gangrene of the intestines, and there 
are rare cases where gall-stones, having escaped into the intestines, have 
caused death by intestinal obstruction. 

Etiology. — Gall-stones may be formed at any period of life, but are most 
frequent after thirty-five. A sedentary, physically inactive life is a great 
factor in their etiology, and I regard the greater prevalence of calculi in 
women than in men as due to their less active mode of life. Those who 
have to pass the greater part of their lives in bed, and prisoners who are 
confined in cells for a long time, are especially liable to the formation of 
gall-stones. A diet over-rich in fats, animal food, or alcoholic beverages, 
predisposes to the formation of biliary calculi. Cancerous growths in the 
liver and gall-bladder, catarrh of the gall-bladder, and in fact any morbid 
condition interfering with the excretion of bile and favoring its retention 
in the gall-bladder, predispose to the development of calculi. I have been 
able in a few cases to make out an hereditary predisposition to the forma- 
tion of gall-stones. The menstrual epoch seems to have some peculiar 
influence upon their formation. 

Symptoms. — Small gall-stones, — "gravel," — in the hepatic ducts may cause 
hepatic congestion, but without enlargement of the liver, and give rise to 
dull pain, a sense of weight and constriction in the right hypochondrium, 
with nausea and the other symptoms of gastric disturbance. Jaundice in 
these cases is of rare occurrence. When the hepatic and larger ducts are 
occluded, the liver becomes enlarged, and there is jaundice, sharp pains, 
colic, and sometimes rigors and sweats. If the hepatic duct is closed, the 
gall-bladder is normal in size. Fatal rupture of the ductus hepaticus 
sometimes, though rarely, is the result of the impaction of a calculus in it. 

When small calculi are formed within the gall-bladder, they often cause 
no inconvenience ; when they reach a large size they excite inflammation, 
which may ultimately cause closure of the neck of the gall-bladder. When 
the gall-bladder contains a large number of calculi, violent physical exer- 
tion causes pain, which disappears during rest. Sometimes the patient may 
actually "feel something rolling around " in the vicinity of the gall-blad- 
der, which on a physical examination is found enlarged, more or less 
tender, hard, and nodulated, and by a stethoscopic examination gives to 
the ear the impression of a number of pebbles being grated together in 
water. 

If biliary calculi in this situation cause perforation of the gall-bladder, 
a fatal peritonitis follows, or a biliary fistula may be formed between the 
gall-bladder and the stomach, which will be attended by sudden intense 
pain, with obstinate vomiting ; sometimes one or more calculi are found in 
+ Jie vomited matter. The vomiting of a gall-stone cannot be accounted for 



438 



DISEASES OF THE DIGESTIVE SYSTEM. 



on the ground of reversed peristaltic action after the stone has passed the 
ductus communis into the duodenum. Again, when calculi are formed in 
the gall-bladder, a fistulous opening into the duodenum may occur, followed 
by vomiting and signs of a local peritonitis, or of intestinal hemorrhage 
and haematemesis. An opening from the bladder into the colon is exceed- 
ingly rare, for the colon is very movable. The symptoms which attend 
such a perforation are obscure. The gall-bladder may open into the pelvis 
of the right kidney, and then biliary concretions will be voided in the 
urine. There is an instance on record where, during pregnancy, a com- 
munication was made between the gall-bladder and the uterus, the discharge 
of the calculi taking place at the birth of the infant. If an opening from 
the gall-bladder into the vena portae occurs, symptoms of pyaemia will de- 
velop very rapidly. If perforation of the left pleural cavity occurs, fatal 
pleurisy will result. A single, rarely a double, fistulous canal may connect 
the gall-bladder with the external surface ; the opening is usually near the 
umbilicus, and may discharge for months. It may cicatrize, and form a 
mass of fibrous induration ; or abscesses may form when a large calculus 
plugs the fistula formed by previous perforation. If perforation occurs, 
recovery is most frequent when an external opening is established. 

When a gall-stone has by any means entered the intestinal canal, it may 
be voided per anum or it may lead to an intestinal obstruction, ulceration, 
or gangrene of the intestine. Obstruction in the common duct may be 
temporary or permanent. If temporary there is no jaundice ; if the 
obstruction is complete and is continued for twenty-four hours, jaundice is 
added to the other symptoms ; this jaundice increases and is persistent 
when the obstruction is permanent. 

Biliary colic, or the passage of gall-stones, is the name applied to the pe- 
culiar and severely painful symptoms produced by the passage of one or 
more calculi along some one of the larger biliary ducts. Usually after a 
hearty meal, or after some jolting exercise, as horseback riding, the patient 
is suddenly seized with a severe pain in the epigastrium, which is increased 
by change of position or pressure. Sometimes slight rigors, nausea, eruc- 
tations, and attacks of yawning precede the colic. The pain is paroxysmal, 
and has its seat at a point where a line from the right nipple to the anterior 
superior spinous process of the left ilium crosses the free margin of the 
ribs. It radiates backward and upward, often as far back as the right 
shoulder, and may extend over both hypochondriac regions. It has been 
described by patients as boring, tearing, piercing, or lancinating. It is 
often so agonizing that patients will roll about the floor or bed, double 
themselves up, and groan with the pain. The face is pale and covered with 
cold sweat, and the pulse is very small. The abdominal muscles are rigid, 
and pressure greatly augments the pain. Vomiting, hiccough, a distended 
and tympanitic abdomen are often present during an attack, and a weak or 
feeble subject may faint, or pass into convulsions, which are epileptiform 
in character. Fatal syncope has occurred during an attack of gall-stone 
colic. After a few hours, sometimes a day, of exhausting and intense pain, 
the patient experiences sudden relief, and the pain entirely disappears; 



GALL-ST0XE8, 



439 



often the pain remits, but does not cease until the calculus enters the du- 
odenum ; an exacerbation occurs at the moment the calculus enters the in- 
testinal canal. Jauudice is often present, but not until the attack has con- 
tinued for twenty-four hours. During the colic, the gall-bladder is very 
sensitive to pressure ; during and after the attack, the patient is yery much 
exhausted, and shows great lassitude. When jaundice is present the faeces 
are clay-colored, and the bowels are apt to be constipated. After the at- 
tack, gall-stones may be found in the faeces. It is to be remembered that 
fresh gall-stones are slightly heavier than water. The urine, if jaundice 
exists, contains bile-pigment and is mahogany in color ; after the colic, it 
deposits lithates and lithic acid. 

Differential Diagnosis.— Gall-stone colic may be mistaken for cardialgia, 
intestinal and venal colic. Cardialgia may be mistaken for biliary colic 
when there is no jaundice present. In cardialgia, pain comes on immedi- 
ately after. eating ; gall-stone colic has no necessary connection with taking 
food. In cardialgia, the symptoms are referred to the epigastrium alone, 
while in biliary colic the pain shoots to the right shoulder and back. In 
cardialgia, the pain gradually diminishes ; in biliary colic it suddenly 
ceases. In gall-stone colic, the presence of a gall-stone in the faeces is 
pathognomonic. 

In intestinal colic, the pain begins at the umbilicus, and radiates over 
the abdomen ; in gall-stone colic it has its seat at the free border of 
the ribs, and shoots to the back and upward to the right shoulder. In in- 
testinal colic, pressure relieves the pain ; in gall-stone colic it aggravates it. 
In intestinal colic, the pain is intermittent ; in gall-stone colic it is con- 
stant, though paroxysmal. In intestinal colic, jaundice is never present, 
while it may exist in biliary colic. Intestinal colic accompanies or is fol- 
lowed by diarrhoea ; in gall-stone colic, the faeces are firm and may be clay- 
colored. 

"With renal colic, the pain shoots from the region of the affected kidney 
to the inner part of the thigh and end of the penis, and the testicle is 
retracted ; in gall-stone colic, the direction of the pain is upward and back- 
ward. In renal colic there is a constant desire to micturate. There is no 
urinary disturbance in biliary colic. In renal colic, after the cessation of 
pain, pus, blood and epithelium are found in the urine ; after gall-stone 
colic, bile-pigment is found in the urine. Jaundice and clay-colored stools 
frequently containing gall-stones may be present in biliary colic ; they are 
all absent in renal colic. The gall-bladder is very tender after biliary colic ; 
while there may be dull pains in the region of the loins after the passage of 
a renal calculus. 

Cancer of tlie head of the pancreas may readily be mistaken for gall-stones 
in the common duct. 

Prognosis. — The sudden and unexpected terminations and varied conse- 
quences due to the formation of a gall-stone, render it impossible to 
give any rule for the prognosis. When a large stone, without facets, 
has been voided, in any manner, from the bile passages, the prognosis is 
better than when small facetted calculi are found. Oft-repeated at- 



440 



DISEASES OF THE DIGESTIVE SYSTEM. 



tacks of biliary colic are bad. Catarrhal and exudative inflammations of 
the bile passages are frequent accompaniments of gall-stones ; and pul- 
monary gangrene, empyema, and pneumonia may sometimes complicate. 
Though it is not necessarily a fatal disease, death may result from peri- 
tonitis, ulceration, gangrene or obstruction of the intestines, pyaemia, 
pylephlebitis, abscess of the liver, from exhaustion, or from the escape of 
bile through an external opening. Death may occur during an attack of 
colic, from unexplained causes. 

Treatment. — An attack of biliary colic demands that attention be given, 
first, to the pain : this is best relieved by morphine, which should be given 
hypodermically, but never in such amounts as would be toxic were the pa- 
tient free from pain. Inhalations of chloroform or ether may be employed 
to relieve the severity of the spasm. The application of two or three leeches 
over the gall-bladder is often followed by relief, and diminishes the chances 
of inflammation of the bile-ducts. Large draughts of warm water, con- 
taining bicarbonate of soda, often relieve the pain at the onset of the 
attack. At the same time put the patient in a tepid bath, or wrap warm 
cloths about the abdomen. In mild cases, and when opium is contra^- 
indicated, belladonna will be sufficient, in connection with anodyne fomen- 
tations over the region of the gall-bladder. If the patient shows signs of 
collapse, stimulants, ammonia and brandy should be administered. 

A patient who has passed gall-stones must be put on a restricted diet ; 
wines or fats should be prohibited ; exercise in the open air, and an entire 
change in the mode of life, are important. Mineral waters, whether by 
giving an alkaline bile or by an increase in the amount secreted, cause the 
number of gall-stones to diminish, and also allow them to be passed with 
less pain. A prolonged course of alkaline mineral water has been found 
the best remedy against the formation of gall-stones. Ether, turpentine, 
chloroform and hydrate of chloral have been proposed as specifics, it being 
thought that they have the power of dissolving the gall-stones. 

FUNCTIONAL DERANGEMENTS OF THE LIVER. 

The terms biliousness and torpid liver were more frequently used 
twenty years ago than now. Many, indeed, have denied that any such con- 
ditions exist, but there is undoubtedly a variety of symptoms (such as 
constipation, yellow and itching skin, dark urine, headache, lassitude, 
furred tongue, bitter taste in the mouth, etc.), which can properly be 
classed as dependent upon functional derangement of the liver. Writers 
describe ten varieties; I shall only briefly consider those which are the most 
common. In these functional hepatic derangements there are no morbid 
appearances in the organ itself to account for the symptoms. 

Etiology. — Functional derangement of the liver may be due to structu- 
ral diseases (e. g., cirrhosis, abscess, and acute yellow atrophy), to dyspep- 
sia, both gastric and intestinal, to atony of the bowels, to obstructive 
diseases of the heart and lungs, to the specific fevers, malaria especi- 
ally, to faulty diet, the food being too rich, to the daily use of alcoholic 



FUNCTIONAL DERANGEMENTS OF THE LIVER. 



441 



beverages, especially ales and sweet wines and liquors (not from whiskey, 
brandy or gin, unless in the form of a hot toddy or sweet punch), to badly 
ventilated, hot, and moist apartments, sedentary habits, a deficient supply 
of oxygen, a warm climate (India, for instance), and finally to anxiety and 
prolonged mental labor. In many cases the tendency to " liver complaint" 
is inherited ; the children of the diabetic or gouty are very prone to func- 
tional derangements of the liver. 

Symptoms. — Few cases are exactly alike. The prominent symptoms 
which usually first attract the patient's attention are anorexia, a bitter 
taste in the mouth (due to taurocholic acid in the blood), flatulency, 
"acidity" and pyrosis. 1 The tongue is large, pale, and flabby, with inden- 
tations of the teeth along its edges. It may be white, showing elongated 
papillse-like villi. The faeces are pale, unless they have remained long in 
the large bowel, when they are blackish. Constipation and diarrhoea may 
alternate. When bile is in excess the faeces are semi-fluid and contain more 
bile than normal. It is a question whether melasna ever occurs as a sole 
result of hepatic derangement, but hemorrhoids are very common. There 
is often a sense of weight, fulness, tightness, burning, or even actual pain 
over the liver. Those who suffer from functional derangement of the liver 
may become very fat, or they may emaciate rapidly. Emaciation results 
either from deficient production of bile or from derangement of the glyco- 
genic function of the liver. Bile may saturate the texture of the body for 
months, and yet no symptoms of blood poisoning occur so long as the 
eliminating function of the kidneys is not impaired. 

A deficient elimination of cholesterin may give rise to " biliousness," 
and thus be a part of functional derangement of the liver. 2 " Cholester- 
semia " is said to be associated with obstinate constipation, and Dr. Murchi- 
son regards this as "torpor of the liver," or at least one, and a frequent, 
form of it. Lithates and pigments deposited in the urine should al- 
ways be regarded as signs of functional derangement of the liver arising 
from causes sometimes temporary and sometimes permanent. Murchison 
says "lithuria, like glycosuria, must be classed as a functional derangement 
of the liver," and he calls the antecedent morbid blood state litlmmia. In 
many, who by heredity are predisposed to "liver troubles," the liver is 
capable of performing its healthy functions only under the most favorable 
circumstances, and functional derangement is at once induced by articles 
of diet which most persons can easily digest. 

" Gouty dyspepsia," "latent gout," suppressed, anomalous or irregular 
gout, are terms which in many instances should be dismissed, and "func- 
tional derangement of the liver " substituted for them, for the symptoms 
which have been ascribed to them occur in those who neither inherit nor 

1 The functions of a healthy liver are. first, sanguinification ; second, the re-combination of albuminous 
matter derived from the food and tissues ; third, the formation of urea and lithic acid, both of which are 
afterward eliminated by the kidneys ; fourth, the secretion of bile, most of which is reabsorbed ; fifth, the 
glycogenic function. Among the most constant results of functional hepatic derangement is imperfect 
formation of urea' evidenced by the deposit of lithic acid or lithates in the urine. When a great part of the 
liver has been destroyed by disease the urea is lessened or disappears from the urine. Destructive 
nitrogenous metamorphosis is unquestionably an important function of the liver. 

2 Virchow'e Archiv. Bd. 65, p. 410. 1875. 



442 



DISEASES OF THE DIGESTIVE SYSTEM. 



ever have shown any gouty tendencies. 1 Biliary calculi (cholesterin and 
bile-pigment) may result from hepatic derangement. Frerichs regards 
the coincidence of gall-stones and urinary calculi in the same individ- 
ual as purely accidental. Since the kidneys eliminate certain products 
of the liver, renal derangements may be a consequence of faulty hepatic 
digestion. Hence Murchison places lithaemia among the chief causes of 
Bright's disease of the kidneys. 2 Many suppose that albuminuria may be 
induced by functional derangement of the liver, independent of any mor- 
bid kidney change, and this accords with the modern theories of albu- 
minuria. 

After the functions of a liver have been interfered with for some time, 
the structure of the liver is very liable to become diseased. Fatty liver and 
cirrhosis are common sequelae, and their causes are closely allied to func- 
tional derangement of the liver. 3 Senile decay (sometimes premature), 
fatty, calcareous and atheromatous arterial changes are very frequently 
direct sequelae of functional hepatic derangement. It is questionable 
whether the rheumatic hyperinosis is due to non-destruction of fibrin in 
the liver, as Murchison would have us believe. But the anaemia of this 
cachexia is undoubtedly often due to it. 

Symptoms. — Those who suffer from torpor of the liver complain of lassi- 
tude, drowsiness, pain in the limbs, dull pain in the right hypochondrium 
often shooting up the right side to the shoulder, and not infrequently of 
sciatica and lumbago. Circumscribed patches of skin, usually on the ex- 
tremities, often become hot and burning. Headache, usually frontal, is 
very common, and when induced by indiscretions in diet it is called " bil- 
ious " or " sick headache," and the patient states that he has had another 
" bilious attack." Dizziness, dim vision, and muscae volitantes are fre- 
quent results of over-eating in those whose livers are functionally deranged. 
Convulsions, paresis and cramps in the legs are rare, but they may occur. 
Melancholia, insomnia, hypochondriasis, irritability of temper, and moodi- 
ness are consequences of deranged liver-function. The term " bilious 
temperament " has passed into common use. In some cases there are car- 
diac palpitations, an irritable, irregular or even intermittent pulse, cold 
extremities, and slight lividity or cyanosis, and, according to Sir James 
Paget, venous thrombosis may result from functional derangement of the 
liver. Paget and Murchison regard lithaemia, i. e., functional derange- 
ment of the liver, as causing acute urethritis (non-specific) in many in- 
stances. 4 

After prolonged hepatic derangement psoriasis, lichen, eczema, lepra, 
urticaria, boils, carbuncles, pigment-spots (popularly called liver spots), 
and pruritus are liable to appear. Frequently the same individual will 
within a year have three or four of the above-named skin diseases as a 
direct result of functional derangement of the liver. 

CD 

1 Gout is one result of lithaemia ; and urinary calculi are frequently but an exhibition of functional de- 
rangement of the liver. 

3 Clin. Lec. Dis. Liver, pp. 572-573. 

8 Trousseau describes a chronic gouty hepatitis that comes under this head. 

4 British Med. Journal, 1875, i. 701. 



FUNCTIONAL DERANGEMENTS OF THE LIVER. 



443 



The diagnosis is made by a consideration of the conditions and habits of 
life of the patient, the sequence of symptoms, its long duration, inter- 
rupted by " acute bilious attacks," and by the exclusion of structural 
hepatic and kidney disease. 

The prognosis depends on the cause : if due to diet, a cure can be easily 
effected if the individual obeys instructions ; if hereditary, a definite prog- 
nosis should never be given. 

Treatment. — The treatment in the main is dietetic and hygienic ; no inflexi- 
ble rule of dietetics can be laid down. Some patients do best on albumi- 
noids, others on the hydrocarbons. The essential point is to restrict the diet 
to one or the other class of foods. Wines and ales should be wholly discarded. 
Fresh air, sea-air especially, and moderate exercise, attention to the cutane- 
ous functions, and abandonment of severe mental work, should be recom- 
mended. Mineral waters (Hunyadi Janos and Pullna especially) should be 
freely drunk at all times. Eochelle, Glauber's, and Epsom salts are beneficiaL 
The bowels should always be kept freely opened. Alkalies, especially the 
carbonate of lithia, are always of service. Chlorine, bromine, and iodine are 
useful in some cases, and the bromide of potash is highly beneficial 
when combined with ammonium chloride. The mineral acids are apt to 
do more harm than good, although in works on materia medica the nitro- 
muriatic acid is said to be almost a specific for torpor of the liver. 1 Acetic 
extract of colchicum is indicated in gouty and rheumatic subjects. Tar- 
axacum was formerly thought to have a powerful effect on the liver ; its 
only action is that of a cathartic. 

Mercury, in the form of blue pill, is more efficacious in affording tem- 
porary relief in the so-called bilious attacks than any other drug. It is 
denied by many that mercury is a cholagogue ; still there are few who do 
not recommend "blue-mass" in functional hepatic disturbances, and 
although experimental therapeusis shows that mercury simply increases the 
biliary secretion by acting on the upper portion of the small intestine, yet 
there must be some action of mercury now unknown, which makes it the 
most reliable drug in functional derangement of the liver. It is suggested 
that by promoting or in some way influencing the disintegration of albu- 
men the liver is relieved, and thus the effects of an overtasked or naturally 
feeble organ are overcome. A dose of calomel at night, followed in the 
morning by a saline purge, relieves both the hepatic and urinary symptoms. 
Podophyllum (I gr. of the resin) given with cannabis indica or henbane is 
by many thought equal to mercury. Tonics and opium are to be expressly 
forbidden ; iron does positive harm. 



1 Prof. Rutherford states that in dogs it has no effect upon the bile secretion. 



444 



DISEASES OF THE DIGESTIVE SYSTEM. 



DISEASES OF THE PANCREAS. 

Diseases of the pancreas are almost always secondary to, or associated 
with, disease of neighboring organs ; I shall briefly consider them under the 
following heads : 

I. Acute and Chronic Pancreatitis. IV. Cysts of the Pancreas. 
II. Degenerations, Fatty and Waxy. V. Calculi and Parasites. 
III. Morbid Growths: — Cancer, Tubercle, Sarcoma, and Gummata. 

ACUTE PANCREATITIS. 

This is a rare affection, and is chiefly of interest from a pathological 
standpoint. 

Morbid Anatomy. — The pancreas is enlarged, hyperaemic and firmer than 
normal. When the hyperemia is intense, small hemorrhages occur in its 
substance. In febrile diseases the whole organ is seen to have undergone 
diffuse parenchymatous changes. In suppurative pancreatitis there is 
either a diffuse infiltration of pus, or numerous small abscesses are 
formed. In some instances the surrounding connective-tissue and lym- 
phatic glands are involved and the pancreas is surrounded by pus. Pus 
may form in the ducts, acini, or the cellular tissue. Pancreatic abscesses 
may open into the stomach, peritoneal cavity, duodenum, or externally. 

Etiology. — This is obscure ; it may possibly be caused by acute alcoholis- 
mus and by blows over the organ. It occurs more frequently in men than 
in women. Acute tuberculosis, typhoid fever, pyaemia, septicaemia, and 
parotitis (from metastasis) are sometimes followed by it. It has appeared 
in some cases to depend upon the prolonged use of mercury. 

Symptoms. — These are obscure and variable, the most constant is colicky 
or deep-seated dull pain over the pancreas, shooting to the back and shoul- 
der. Fever, dyspnoea, anorexia, and vomiting of a thin, viscid fluid, some- 
times containing bile, are nearly always present. There is great thirst and 
restlessness. The pulse is rapid, the pain is greatly increased by firm press- 
ure over the pancreas, and symptoms of collapse are often present. There 
is marked anxiety and depression from its onset. The bowels are consti- 
pated. In some cases of metastatic pancreatitis the stools are watery and 
like saliva. In these cases diarrhoea is generally present. 

Differential Diagnosis. — Hepatic diseases are excluded by the absence of 
jaundice. But it is frequently impossible to exclude acute gastritis or duo- 
denitis except by the site and distribution of the pain, and by the presence 
of fever and the irregular heart-action. 

Prognosis. — It usually terminates in death after a very rapid course. It 
may become chronic, terminating in abscess or induration. 

Treatment. — Eest, a mild, fluid diet, and anodynes are the only means to 
be employed in its treatment. The efficacy of ice or poultices over the 
epigastrium is questionable. 



CHROMIC PANCREATITIS. 



445 



CHEONIC EANCEEATTTI5. 

Morbid Anatomy. — The changes are identical with cirrhotic processes 
elsewhere, e. g.. in the liver and spleen. This process may lead to complete 
disappearance of the gland substance or to closure of the duct and the con- 
sequent formation of cysts. The head of the gland is most involved in the 
cirrhotic process. Interstitial hemorrhages may occur, or little cvsts mav 
stud the gland. Adhesions generally bind the organ to the adjacent parts. 
In chronic suppurative pancreatitis the pus may infiltrate the gland, or 
there may be one or more small abscesses. The contents of the latter may 
become cheesy or calcareous. 

Etiology. — The causes are similar to those of cirrhosis of the liver : — cal- 
culi, the pressure of an adjacent tumor, or extension of inflammation from 
adjacent parts, especially ulcers of the stomach and duodenum. It may be 
associated with syphilitic infection. 

Symptoms. — The only symptoms that could lead to a diagnosis are fatty 
stools, intercurrent ruellituria. neuralgic pains, and the presence of a trans- 
verse tumor in the epigastrium. Abdominal dropsy and signs of intestinal 
obstruction may be caused by the pressure of the hard gland which acts as 
an abdominal tumor. A peculiar cachexia is usually present. 

FATTY DEGENERATION. 
Two forms are recognized : 

L Fatty infiltration of the connective-tissue investing the gland and sur- 
rounding the acini, where the new growth of fat-tissue causes atrophy and 
disappearance of the gland cells by its pressure. The whole gland may 
look like a mass of fat with only a central canal. 

II. Fatty degeneration affects the gland cells and ultimately destroys 
them ; the acinous structure is preserved in the midst of a soft, flaccid and 
wasted gland. A more or less abundant fatty emulsion is found in the 
ducts. 

Etiology. — The first form occurs in general obesity and in chronic alco- 
holismus. The second is due to the same causes, and a 1 so to heart disease 
or obstruction to the outflow of the pancreatic secretion. 

VTA XT DEG-ENEEATION. 

The vessels of the pancreas and the cells of the acini may exhibit amy- 
loid change. This is the rarest disease of the pancreas. 

CANCEE OE THE EANCEEAS. 

This is the most frequent form of primary disease of the pancreas. In 
one hundred cases of cancer the pancreas was found involved in five. 
Scirrhus is the most frequent variety of cancer found here. Pancre* 



446 



DISEASES OF THE DIGESTIVE SYSTEM. 



atic cancer tends to involve adjacent organs ; the bile-duct and left 
ureter may be pressed upon and obstructed, and the mass may com- 
press the splenic or superior mesenteric vessels, the vena porta?, the in- 
ferior cava, or even the aorta. The cancer may ulcerate into neighboring 
structures. The canal of Wirsung may be obstructed, and then cysts will 
form. 

Etiology. — It occurs chiefly in men after the fortieth year ; further than 
this little can be said. 

Symptoms. — The symptoms are varied, because the neighboring organs 
are so frequently and extensively involved. Neuralgic and paroxysmal 
pain, is an important symptom. The presence of a tumor with enlarge- 
ment of the adjacent lymphatic glands is essential for a diagnosis. Vom- 
iting, jaundice, dyspepsia, dropsy, oedema of the feet, — all may be present. 
Sometimes the stools may be fatty. There may be constipation or diarrhoea, 
or the two may alternate. The general symptoms are those of anaemia. 

Differential Diagnosis. — A pancreatic cancerous tumor may pulsate and 
have a bruit conducted from the aorta, and therein simulate aortic aneu- 
rism. 

Prognosis. — Cancer of the pancreas usually causes death within a year. 

The treatment is symptomatic. 

Small-celled Sarcoma usually occurs as a melanotic tumor. It is very 
rare, and clinically indistinguishable from carcinoma. 

Tuberculosis of the pancreas, secondary to that of the lungs and peri- 
toneum, develops in the connective-tissue between the acini. Caseous 
nodules are oftener met with than diffuse miliary tubercles. It is denied 
that the pancreas ever is involved in acute miliary tuberculosis. 

Syphilitic Gummata are usually found in connection with syphilitic in- 
terstitial pancreatitis. They have been described by Rostan and Rokitansky. 
It is believed that more frequent examinations of the gland would reveal a 
larger number of gummata. 

CYSTS IN THE PANCKEAS. 

Cysts in the pancreas are due to retention of the pancreatic secretion, 
from obstruction of the duct by calculi, or from external pressure of tumors. 
Hemorrhagic cysts are very rarely found. When the duct is closed near 
its mouth, the canal and its branches look like a bunch of currants. Atro- 
phy and cirrhosis of the gland may result from these cysts, which at first 
contain a normal secretion which afterword becomes purulent, hemorrhagic, 
or albuminous. Haematoidin crystals, lime-salts and urea have been found 
in these cysts. The cyst-walls thicken from connective-tissue develop- 
ments. 

Etiology. — Any tumor, either of the pancreas itself or of neighboring 
parts, calculi, cirrhosis of the pancreas, or angular displacements of the 
pancreas may cause it. 

Symptoms. — The only symptom is the disoovery of a smooth lobulated tu- 
mor in the region of the pancreas. 



HYPEKJEMIA OF THE SPLEEN". 



447 



CALCULI OF THE PA3TCEEAS. 

Calculi of the pancreas are usually gray-white, rounded masses of car- 
bonate or phosphate of lime. They are situated anywhere in the pancreas, 
are either free or embedded, vary in size from microscopic dust to a walnut, 
and also vary in number, but rarely exceed fifteen or twenty. Laminated 
protein concretions are described by Virchow. 

Etiology. — Anomalies in the pancreatic juice itself, catarrh of the ducts, 
and retention cysts are the most frequent causes. 

Symptoms. — There will be no symptoms except when interstitial inflam- 
mation is excited, or the common duct is pressed on so as to cause jaundice. 
Round worms have been found in the pancreas. 

DISEASES OF THE SPLEEN". 
Diseases of the spleen will be considered in the following order : 

I. Hyperemia. . IV. Degenerations, Waxy or 

II. Inflammation, or Splenitis, includ- Sago-spleen. 

ing Embolism and Infarction. V. Morbid Growths. 

III. Hypertrophy, or Chronic Enlarge- VI. Parasites, 
merit. 

HYPEKiEMIA. 

Splenic hyperemia may be active or passive. 

Morbid Anatomy. — The accumulation of blood in the vessels and inter- 
vascular spaces of the spleen, causes the enlargement which occurs in 
hyperemia ; the organ may be increased to five or six times its normal size 
and yet retain its normal shape. Its color is darker than normal, its cap- 
sule is usually tense and shining, and its consistency is often diminished, 
being sometimes as soft as pulp. A microscopic examination shows no new 
elements in the spleen, only an increase in the number of its normal ones. 

Etiology. — A physiological congestion of the spleen takes place after every 
meal. A pathological engorgement occurs : (1) when there is any ob- 
struction to the venous flow from the spleen, as happens in certain cardiac, 
hepatic, and pulmonary diseases ; (2) in the acute infectious diseases, such 
as typhus, malarial fevers, and pyaemia ; (3) at the menstrual epoch, de- 
pending upon an abnormality of menstruation ; (4) as the result of inju- 
ries and inflammation, when the hyperemia will be circumscribed. 

Symptoms. — The symptoms of simple hyperemia of the spleen are usually 
not well marked ; the patient may complain of a sense of weight in the 
left hypochondrium and more or less tenderness on pressure over the 
splenic region. Palpation and percussion will discover a tumor in this 
region of greater or less size ; this tumor extends obliquely downward to- 
ward the umbilicus, rises and falls with each respiratory movement, and 
has the outline of the spleen, with the characteristic notches on its lower 
rounded edge. The pale and anaemic appearance often met with in those 



448 



DISEASES OF THE DIGESTIVE SYSTEM. 



having splenic hyperemia is due to the overloading of the spleen with 
blood at the expense of the rest of the body, rather than to any change in 
the composition of the blood. 

Prognosis. — The prognosis is good, although in certain rare cases death 
has occurred from rupture of the distended organ. 

Treatment. — The treatment is directed rather to the disease which gives 
rise to the hyperemia than to the condition itself. Quinine in large doses 
has been found in most instances to remove the splenic congestion and 
relieve the accompanying symptoms. 

INFLAMMATION OF THE SPLEEN. 

{Splenitis.) 

Primary splenitis is exceedingly rare ; it is generally due to injury, em- 
bolism, or infarction, especially when occurring with pyaemia or septic 
diseases. It may occur in connection with morbid growths and abscesses 
in the spleen. There is a condition of the spleen resembling cirrhosis of 
the liver, called by some chronic or interstitial splenitis. 

Morbid Anatomy. — The anatomical arrangement of the splenic arteries 
renders the spleen a favorable seat of metastatic inflammation. In acute 
splenitis a part or all of the organ may be attacked ; the involved portions 
are congested and swollen, and the peritoneum over them is injected and 
^covered with a fibrinous exudation. The spleen is of a deep purplish color 
and friable, being broken down as easily as coagulated blood. When a 
hemorrhagic infarction is formed in the spleen, it is usually without rupt- 
ure of the blood-vessels, and is encircled by a zone of sero-hemorrhagic 
infiltration. These infarcts are at first of a brownish red color and of a 
firm consistency ; later, they become dirty yellow in color, and either under- 
go fatty degeneration and become absorbed, or remain as cheesy and 
calcareous masses ; or, lastly, the infarctions soften and abscesses form, 
which are single or multiple, sometimes fusing together, and again in- 
creasing by peripheral extension. 

In a few instances these abscesses are found incapsulated in a proliferation 
of connective-tissue, but in most cases this is not the case ; the connective- 
tissue breaks and a large sac is formed filled with pus ; as much as thirty 
pounds have been found in one of these sacs. At last the capsule becomes 
involved, perisplenitis is set up, and, adhesions having formed between the 
spleen and adjacent parts, the abscess may open into some adjacent organ, 
as the stomach and colon, into the thorax or abdominal cavity, or an 
external fistulous opening may be formed. Localized suppurative inflam- 
mation of the small Malpighian bodies in the spleen has been found to occur 
in typhus and other fevers. 

" Necrotic splenic softening " may occur from an infarction caused by 
atheroma and endocarditis : the latter is not necessarily ulcerative. In these 
cases the lymph-cells in the fibrinous reticulum of the clot become fatty, 
and then they mass themselves into spheres of fat-crystals. The whole 
infarction softens and becomes a fatty, pulpy mass. The capsule over such 



INFLAMMATION OF THE SPLEEN. 



449 



a spot is villous and appears covered with vegetations. A gangrenous con- 
dition of the left lower lobe of the lung has been caused by such a form of 
metastatic splenitis ; with the intense engorgement which accompanies 
acute splenitis, hemorrhage into the organ may occur, the capsule may 
be ruptured, and a fatal peritonitis may be induced. 

Chronic splenitis is the result of long-continued splenic congestion. The 
spleen is of a brownish-red or slate color, its capsule is thickened, and 
covered with very firm vegetations and new connective-tissue formations, 
which are highly vascular. The organ is more or less pigmented, owing 
to the pigmentary deposit in the endothelia of the veins. This whole proc- 
ess is analogous to that which occurs in cirrhosis of the liver, except 
that a spleen which is the seat of interstitial inflammation is larger than 
normal. 

Etiology. — It is very doubtful whether idiopathic splenitis ever occurs. 
Blows and severe muscular exercise are said to have caused it. Splenitis 
is usually metastatic, the embolic plug, the result of endocarditis and 
valvular disease, most often having its origin in the left heart, although it 
may be induced by thrombotic changes in the aorta. Earely the embolus 
comes from the lungs, having passed through the pulmonary vein and left 
heart. In pyaemia and its allied states hemorrhagic infarctions of the spleen 
are of frequent occurrence, and a similar condition has been noticed in 
Bright's disease and in the infectious diseases. Extension of inflammation, 
especially the result of ulcerative changes in the stomach, is an occasional 
cause of acute splenitis. 

Symptoms. — These are vague ; often there is nothing except the local 
changes to direct attention to the spleen as the seat of disease. There is 
no pain, unless the capsule is involved ; if pain is present it will be in- 
creased by a full inspiration. There may be hectic fever, but, as splenitis 
is secondary to some febrile disease, the fever may be attributed solely to 
the latter. There may be a sense of weight and pain in the left hypo- 
chondrium, and even snooting pains in the left shoulder and arm. 

Vomiting of blood and pus, or the simultaneous passing of blood and pus 
with the faeces is indicative of rupture of a splenic abscess into the stomach; 
this, hoAvever, is an exceedingly rare event. The recognition of a splenic 
abscess will depend upon its attaining a sufficient size to form an appreciable 
fluctuating tumor in the splenic region. 

Physical Signs. — Inspection will show a marked enlargement in the splenic 
region. 

Palpation may discover a fluctuating mass. The " notchings " on the 
anterior margin of the spleen are usually readily made out. The mass is 
more or less movable, unless adhesions have formed between the splenic 
capsule and adjacent parts. 

Differential Diagnosis. — Acute splenitis may be mistaken for cancer of 
the stomach, disease of the pancreas, or hepatic disease, especially that in- 
volving the left lobe of the liver. Ovarian tumors will rarely be con- 
founded with it. In stomach diseases the absence of fever, the vomiting,, 
pain and discomfort dependent on the ingestion of food, the long dura- 
29 



450 



DISEASES OF THE DIGESTIVE SYSTEM. 



tion, and the peculiar haematemesis will readily distinguish them from 
acute splenitis. 

Cancer, abscess, or cirrhosis of the liver would give physical signs which 
could hardly be confounded with those of acute splenitis — the position of 
the area of dulness would of itself be sufficient for a diagnosis. The con- 
dition of the stools, the urine, and the color of the skin are often sufficient 
to lead to a diagnosis of hepatic diseases. If the tumor is of considerable 
size, the diagnosis of splenic abscess can always be safely reached by the 
aid of the exploring trochar. 

Prognosis. — Suppurative splenitis is always a dangerous disease, and is 
rarely recovered from, even when an extensive opening is established. 

Treatment. — No special treatment is called for unless the pain is severe, 
when anodynes and fomentations may be used. When an abscess can be 
made out it should be treated in the same manner as an hepatic abscess. 



HYPERTROPHY OF THE SPLEEN. 

{Enlarged JSpfcen.) 

Enlargements of the spleen are of two kinds : (1) acute and transient ; 
and (2) chronic and permanent. The first class occurs in fevers, e. g., 
typhoid ; the second from long-continued and repeated congestion, as in 
chronic malarial infection. 

Morbid Anatomy. — In acute enlargement, the spleen may reach four or 
five times its normal size. The capsule becomes thin and tense. The 
spleen pulp varies in consistence, and may even be completely diffluent ; 
its color varies from a bright pink to a red black. Hemorrhagic foci in- 
dependent of embolism may occur. Many lymphoid cells contain one or 

more red corpuscles, the latter either being 
normal in size or smaller (1-8000 of an 
inch). This microscopical appearance is 
best marked in typhoid fever. 1 

Chronic Enlargement of the Spleen. — The 
organ is enlarged without any obvious 
change in texture ; there is an increase in all 
its elements, and it acquires a more or less 
fleshy consistency. It sometimes reaches a 
very great size, filling the left side of the 
abdominal cavity from the ribs to the pelvis; 
it may be increased to twenty pounds in 
weight. Its normal shape is unchanged and 
the notches on its edges are distinctly re- 
fig. 90. tained. In rare cases chronic enlargement 

Diagram illustrating the abdominal areas of -i j , ^ -. 

percussiou-diilnessin Splenic Enlargement. OCCUl'S as a multiple nodular hyperplasia. 




1 The color of the spleen in congestive enlargement is always paler than that of the other viscera, on 
account of the presence of a larger quantity of white blood corpuscles than are found elsewhere in the 
body. 



AMYLOID DEGENERATION OF THE SPLEEJS". 



451 



Etiology. — Acute enlargement of the spleen is met with most frequently 
in acute infectious diseases. Many regard the accumulation of micrococci 
in the spleen and their retention within the splenic protoplasm as a cause 
of acute swelling. 1 Of all the diseases that cause sudden and great enlarge- 
ment of the spleen, the most frequent are typhoid and intermittent fevers. 

Chronic enlargement of the spleen is frequently associated with cirrhosis 
and other chronic affections of the liver, and with chronic cardiac- and 
pulmonary diseases that induce long-continued or repeated congestion of 
the organ. But chronic malarial infection is its most common and constant 
cause. Chronic enlargement of the spleen is part of the history of leucocy- 
thaemia; it is never idiopathic. Chronic mercurialism disposes to en- 
largement of the spleen. 

Symptoms. — Acute enlargement of the spleen is part of the history of 
acute general diseases ; its natural symptoms are few : pain on pressure, 
dyspnoea, and an increased area of splenic dulness are the most constant 
and prominent. Chronic enlargement of the spleen is attended by no 
symptoms except the physical signs of splenic enlargement. 

Treatment. — Quinine and iron are always indicated, but they should be 
given alternately and never at the same time; they may be combined with 
arsenic and cod-liver oil. In malarial hypertrophy of the spleen the patient 
should reside in a non-malarial district. Inunctions of the biniodide of 
mercury are strongly recommended by English authorities, but I have 
never seen any beneficial results from their use. 

AMYLOID DEGENEKATION OF THE SPLEEN. 

{Sago Spleen.) 

Waxy or lardaceous degeneration of the spleen, also called the "sago 
spleen," is a part of a general cachexia in which other organs are primarily 
involved. 

Morbid Anatomy. — It occurs in two forms ; in one it is limited to the 
Malpighian bodies, in the other it is diffused. In both the organ is en- 
larged, rounded and doughy. The capsule is tense, but not thickened, and 
is usually smooth and glistening. 

On section the first variety presents the appearance of a number of sago 
granules, the Malpighian bodies being enlarged to 1-25 or 1-12 of an inch 
in diameter, and filled with waxy material which gives the characteristic 
reaction with iodine. The corpuscles through which the arteries pass are 
involved, but the wall of the in-going vessels may remain normal. The 
"adenoid" or " cytogenic " tissue, the lymph -corpuscles, and the capilla- 
ries of the spleen are, however, infiltrated with waxy material, massed to- 
gether, and channelled by healthy capillaries. The veins near the diseased 
Malpighian bodies are sometimes involved. In diffuse lardaceous degenera- 
tion, the spleen, on section, is pale, homogeneous, glistening and anaemic ; 
all the vessels, the trabeculae, and capsule are involved. 2 

Etiology. — The causes of waxy spleen are identical with those of waxy 

1 Mosler and Birch-Hirschfeld. 

2 Eokitansky regards this form as but a later stage of " sago spleen." 



452 



DISEASES OF THE DIGESTIVE SYSTEM. 



liver ; it is met with in chronic bronchitis with bronchiectasis, in phthisis, 
chronic Bright's disease, chronic peritonitis, cirrhosis of the liver, chronic 
alcoholismus, and intermittent fever. Sago spleen frequently accompanies 
chronic intestinal catarrh in children. Syphilis is probably its most fre- 
quent cause. 

Symptoms. —As the liver and intestines are generally involved in the same 
change, the waxy cachexia will not be characteristic of splenic changes. 
There will be anaemia, accompanied by a great increase in the area of splenic 
dulness. Late in the disease there is usually anorexia, vomiting, and 
hemorrhages, but it is not possible to determine to what extent these vari- 
ous symptoms depend on the splenic disease. 

The diagnosis rests mainly on its etiology. 

The prognosis is unfavorable. 

Treatment. — It never calls for independent treatment. Niemeyer regards 
iodide of iron as the most efficacious drug. Our first efforts should be to 
cure or remove the causes or conditions which have led to its development, 
and to improve the general condition of the patient by tonics, hygienic 
measures, and a carefully regulated, nutritious diet. 

MORBID GROWTHS OF THE SPLEEN. 

Cancer of the spleen is very rare ; it may be secondary to cancer of the 
stomach, mamma, liver, or brain. When disseminated, it is generally of 
the eneephaloid variety. It may develop in the hilum by contiguity of can- 
cer in the other organs. Secondary isolated growths may be scattered 
through its substance, or in many more instances it may be the seat of pri- 
mary cancer. In pigment-cancer of the spleen, the organ rapidly enlarges 
to nearly double its size ; in other forms it is but slightly enlarged. The 
symptoms are obscure and of little clinical importance. 

Gummata, or syphilitic tumors of the spleen, are only met with in con- 
nection with amyloid changes, and are accompanied by similar develop- 
ments in the liver. Syphilis thus shows itself in the spleen in one of four 
ways, — waxy degeneration, gummata, inflammation of the spleen- pulp, or 
hypertrophy of the spleen with increase in interstitial tissue. Syphilomata 
are of no clinical importance. 

Tubercles in the spleen develop in the spleen-pulp. The nodules may be 
small and gray, or large, yellow and cheesy. In acute tuberculosis, the 
spleen rapidly enlarges as the tubercles develop. Tubercular formations 
are very common in young children. Yellow tubercular masses, varying 
in size, are frequently found in the spleen in connection with similar form- 
ations in other parts of the body ; occasionally they soften and form ab- 
scesses. The small splenic vessels are often clogged with lymph and fibrin. 
Tubercles of the spleen cannot be recognized during life. 

Cysts have been found in the spleen. They are associated with cystic 
developments in the liver and omentum. 

Hydatids, when occurring in the spleen, usually accompan}^ similar de- 
velopments in the liver and peritoneum. The enlargement of the spleen 



MORBID GROWTHS OF THE SPLEEN". 



453 



may cause a sense of weight in the splenic region, and if the splenic capsule 
becomes inflamed their development will be accompanied by sharp pains in 
the left side. An hydatid tumor in the spleen usually fluctuates, but it 
rarely gives the hydatid fremitus. An exploratory puncture decides its 
character. 

The prognosis and treatment are the same as in hydatids of the liver. 



SECTION III. 



DISEASES OF THE HEART, BLOOD-VESSELS AND KIDNEYS. 



Diseases of the heart may be classified as follows 



I. Pericarditis. VIII. 

II. Endocarditis. IX. 

III. Valvular Lesions. X. 

IV. Cardiac Hypertrophy. XI. 
V. Cdrdiac Dilatation. XII. 

VI. Myocarditis. XIII. 

VII. Cardiac Degenerations. XIV. 



Cardiac Atrophy. 

Cardiac Thrombosis. 

Cardiac Aneurism. 

Morbid Growths and Parasites. 

Tuberculosis of the Pericardium. 

Cardiac JSeuroses. 

Hydro-pericardiu in. 



XV. Pneumo-hydro-yericardium. 



PERICARDITIS. 



The pericardium is a fibro-serous sac ; the fibrous layer is firmly adherent 
to the diaphragm and is attached to the large vessels about two inches 
above the heart ; it forms a closed sac. The serous layer is in close appo- 
sition to the internal surface of the fibrous layer, is reflected from the large 
vessels, and completely invests the heart itself. This shut serous sac, when 
diseased, behaves in all respects like the pleura. Inflammation of the 
pericardium may be acute or chronic. Chronic pericarditis is usually the 
sequel of acute. 

ACUTE PERICARDITIS. 

Acute pericarditis is perhaps more frequently overlooked than any other 
acute disease, for its subjective symptoms are rarely, if ever, well marked. 

Morbid Anatomy. — At its commencement, the serous surface of the 
pericardium becomes more or less reddened, with here and there ecchy- 
motic spots of irregular shape. The reddening may be circumscribed about 
the roots of the great vessels, or it may involve the whole visceral and 
parietal pericardium. The reddening is due to hyperemia of the sub- 
serous capillary vessels. With the redness there are swelling and infil- 
tration of its serous and sub-serous tissue. Following the hyperemia 
and infiltration the epithelium desquamates and the membrane loses its 
natural glistening appearance. If the inflammatory action is continued, 
an exudation is poured out- on its free surface : it may consist of but a few 
shreds of lymph, or a fibrinous layer may cover the whole of its car- 
diac or parietal surface. It varies in thickness from a line to three-fourths 



ACUTE PERICARDITIS. 



455 



of an inch, or even more. This exudation is composed of fibrin, a few pus 
cells and detached epithelia ; it causes the free surface of the pericardium 
to assume a roughened appearance ; it is this appearance which has given 



rise to the expression "hairy heart 
amount of plastic exudation, it 
will usually be confined to that 
portion of the pericardium which 
covers the blood-vessels. 

With or following the plastic 
exudation there may be a fluid 
effusion which varies in quantity 
and in quality. It may be sero- 
albuminous, sero-fibrinous, hem- 
orrhagic, or purulent. It varies in 
quantity from three fluid ounces 
to several pints. In most instances 
it will be sero-fibrinous in char- 
acter ; it is rarely sero-albuminous. 
When it is small in amount it will 
gravitate to the most dependent 
portion of the pericardial sac. 
Wlien it is large in quantity, the 



When there is only a very small 




Fig. 91. 

entire pericardial Sac is filled, and Diagram Illustrating the Morbid Anatomy and Physical 

Signs of Sero-plastic Pericarditis. 

A. Line of diaphragm. 

B. Heart. 

C. Serous effusion into lower portion of pericardial sac. 

D. Plastic exudation upon both visceral and parietal 
layers of the pericardium. 



the adjacent lung-tissue com- 
pressed, and the surfaces of the 
membrane have a reticulated or 
honey-combed appearance. It is 
always turbid from the molecular fibrin suspended in it, and may be 
yellow, green, brown, or red in color. 

Hemorrhagic pericarditis is rare, except with purpura, scurvy, cancer of 
the lung, and tuberculosis. In this variety the line of demarcation between 
the false membrane and the pericardium is very indistinct. 

Tuberculous pericarditis is attended by the development of tubercles in 
the pericardium and in the substance of the heart ; the blood elf used forms 
ochre-colored masses in the exudate. The exudations and effusions in 
pericarditis may all undergo 'absorption. The serous effusion is removed 
rapidly, the hemorrhagic with less facility, the plastic and purulent with 
still greater difficulty. The fluid disappears first, then the granular, and 
last the coagulated fibrin. The lymph and purulent exudations may 
undergo fatty metamorphosis and be absorbed, or remain in a cheesy, 
mortar-like mass, and finally become calcareous after the absolution of the 
more fluid portion of the degenerated mass. The calcareous material with 
connective-tissue formations may form ossified plates upon the surface of 
the heart and pericardium. 

New connective-tissue formations may take place upon the surface of 
the pericardium under the layer of plastic exudation ; if the inflamma- 
tory process is continued sufficiently long, these are converted into a firm 



456 



DISEASES OF THE HEART. 



fibrinous mass, causing either a permanent thickening of the pericardium, 
or adhesions between its two surfaces. Sometimes these adhesions are by 
bands stretching across from one portion to the other ; at others there is 
complete agglutination of the two surfaces, and an entire obliteration of the 
pericardial cavity ; in either case more or less complete organization takes 
place. The adhesions about the base are the most dense. Those at the; 
apex are drawn out into fibrinous strings. 

With inflammatory changes in the visceral pericardium, there will be 
more or less inflammatory change developed in the muscular tissue of the 
heart immediately beneath the pericardium. If the pericarditis has been 
extensive and long continued, the walls of the heart will become weakened ; 
indeed, they are somewhat weakened in every attack of pericarditis. The 
development of myocarditis will be considered more fully under its appro- 
priate head. Dilatation of the cavities of the heart may take place in con- 
sequence jf the weakened condition of the cardiac walls, and cardiac hy- 
pertrophy may be developed as a result of this weakening and dilatation. 
Upon post-mortem examination not infrequently smooth, opaque, pearly- 
white patches are found upon the external surface of the heart. They are 
slightly elevated, variable in size, have irregular sinuous margins, and are 
usually located on the anterior surface of the ventricle. As to the nature 
of these spots there has been considerable discussion. These " milky 
patches " are, however, nothing more than growths of white, laminated con- 
nective-tissue with elastic fibres, immediately beneath the cardiac pericar- 
dium, and indicate the previous existence of a localized pericardial inflam- 
mation which has been recovered from without adhesions. In rare instances 
the two surfaces of the pericardium will become firmly agglutinated through- 
out their entire extent, and the pericardial sac will remain completely oblit- 
erated, and if attempts are made to separate them the cardiac muscle is 
torn. Under such circumstances, the movements of the heart carry with 
them the pericardium, and with each cardiac pulsation there is a lifting of 
the diaphragm. 

Etiology— Acute pericarditis rarely occurs as a primary affection, but is 
usually secondary, or is developed during the course of some other disease. 1 
It may be produced by injuries to the pericardium, — by extension of inflam- 
mation from neighboring organs, as when it occurs with pleuro-pneumonia, 
pleurisy, necrosis of the sternum, ribs, rupture of abscesses, etc. It occurs 
most frequently in connection with that class of diseases which depend upon 
well-recognized blood-changes, and especially with those due to a specific 
infection ; under this head are included pericarditis which accompanies 
acute rheumatism, Bright's disease, acute infectious diseases, as scarlatina, 
small-pox, typhus and typhoid fever, pneumonia, tuberculosis, syphilis, 
chronic alcoholismus, etc. Occasionally it is developed in connection with 
scurvy and purpura ; then it is of the hemorrhagic variety. Cancer of the 
lung and tuberculosis also cause ' k hemorrhagic pericarditis." 

When pericarditis occurs in connection with pyaemia and septic condi- 
tions, the effusion is purulent in character and accumulates rapidly. It is 



1 A case of " Idiopathic Pericarditis.' 1 '' Glasgow Med. Journal, Sept., 1878. 



ACUTE PEKICAKDITIS. 



457 



of most frequent occurrence in connection with acute articular rheumatism, 
Bright's disease and pneumonia. Often in rheumatic pericarditis, the ar- 
ticular rheumatic development occurs subsequent to the pericarditis. In 
rheumatism it is an early, in Bright's disease a late occurrence. Pericar- 
ditis occurring in connection with scarlet fever is especially liable to be 
overlooked, for its presence is not revealed until a large fluid effusion takes 
place. 

Symptoms. — The symptoms cf acute pericarditis are rarely well defined. 
It is very difficult to give a clear description of the rational symptoms which 
attend its development, for it is usually associated with some other affection 
whose symptoms tend to obscure those of pericarditis ; more than one-half 
of the cases are latent, and come on so insidiously that they would go un- 
recognized were it not for the physical signs which attend them. 

The two prominent rational symptoms are pain in the precordial region 
and cardiac palpitation. The pain is usually confined to the precordial 
space ; occasionally it involves the brachial plexus, and extends down the 
left arm ; under such circumstances it is probably reflex in character. The 
pain may be increased in severity by pressing the left lobe of the liver 
against the diaphragm. It varies in severity ; sometimes it is very slight, 
again it is of a sharp, lancinating character, and sufficiently severe to de- 
mand immediate relief. With the pain there is always more or less cardiac 
palpitation, a dry irritable cough, and a sense of constriction over the whole 
chest, with more or less dyspnoea ; the intensity of the dyspnaea will vary 
with the amount of the fluid effusion. When the effusion is considerable 
and there is orthopncea the patient becomes restless and the eountenance 
assumes an anxious expression, with a painful look of suffering somewhat 
characteristic ; he assumes the half-sitting posture, leaning somewhat 
toward the left side. Lying on the back with the head elevated, is the 
position usually preferred when the effusion is not large. The face is often 
livid. 

At first the pulse is full and strong, ranging from 90 to 120 beats in the 
minute, — after the fluid effusion has taken place, it becomes feeble, sup- 
pressed and sometimes delayed. If the effusion is abundant the pulse has 
a tendency to become irregular, and not infrequently intermitting ; it is 
always out of proportion to the activity of the heart and strongly dicrotic. 
The temperature usually rises one or two degrees, — in some cases it may 
rise as high as 10£-° F. In fatal cases the temperature falls toward the 
close of life, sometimes below normal. Jaundice sometimes occurs and 
headache and dizziness are frequently present ; in the severe forms of the 
disease there is often delirium, the patient sometimes becoming so furious 
as to require restraint ; at other times it is low and muttering. The de- 
lirium is often accompanied by delusions, tetanic or clonic spasms, and in 
rare cases convulsions occur, rapidly passing into coma and followed by 
death. Usually when the fluid effusion takes place, the acuteness of the 
symptoms subsides, and the patient experiences a sensation of oppression 
referable to the precordium, — he is disinclined to make any movement, for 
the least motion of the body gives rise to a sinking sensation with a 



458 



DISEASES OE THE HEAKT. 



tendency to syncope. Painful hiccough accompanies this symptom. The 
patient is now constantly in danger of sudden and fatal syncope from press- 
ure of the pericardial accumulation upon the heart. Some maintain that 
sudden and fatal syncope never occurs in primary pericarditis, but that it 
is met with only after several attacks have occurred, and more or less ex- 
tensive pericardial adhesions have taken place. This is not necessarily the 
case, for whenever large fluid effusions are developed, with the attendant 
weakening of the cardiac walls from superficial myocarditis, patients are 
constantly in danger from sudden syncope. 

The severity of the symptoms in pericarditis corresponds to the intensity 
of the inflammation and the amount of the effusion ; if the inflammation 
is slight and the effusion moderate, the plastic exudation predominating, 
none of these symptoms will be present, and the subjective symptoms will 
only serve to attract attention to the heart as the seat of disease. 

The subjective symptoms in many cases of pericarditis being so obscure, 
often altogether wanting, the physical signs become all important. In fact, 
in all cases of acute articular rheumatism, for the first two weeks it is an 
imperative duty each day to make a careful physical examination of the 
heart, especially if its action becomes irritable and the apex-beat is increased 
in force. Delirium in acute rheumatism ought at once to direct attention 
to the heart. The same care in examination should also be exercised in 
Bright's disease when convulsions or coma occur ; and in severe acute infec- 
tious disease the heart will often be found implicated. 

Physical Signs. — These vary with its different stages. In the early stage 
the only sign, furnished by inspection and palpation is an irritable, turbulent, 
forcible, and sometimes irregular action of the heart. 

Palpation gives a friction-fremitus in a few cases. There is no change 
in the normal area of precordial dulness. 

On auscultation the first positive physical signs of pericarditis are the 
pericardial friction sounds. They may be grazing, rubbing, or creaking 
in character. These friction sounds may be single or double, and may 
accompany the heart sounds or occur independently of them. They are 
always superficial in character and are generally restricted to the precordial 
space. Their point of maximum intensity is usually at the junction of the 
fourth rib with the sternum on the left side ; occasionally they will not be 
audible at this point, but will be heard over the large vessels at the base of 
the heart ; when this is the case it indicates that only a small extent of the 
pericardium is involved, and that the inflammatory changes are confined 
to that portion of the pericardium which covers the large vessels. When 
absent, as they sometimes are, their absence may be due to softness of the 
fibrin, feebleness of heart action, or alteration in, or abnormal position of, 
the lungs. Pericardial friction sounds may be increased in intensity by 
changing the position of the patient : when the body is thrown forward 
the heart will be brought nearer to the anterior wall of the chest and the 
friction sound will be more distinctly audible. These friction sounds will 
also be increased in intensity by a full inspiration, for the distended lung 
will press the two pericardial surfaces together and thus intensify the rub- 



ACUTE PERICARDITIS. 



459 



bing sounds. In this way a single friction sound may become double. 
These sounds are usually of short duration, disappearing after a few hours, 
or at most in a few days. 

As soon as the stage of effusion is reached and liquid is poured into the 
pericardial sac, the friction sounds disappear and another class of physical 
signs are developed which mark the effusive stage of pericarditis. 

Inspection now shows a diminution in the respiratory movements over 
the precordial space, and if the pericardial sac is distended — especially in 
children and young persons — there will be arching forward of the precordial 
region ; this arching forward may extend from the second to the sixth in- 
tercostal space. On lying down the apex-beat often becomes more promi- 
nent. This bulged portion does not move with the rest of the thorax in 
respiration. 

Palpation shows the point of the apex-beat to be raised and carried to the 
left of its normal position. This raising of the apex-beat is never actual 
— only apparent — for as the fluid accumulates the apex is pushed further 
back from the anterior wall of the chest, and the portion of the heart that 
is nearest to the chest wall appears to strike it and cause an "apex- 
beat," which is nearer the base the more fluid there is in the pericardium 
— a simple physical phenomenon dependent upon the " conicity " of the 
heart and the pear-shaped sac in which it hangs. The cardiac excitement 
and friction-fremitus which might have been present before the effusion 
occurred disappear, and if the effusion is large the apex-beat becomes im- 
perceptible. Sometimes in extreme pericardial effusion an undulating 
impulse is communicated to the hand as it rests on the chest walls, by 
the action of the heart in the fluid 

On percussion, if the pericardium is distended with fluid, the area of 
precordial dulness is found to be 



increased in every direction, espe- 
cially laterally and vertically. The 
shape of the enlarged area corre- 
sponds to the pyramidal form of 
the pericardial sac. Eecent experi- 
ments prove that the triangular 
or pyramidal dulness is not due to 
the shape of the pericardial sac, 
but to the retraction of the edges 
of the lung. In a lateral direc- 
tion the precordial dulness may 
extend from one nipple to the 
other ; it may extend upward as 
high as the second or the first rib, 
or above the clavicle, and down- 
ward somewhat beyond the nor- 
mal limits. A small amount of 
effusion is denoted by an increase 
in the width of the precordial area 




Fig. 92. 

Diagram illustrating the Physical Signs of Pericarditis 
when the pericardial sac is distended with fluid. 



460 



DISEASES OF THE HEART. 



of d ulness at the lower portion of the precordial region ; if emphysema 
exists the changes in the area of dulness will be less marked. 

Upon auscultation an absence of respiratory murmur is noticed over all 
that space which is normally occupied by lung tissue, the lungs being 
pushed to the right and left by the distended pericardial sac. The friction 
sound which may have been present before the occurrence of the effusion 
disappears and the heart sounds become feeble or indistinct. In most 
cases the fluid disappears rapidly within a week or ten days. 

Stage of Absorption. — As recovery takes place and the effusion is absorbed, 
the area of precordial dulness decreases and the pericardial surfaces again 
come in contact and the friction sound reappears, the heart sounds will be- 
come more distinct, the apex will assume its normal position, the cardiac 
impulse will regain its normal force, and the respiratory and vocal sounds are 
again heard over the space formerly occupied by the distended pericardium. 
If the anatomical changes developed in the substance, and on the surface of 
the pericardium, have been extensive, as the two pericardial surfaces come 
together they may become firmly adherent and all motion between the 
heart and pericardium cease. This condition cannot be recognized by phys- 
ical examination — it is only to be inferred from the history of the case. 
If one who has had all the symptoms of pericardial effusion which has 
been followed by a friction sound that has gradually disappeared, leaving 
a slight intermittent action of the heart, suffers on active exertion from a 
sense of constriction above the precordial region, it may be inferred that 
the two surfaces of the pericardium have become adherent. Pericardial ad- 
hesions, whether general or in bands, may undergo absorption, and if a sec- 
ond attack of pericarditis is not developed motion between the two surfaces 
will be restored, and the only evidence of the disease will be the milky 
patches on the pericardial surface found at the autopsy. 

Differential Diagnosis. — The existence of pericarditis can never be positive- 
ly determined except by its physical signs ; even when attention has been 
directed to the heart it is not always easily recognized. Its physical signs may 
be confounded with those of endocarditis, pleurisy, and cardiac hypertrophy. 

The friction murmurs of pericarditis may be distinguished from endocar- 
dial murmurs -.—first, by their superficial character. Second, by their lim- 
ited area of diffusion, their maximum area of intensity being over the right 
ventricle and the junction of the fourth rib with the sternum ; while endo- 
cardial murmurs are audible beyond the pericardial limits to the right and 
left, upward along the course of the vessels and sometimes in the back. 
Third, the intensity of a pericardial friction sound may be increased or di- 
minished by inclining the body of the patient forward or backward, and 
it is rendered more distinct by a full inspiration ; whereas endocardial 
murmurs are not changed in intensity by a change in the position of the 
patient, nor by the period of time of the respiratory movement. Fourth, 
pericardial friction sounds are not necessarily synchronous with the heart 
sounds and may be double; while endocardial murmurs always pre- 
cede, take the place of, or follow heart sounds. Pericardial sounds are 
more grating, rubbing or creaking in character than endocardial. 



ACUTE PERICARDITIS. 



461 



Pericardial friction sounds may be distinguished from the friction 
sounds of pleurisy when the pleurisy occurs over the precordial space, by 
directing the patient to hold his breath for a moment ; if the friction 
sound is pericardial it will continue during the suspension of the respira- 
tory act — if it is pleuritic the friction sound will cease during the arrest of 
respiration. Occasionally, however, where there is consolidation of the 
lung directly over the heart, accompanied by a pleuritic friction, and firm 
adhesions having taken place between the two surfaces of the pericardium, a 
distinct friction sound may be produced in the pleura by the motion of the 
heart. This is of rare occurrence and is hardly to be taken into considera- 
tion. In this case the general bodily condition and the state of the pulse 
may aid us. 

The abnormal area of percussion dulness produced by hypertrophy or 
dilatation of the right ventricle very closely resembles that produced by peri- 
cardial effusion, and it is often exceedingly difficult to draw a distinct line 
between them. There is one point which may be regarded as diagnostic : 
that is, in enlargement of the right heart the precordial dulness never ex- 
tends to the left beyond the apex-beat, while in pericardial effusion it may 
extend one or two inches beyond the apex-beat. The fact that cardiac 
dulness extends to the left of the apex-beat proves that there is more or 
less fluid in the pericardial sac. The outline of dulness is quadrilateral 
in dilatation, and triangular in pericardial effusion. Besides, in cardiac 
hypertrophy there is an increase in the force of the apex- beat, and an ab- 
normal intensity to the heart sounds ; in pericarditis both will be dimin- 
ished in intensity. Pericardial effusion is distinguished from hypertrophy 
or dilatation of the left heart by the fact that in left cardiac hypertrophy the 
apex-beat is carried downward and to the left, and the area of precordial 
dulness is increased in the same direction and not to the right. The 
force of the heart's action is greatly increased in left ventricular hypertrophy. 

Prognosis. — In most instances pericarditis ends in complete recovery. 
The exceptions to this rule are met with almost exclusively in connection 
with Bright's disease and septic or pysemic conditions. In connection with 
either of these diseases there is always more or less danger ; if it occurs in 
connection with pyaemia, the danger is very great, for the exudation in 
such cases is usually purulent and its absorption can hardly be expected, 
although it does occur. A large amount of fluid may compress, and cause 
paralysis of the heart, death resulting in a few hours. The nature of the 
exudation determines to a great extent the prognosis ; when it is hemor- 
rhagic or purulent, the prognosis is bad. Eheumatic pericarditis is rarely 
fatal. Occasionally, acute pericarditis passes into chronic, or rather is ac- 
companied by a large serous effusion, which disappears slowly, and is es- 
pecially liable to be accompanied by relapse, and thus the disease goes on 
for months. During its progress the patient suffers from repeated attacks 
of extreme dyspnoea ; in rare instances a fatal syncope occurs. 

As a result of the long continuance of the fluid effusion the substance of 
the heart becomes softened and its muscle undergoes more or less degener- 
ation, on account of which its propelling power is diminished, and death 



462 



DISEASES OE THE HEART. 



by oedema of the lnngs may occur ; or any sudden effort may result in in- 
stant death. This form of subacute or chronic pericarditis is generally as- 
sociated with blood changes attended by a loss of red corpuscles and fibrin, 
and must always be regarded as a grave disease. The most frequent 
sequelae of acute pericarditis are adhesions of the two surfaces of the peri- 
cardium, cardiac dilatation, and hypertrophy. Cardiac dilatation occurs 
as the result of the weakening of the cardiac walls from myocarditis. The 
hypertrophy of the cardiac walls which follows this dilatation is compensa- 
tory. Occasionally the pericardial exudation is abundant, and extensive 
pericardial adhesions take place at the base of the heart, which, by their 
contraction and pressure, interfere with the current of blood through the 
coronary arteries, and as a result the nutrition of the heart is impaired and 
fatty degeneration of its walls may be developed. The duration of peri- 
carditis is from one to three weeks ; some cases end fatally in a few hours 
from sudden heart failure. 

Treatment. — We have to deal with an inflammation of considerable sever- 
ity, yet from our knowledge of its etiology and morbid anatomy we are not 
warranted in the use of a single antiphlogistic measure. Blood-letting, 
hydragogue cathartics, diuretics and blisters, which at one time were 
almost universally employed, are now abandoned ; the tendency is toward 
a supporting plan of treatment. As soon as it is discovered that peri- 
carditis exists, endeavor to determine its cause, and, if possible, remove it ; 
if this is not possible, endeavor to counteract it. If the pericarditis is due 
to uraemia, employ those means which favor elimination of urea. If it ac- 
companies articular rheumatism it must be treated as a rheumatic affection. 
In those acute diseases marked by great depression the occurrence of peri- 
carditis is an indication for an increase in stimulants. Under all such cir- 
cumstances, especially in connection with septic and pyaemic developments, 
supporting measures are early called for. The favorite local applications 
in its early stage are hot anodyne poultices over the precordial space in con- 
nection with the internal administration of opium ; absolute rest in bed 
must be enjoined. If the pulse exhibits diCrotism, stimulants in small 
quantities may be given. 

Opium is the most valuable internal agent. It should never be given in 
large doses, but only in sufficient quantities to relieve pain and arrest or al- 
lay an irritable action of the heart. The largest doses administered should 
be given at night, in order that the patient may secure quiet sleep ; the 
heart is more liable to become irritable at night, and the patient usually be- 
comes more restless. Great care should be exercised in the administration 
of opium ; it should never be carried to semi-narcotism. Chloral is thought 
to be equally good, since it does not interfere with secretions ; my expe- 
rience is against its use. 

The means usually employed for removal of the fluid are hydragogue 
cathartics, diuretics and blisters. I am convinced that this plan of treat- 
ment will not hasten, but will rather delay the removal of the fluid. Ex- 
perience teaches that pericarditis is an inflammation which occurs in the 
weak and feeble, and not in the strong and vigorous ; it is met with among 



CHROMIC PERICARDITIS. 



463 



the young rather than in healthy persons in the prime of life. In almost 
all instances it is associated with those diseases that are especially marked 
by a loss of vitality ; consequently all measures that have a tendency to 
depress .the patient are to be avoided. Blisters are apt to accelerate the 
heart's action and should never be applied directly over the precordial 
space ; leeches are less painful and more efficacious, and may be applied 
over the precordial space. The same general rules which were given as 
guides in promoting the absorption of the inflammatory product in pleu- 
risy are to be followed in the treatment of pericarditis. Iron, stimulants, 
and a highly nutritious and readily digestible diet are the most efficient 
remedies. Anything which accelerates the heart's action should be 
avoided. 

The surface of the chest must be carefully protected from changes in tem- 
perature ; any exposure incident to a physical examination of the chest must 
be carefully avoided. The Germans advocate cold to the precordia ; it is said 
to diminish pain and frequency of the heart's action. They direct that an 
ice-bag shall be kept over the precordial space until all evidences of peri- 
carditis have disappeared. I cannot recommend this plan of treatment. 

During the period of convalescence the patient must be very strictly 
guarded, for the walls of the heart are in a weakened condition, and 
should not be overtaxed. Everything which will have a tendency to 
increase the action of the heart must be carefully avoided. Children 
should not be allowed to go up and down stairs or to play with other 
children during the period of convalescence. Patients convalescing from 
pericarditis must be placed under the very best hygienic conditions for two 
or three months after the disappearance of the pericardial symptoms. 

Sometimes the symptoms which attend a large fluid effusion become very 
urgent, and the question presents itself : — shall aspiration of ilie pericar- 
dium be performed ? It has been claimed that little danger attends its per- 
formance, but it should never be rashly undertaken. When it is positively 
determined that pus is in the pericardium aspiration should be practised. 
When the effusion is sero-fibrinous it must be remembered that the urgent 
symptoms, for the relief of which aspiration would be resorted to, are usu- 
ally of short duration, and patients rarely die from the pressure produced 
by the effusion. Whether aspiration shall be performed under such cir- 
cumstances is a question for most careful consideration. 1 

CHEO^IC PERICARDITIS. 

Chronic pericarditis is rare except as a sequela of acute ; occasionally it 
may be sub-acute from its commencement. When, after three or four 
weeks, acute pericarditis does not terminate in recovery, it becomes chronic. 
In some cases of chronic pericarditis the pericardial sac contains several 
pounds of fluid. In others firm adhesions form between the pericardial sur- 

J In a monograph by Dr. Roberts, who gives an account of sixty cases with twenty-four recoveries 
(forty per cent.), he states that the best points to tap are in the fossa between the ensiform and costal 
cartilages on the left side, or in the fifth left interspace near the junction of the sixth rib with its carti- 
lage. In Huidenlang's case 1000 c. c. were withdrawn at two tappings and recovery followed. ( A.rchiv. f. 
klin. Med. 24, p. 452.) 



464 



DISEASES OF THE HEART. 



faces, binding them more or less closely to each other ; mingled with these 
adhesions are chalky debris and calcareous plates. The adhesions which 
form in acnfce pericarditis are not regarded as a part of the history of 
chronic pericarditis. The fibrous changes of chronic pericarditis only 
occur when the sub-pericardial tissue is involved. The heart may then 
be encased in a calcareous wall, and a fibrous degeneration of the cardiac 
muscles result, which may lead to local aneurismal dilatation. 

The Symptoms of chronic pericarditis are those which give evidence of 
obstructed circulation with signs of enlargement of the heart. This en- 
largement may be due to hypertrophy, but is more frequently dependent 
upon dilatation of the cardiac cavities. There is dyspnoea sometimes 
amounting to orthopncea and uneasiness or a sense of weight in the pre- 
cordial region. In some instances this condition is associated with attacks 
of angina pectoris. The heart's action is easily disturbed, and cardiac 
palpitation is present on slight physical exertion or mental excitement. 

The Physical Signs of chronic pericarditis closely resemble those of eccen- 
tric cardiac hypertrophy ; in both cases there is increased dulness in the pre- 
cordial region, but in pericarditis the apex-beat is indistinct and is raised 
above its normal position ; while in hypertrophy the apex-beat is distinct 
and is carried downward and to the left of its normal position. A friction 
murmur is usually heard even when a large amount of fluid is present. 
There is no murmur in hypertrophy. Bulging sometimes occurs, and 
there may be fluctuation when the fluid is large in amount. If the two 
surfaces of the pericardium are closely agglutinated, and the pericar- 
dium is adherent to the costal pleura, so that firm adhesions are formed 
between it and the chest wall, there will be more or less depression of the 
precordial region — so-called "systolic depression;" the cardiac impulse 
will be permanently displaced upwards, and will be unaltered either by 
change of posture or by a full inspiration, and there will be an irregular 
jogging motion of the heart during both its systole and diastole. Some- 
times there is a depression over the scrobiculus cordis, caused by adhesion of 
the two layers of the pericardium to each other and to the pleura covering 
the diaphragm, and concomitant adhesion of the diaphragm with the liver. 

Although the Diagnosis of chronic pericarditis is always difficult, and its 
existence is rarely, if ever, positively determined unless there is a large 
amount of fluid effusion in the pericardial sac, still, if the symptoms and 
physical signs already detailed follow an attack of acute pericarditis, there 
is presumptive evidence of its existence. 

The Prognosis in this affection, as regards complete recovery, is always 
unfavorable, and when it is accompanied by degeneration of the cardiac 
walls, and dilatation of the cardiac cavities with or without valvular in- 
sufficiency, sudden death is liable to occur during violent physical exertion. 

The Treatment consists in limiting physical exercise so as not to overtax the 
embarrassed heart; at the same time in furnishing the patient with a most nu- 
tritious but non-stimulating diet, and in administering daily some preparation 
of iron. When there is a large amount of effusion the same rules for the per- 
formance of paracentesis are to be followed as in acute pericarditis. The oper- 
ation will be resorted to in chronic cases with better success than in acute. 



ACUTE ENDOCARDITIS. 



465 



ENDOCARDITIS. 



Endocarditis is an inflammation of the endocardium. I shall describe 
it under three heads, grouping the first two together : — 

I. Acute N on- infectious Endocarditis. 
II. Infectious or Ulcerative Endocarditis. 
III. Interstitial Endocarditis. 

In most instances this disease depends upon a constitutional dyscrasia 
characterized by alterations in the vital, physical, or chemical properties 
of the blood. Etiologically, all the different varieties are closely con- 
nected ; clinically and pathologically, they are distinct. They cannot be 
classified as acute and chronic m the ordinary acceptation of the terms, for 
some cases are at no time acute, and even in so-called chronic endocarditis 
the changes are but an advanced stage of an acute process. 

So-called acute endocarditis is accompanied by a fibro-cellular exudation 
into the substance of and underneath the endocardium, causing elevations 
of its surface. A common term for 
this variety is "acute exudative endo- 
carditis," it being understood that no 
exudation occurs on its free surface, 
but underneath it. This form may 
be entirely recovered from, or may 
lead to interstitial formative changes. 
Acute non-infectious endocarditis may 
become ulcerative as the result of sep- 
tic infection, giving rise to changes 
known as acute infectious endocardi- 
tis. 

Chronic or interstitial endocarditis 
is the form in which the endocardial 
and myocardial tissues are involved in 
sclerotic or cirrhotic changes, giving 
rise to the many varieties of valvular 
disease. It may be a sequela of the 
acute exudative variety, or the inflam- 
mation may have been interstitial from its commencement, for the valvular 
changes due to this form are often found in those who never have had 
either acute articular rheumatism, or acute endocarditis, but who are sub- 
jects of chronic rheumatism, syphilis, or gout. 




Fig. 93. 

drawing show ing the changes in a case of Diph- 
theritic Endocarditis. 

A. Thickening of the Endocardium on the free 
border of the mitral valve, with papillary 
elevations surmounted by fibrinous deposit. 



ACUTE ENDOCARDITIS. 

In adults the left, and in intra- uterine life the right, heart is oftenest 

affected. The process rarely extends beyond the valves and valvular 

orifices ; but it may involve the whole or any part of the ventricular or 

auricular portions of the endocardium. 

Morbid Anatomy.— The endocardium becomes infiltrated with cells, the 
30 



466 



DISEASES OF THE HEAET. 




Fig. 94. 

Drawing from the previous case showing similar changes 
upon the Aortic Valves. 



process beginning in the layer of flat cells. The new formative cells are 
developed in the layer underneath the endocardium. This hyperpla- 
sia is accompanied by softening of 
the intercellular structure, which 
is soon destroyed. The endothelial 
elements take part in the process. 
The masses of new cells push out 
the endocardium, and papillary 
elevation s are form ed . These con- 
ical elevations are surrounded in 
the deeper layers of the endocar- 
dium by a zone of proliferation 
which is never distinctly limited, 
but which exhibits progressive 
hyperplasia from the periphery 
toward the centre. All these 
changes may have taken place in 
non-vascular tissue. Where the 
capillaries are most numerous, a 
punctate or arborescent vascularity 
is seen, after which the part be- 
comes opaque. There is no exuda- 
tion upon the papillary elevations, 

A. A. Aortic, B. B. Mitral Valves showing papillae and but fibrin from the blood is depOS- 
fibrinous deposit. ^ j^ Qm ag on f ore jg n bodies. 

These coagula are most numerous on the surface opposed to the blood current. 
They have a cauliflower-like, bulbous extremity connected by a constricted 
neck with a firm, hard base which is contin- 
uous with the subjacent tissue. Each mass 
is covered by a thin hyaline layer. At first 
these vegetations are so small and numer- 
ous that the membrane has a granular look. 
Later, they enlarge, sometimes to the size 
of a pea, and have a conical or raspberry- 
like shape. They are arranged on the bor- 
ders of the aortic valve near the edge, their 

p ' Fig. 95. 

seat being determined by the limit of the Vertical Section of an Aortic V alve in Acute 

vascular network. The bands of tissue 
passing from the attached valvular bor- 
der to the corpus Arantii in the centre 
show the granulations most distinctly. Near the insertion of the tendons 
upon the auricular surface of the mitral valve are irregular wreaths of vege- 
tations enclosing attachments of the chordae tendineae. Friction of these 
vegetations or coagula upon the endocardium, may excite an endocarditis at 
points remote from the valves. The chordae tendineae may adhere to one 
another. From these adhesions stenosis may result, by the flaps becoming 
agglutinated to each other, or regurgitation by their adhering to the heart- 
walls. As a result of these changes, new vessels appear in the substance of 



C 




A. Endocardium. 

B Papillary elevation. 

(J. Fibrinous deposit, x 60. 



ACUTE ENDOCAKDITIS. 



4G7 



the mitral valve, or existing ones become more apparent. The more rapid 
the course, the more marked are these changes. The largest vegetations are 
found on the valves. Young vegetations are translucent, soft, and friable. 

Infectious or Ulcerative Endocarditis. — Necrotic changes with loss of 
tissue may occur in non-infectious endocarditis, but by general usage the 
term "ulcerative" has come to signify the infectious form of the disease. 

It is oftenest met with in pyaemia, puerperal fever, scarlatina and diph- 
theria ; it has been called "septic" and "diphtheritic" endocarditis. 
When ulceration of the endocardium is of specific origin, the primary 
changes are associated with the entrance of bacteria, which invade the 
membrane from the blood-current, and induce necrotic changes that may 
be well advanced before there are any distinct evidences of reactionary 
inflammation. White cell infiltration, however, of both the necrotic mass 
and the surrounding tissue, rapidiy supervenes. This is followed by dis- 
integration and sloughing of the affected portions. The margins of the 
valves are irregular, but well defined. The edges are swollen and thick, 
and their floor is infiltrated with pus. In some case the apices of the 
vegetations which are formed are swept off by the blood-current, and an 
ulcerated surface is left. If their removal causes great loss of substance, 
perforation of the valve may occur. These perforations are sometimes 
closed or hidden by a fibrinous exudation. Micrococci and other bacteria 
are found in ulcerative endocarditis of a septic origin, and have given to 
it the name of "mycosis endocardii. , ' > 1 

The valvular ulcerations in this form of endocarditis may give rise to 
various lesions. If small masses are detached from the cardiac orifices, 
either from deposits on the valves or from ulcerations, and enter the blood- 
current, they originate morbid processes in the organs to which they are 
carried. It is important to distinguish between the results produced by 
displacements into the blood-current of large masses, and those arising 
from the entrance of molecular fragments. Masses from the vegetations, 
or from the ulcerated valves in infectious endocarditis, being stamped with 
a septic element, lead to the development of suppurative infarctions in 
different organs. The size and site of the emboli are important ; they 
may be so large as to obstruct vessels of the largest size, as the external 
iliac. When arteries in the lungs are thus plugged, the result is generally 
an isclimmia, often terminating in gangrene. Capillary embolism may 
occur in a number of organs simultaneously. 

When the cutaneous capillaries are obstructed, ecchymotic spots are 
formed, followed by cellulitis. If in cerebral embolism the occluded ves- 
sel is large, instantaneous hemiplegia and secondary softening will result ; 
if it is very small, softening develops without evidence of obstructed circu- 
lation. Infarctions and suppuration of the spleen (splenitis, so called) are 
not uncommon. The kidneys may be similarly affected. Septic phenom- 
ena are very important. When typhoid symptoms, deep jaundice, and 
symptomatic intermittent fever are associated with endocarditis, it estab- 
lishes its "ulcerative" character. When the inflammation develops rapidly, 
the valves soften, lose their resisting power, and in time become stretched, 

1 Jaccoud. Klebs. 



468 



DISEASES OF THE HEART. 



bulged, or torn by the blood- current. A rupture of the mitral valves will 
open into the auricular, and that of the aortic into the ventricular cavity. 

If the blood penetrates a rent in the flap of the valves, the endocardium 
is puffed out and a "valvular aneurism" is formed; round or funnel- 
shaped aneurismal sacs may project from the valves ; the bottom of one of 
these sacs may be perforated, and long, ragged, gray shreds covered with 
fibrin may hang into the ventricular cavity. When the ulceration is situ- 
ated in the ventricular wall, the pressure of the blood may bulge out the 
heart-wall and give rise to "partial cardiac aneurism." Communication 
between the various heart cavities may thus be established. The results of 
both varieties of acute endocarditis will be considered under the head of 
" interstitial endocarditis.'' 

Etiology. — Acute non-infectious endocarditis is rarely, if ever, idiopathic. 
Germain See claims that all endocarditis is of bacterial origin, but I am 
unwilling to admit this from either a pathological or clinical standpoint. 
It is closely connected with those diseases and dyscrasise in which the 
blood is altered either in the relative proportion of its constituents or in its 
physiological elements. Endocarditis is so frequently associated with acute 
articular rheumatism that they are often described as one disease. It is 
said to occur in fifty per cent, of all cases, but the statistics of Bellevue 
Hospital show that it complicates only thirty-three and one-third per cent, 
of the cases. The irritation caused by blood, the salts of which are 
changed, or which contains excrementitious products or a specific poison, 
is shown most markedly upon the valvular surface of the endocardium ; 
and for this reason the parts most exposed to friction are those which first 
and most extensively exhibit its pathological changes. 1 There is no disease 
characterized by a morbid condition of the blood in which endocarditis 
may not occur : thus it often complicates the essential fevers, the exan- 
themata, diphtheria, Bright's disease, and syphilis. When an individual 
who is already suffering from valvular disease of the heart is attacked with 
acute rheumatism, the liability to endocarditis is much increased. Even 
when rheumatism and chorea are absent, endocarditis is liable to occur 
when valvular disease exists. 

Some regard myocarditis, pericarditis, pleurisy, and pneumonia as capa- 
ble of exciting endocarditis by the extension of the inflammatory process 
from the surface of the heart ; this is questionable, but that it can result 
from traumatism is possible. 2 

Wunderlich ranks measles next to rheumatism as a cause of endocarditis. 
We must remember that not every "blowing" murmur is indicative of 
endocarditis. Bamberger and Nierneyer think that the excited and irregu- 
lar action of the heart in children, by inducing irregular tension of the 
valves, will bring about a "blowing" sound during acute rheumatism 
without endocarditis. 

Infectious endocarditis is met with in pyaemia, puerperal fever, scarla- 
tina, diphtheria, and it may occur secondarily to a septic inflammatory 

1 Charcot records a large number of observations in which endocarditis was developed in patients with 
chronic rheumatism, and in which it never assumed an acute form. It thus seems evident that organic 
valvular lesions from endocarditis may arise during chronic as well as acute articular rheumatism. 

2 Bamberger records two traumatic cases. 



ACUTE ENDOCARDITIS. 



469 



process located in any part of the body. It may also appear without any 
obvious cause, or in connection with some specific form of inflammatory 
disease, as croupous pneumonia. Wicks calls it then arterial pymmia. 
Eecent investigations have shown that infectious endocarditis depends 
upon bacterial action for its specific and ulcerative character. No single 
bacterium has been isolated as its sole cause. On the contrary, it seems 
probable that the bacteria of many different specific diseases may induce 
necrotic changes in the endocardium either directly or by causing such a 
lowered vitality in the endocardial tissue as renders it susceptible to the 
invasion of the common bacteria of suppuration. Experimentation upon 
animals has shown quite conclusively that some precedent lesion of the 
endocardium, either from traumatism or inflammation, is a necessary con- 
dition of such bacterial activity. 

Symptoms. — The subjective symptoms of acute non-infectious endocar- 
ditis are more obscure than those of any other cardiac disease. They are 
few, ill-defined, and without any regular order of development ; when the 
heart-muscle is not involved, the disease cannot be appreciated by a single 
rational symptom, for the urgency of the symptoms of the diseases in 
which it occurs often masks the few symptoms which attend its develop- 
ment. But when it is extensive and the muscular tissue of the heart is 
involved, palpitation and a sense of discomfort in the precordial region 
are present, and there may be attendant dyspnoea and decubitus on the 
left side. Seldom is the palpitation appreciable to the physician, for the 
heart may beat with force and be tumultuous, and yet the pulse remain 
unchanged. At first the pulse is strong and forcible ; later it becomes 
rapid, small, feeble, and irregular ; it is frequent from the onset. As a 
rule, the force of the pulse does not correspond to the cardiac activity, for 
as the heart-muscle becomes involved, its propelling power is diminished 
and the pulse becomes feeble, compressible, and sometimes dicrotic. The 
respirations are accelerated and sometimes labored ; there may be paroxys- 
mal dyspnoea, the face may be flushed, or it may be dusky, pallid, ashy-gray, 
or even cyanotic. Sleeplessness and nocturnal delirium are rare. When 
the muscular tissue of the heart is extensively involved, nausea, vomiting, 
giddiness, and syncope may be present, yet slight pain or a "tightness" is 
not an infrequent symptom when endocarditis occurs in those who have 
chronic valvular disease. The temperature seldom exceeds 103° F. 

When in infectious endocarditis a valve ruptures, usually a typhoid state 
rapidly supervenes. The patient is forced to assume the upright posture 
on account of dyspnoea ; cyanosis is sudden and extreme, and the symp- 
toms of multiple embolism appear. The temperature rises to 106°-107° 
F. There are jaundice, and frequent rigors, which, with the paroxysms of 
fever, simulate the icteric form of malarial fever. The spleen becomes 
enlarged and tender ; the urine is scanty, dark-colored, albuminous, and of 
high specific gravity. Delirium and coma occur in severe cases. Some 
cases are marked by nausea, vomiting, and diarrhoea. The frequency with 
which this form of endocarditis is associated with pneumonia suggests the 
presence of a blood-poison of great intensity. 

The symptoms of embolism are more frequent in infectious than in any 



4:70 



DISEASES OF THE HEART. 



other form of endocarditis. The spleen is much oftener the seat of embol- 
isms than the kidney or brain, but they may occur in any organ and give 
rise to characteristic local symptoms. The occurrence of hemiplegia with 
aphasia, or of severe cerebral disturbance, during the course of an endocar- 
ditis, is indicative of cerebral embolism. 

Physical Signs. — Inspection sometimes shows the area of cardiac impulse 
greater than normal ; the impulse is irregular and often tumultuous. 
Later the apex-beat and the impulse grow more indistinct, but never so 
suddenly or so markedly as in pericarditis. In children the vessels of the 
neck may exhibit venous stasis. 

Palpation. — At the onset of the disease, the cardiac impulse is more 
forceful than normal, and the heart's action is frequently irregular. Some- 
times the heart thumps violently against the chest-walls. The force of the 
cardiac impulse varies from day to clay, being stronger when pain is 
present. If, during the disease, there is no increase in the force of the 
apex-beat, we infer that the muscular power of the heart is deficient. 
When acute endocarditis supervenes upon long-standing valvular disease, 
there is alternate increase and diminution in the area and force of the im- 
pulse. When the heart walls are weakened by myocarditis, or when the 
endocarditis is itself very extensive, the force of the apex-beat is diminished; 
an endocardial thrill is often present. 

Percussion. — The area of cardiac dulness is normal unless changes at 
the valvular orifices retard the outflow of blood from the lungs, and then 
the cavities in the right heart become engorged and the area of dulness 
will be abnormally increased. But this increase is always slight, except in 
those cases where sudden and extreme distention of the heart cavities re- 
sults from the presence of masses of fibrin. Extensive myo- or endocar- 
dial inflammation may so weaken the heart that dilatation results, and then 
percussion will show marked increase in the area of cardiac dulness. 

Auscultation reveals a murmur, or murmurs, over the various cardiac ori- 
fices. The fact that valvular disease may have pre-existed makes it impor- 
tant to carefully examine the heart at the first visit to one suffering 
with acute rheumatism, chorea, Bright' s disease, etc. When hypertrophy 
and old valvular disease of the heart exist, the advent of an attack of 
acute endocarditis generally passes unrecognized, and even its presence is 
often undetermined. The most important constant sign of endocarditis is 
a systolic murmur, heard with greatest intensity at the apex ; this soft, 
blowing, or "bellows" murmur may be ventricular or valvular. In all 
cases it is due to roughening or thickening of the endocardium. It often 
changes its point of maximum intensity during the acute period of the 
disease. It is developed early, and when one is on the lookout for endocar- 
ditis this will be the first evidence of it. In some instances no murmur 
is at any time present. 

A mitral murmur alone occurs in fifty per cent, of cases of rheumatic- 
endocarditis ; it is developed early and is preceded by prolongation of the 
first sound, a " transition " sound, so to speak, feeble and wavering in char- 
acter, extending over the slight interval which normally exists between the 
first and second sounds. Other changes, not murmurs, but which precede 



ACUTE ENDOCARDITIS. 



471 



them in many cases — are loud, ringing normal sounds ; — muffled first 
sound; — feeble first, intensified second sound; — doubling of the first sound; 
— "roughening" of the first sound ; — and a " humming " over the right 
heart. Complete absence of the heart sounds is a rare but possible ante- 
cedent of an endocardia] murmur. A mitral murmur, in acute endocar- 
ditis, is usually audible oyer a limited area. It is the exception to hear it 
both in front and at the back ; very frequently it is heard most distinctly 
over the stomach. When the pulmonary circulation is greatly obstructed, 
it causes an extra strain on the pulmonary valves, and then the second 
sound will be accentuated, while the first pulmonic sound may be feeble or 
absent. Reduplication of the second sound in mitral endocarditis is proba- 
bly due to the difference in time occupied by the ventricles in emptying 
themselves. 

A tricuspid murmur occurs in fifty percent, of the cases of acute mitral 
endocarditis; & pulmonic murmur in about one-third of the cases. They 
are superficial and " scratchy " in character, and indicate a relaxed condi- 
tion of the vessels and a thin state of the blood. They are never perma- 
nent. Mitral endocarditis is accompanied by aortic murmurs in about 
sixteen per cent, of the cases, and these murmurs are usually soft and 
blowing, but may be "musical." "whistling," or " twangy." 

In aortic endocarditis the second sound is usually lost over the carotids. 
In about twelve per cent, of all cases of acute (rheumatic) endocarditis a 
regurgitant murmur will be heard over the tricuspid orifice. Tricuspid 
murmurs are present in fifty per cent, of all cases of recent mitral mur- 
murs ; in forty per cent, of recent aortic murmurs, and in twenty-five per 
cent, of mitro-aortic murmurs. They are due to an increase in the slight 
(normal) insufficiency of the tricuspid valves. Such murmurs are of short 
duration, vibrating in character, and heard over the right ventricle. In 
children aortic endocarditis is rare ; at this period obstruction at, and re- 
gurgitation through, the mitral orifice commonly occur together. 

Differential Diagnosis. — Acute non- infectious endocarclitis may be mistaken 
for pericarditis, and its murmur maybe mistaken for that produced by 
aortitis or for those friction murmurs that develop during fevers. The 
friction-sounds of pericarditis are superficial and limited to the precordial 
space, while those of endocarditis are distant, and each murmur will have 
its area of diffusion beyond the precordial space. A pericardial sound is 
distinctly a friction, creaking, or rubbing sound, and it has a " to-and- 
fro" character, while that of endocarditis is soft and blowing. Endocar- 
dial murmurs accompany the heart sounds, while pericardial friction sounds 
are not always rhythmical with the heart sounds. The intensity of a peri- 
cardial sound is increased when the patient bends forward, at the end of a 
full inspiration, or when the stethoscope is pressed firmly over the pre- 
cordial region, and in the last instance it becomes "grazing " and " rub- 
bing" in character. As soon as effusion occurs in pericarditis, alteration 
in the character of the pulse, increase in the area of precordial dullness, and 
the disappearance of adventitious sounds, will decide the diagnosis. 

Aortitis has many of the symptoms of endocarditis, but in addition the 
pulse is more rapid, the respirations are more hurried, and pain is present 



472 



DISEASES OF THE HEART. 



in the precordial region, shooting down the spine and increased by motion. 
Aortitis is often accompanied by cutaneous hyperesthesia. Acute aortitis 
is very rare. 1 

The functional murmurs which occur in fevers are usually heard only 
at the base of the heart ; while those of endocarditis are most frequent and 
distinct at the apex. There are no signs of obstruction present with febrile 
murmurs, while they are frequent with endocarditis. 

It is difficult to tell whether a murmur is of old or recent origin. If 
during an attack of rheumatism a murmur is developed under daily exami- 
nation, it indicates acute endocarditis. If a murmur exists at the first 
examination, systolic, soft, blowing, and unaccompanied by cardiac hyper- 
trophy, there is reason to believe that it is due to an acute endocardial 
inflammation ; but should it be rough, diastolic, and accompanied by car- 
diac hypertrophy, it is probably not due to acute endocarditis. 

Prognosis. — Acute non-infectious endocarditis is rarely a direct cause of 
death, and is seldom completely recovered from. Acute mitral endocar- 
ditis ends in permanent valvular disease in twenty-five per cent, of the 
cases. The prognosis is rendered unfavorable when the signs of embolism 
or metastasis occur. Sudden splenic enlargement, with tenderness, albu- 
minuria, or hemiplegia, when accompanied by the physical signs of acute 
insufficiency or perforation of a valve, with cyanosis, dyspnoea, and dis- 
turbance of the cardiac rhythm, will render the prognosis bad. All these 
symptoms suggest infectious endocarditis, so that when the symptoms of 
this disease appear during the course of septic diseases, the liability to its 
occurrence must be borne in mind. Typhoid symptoms in acute endocar- 
ditis render the prognosis unfavorable. In children bronchitis, lobular 
pneumonia, and intercurrent diarrhoea may cause death. It may result 
from acute insufficiency of the heart. 

In cardiac aneurism death may result from rupture of the sac, apo- 
plexy, or from secondary disease in organs. 

Treatment. — The treatment of both varieties of acute endocarditis must 
be determined by the conditions under which they occur. The patient 
must have absolute rest in bed in a room whose temperature is never 
below 70° to 75° F. The chest should be covered with flannel, and dur- 
ing the physical examination it should be exposed as little as possible. 
Some claim that an ice-bag over the heart during the acute period will 
arrest or limit the inflammation, but my own experience does not sustain 
this statement. In rheumatic endocarditis anti-rheumatic remedies are 
indicated. The joints must be kept absolutely at rest in the most com- 
fortable position, and the pain relieved. If the urine is kept alkaline, the 
liability to endocarditis is diminished. To ensure rest, small doses of 
opium may be given, but opium cannot be administered as freely as in 
pericarditis. The patient's strength must be sustained by the judicious 
use of concentrated nutriment with some preparation of iron. 

When endocarditis, accompanied by typhoid symptoms, occurs with sep- 
tic lesions, alcohol, quinine, and iron must be freely administered ; when 
it complicates Bright's disease, the rapid elimination of urea must be estab- 

1 Lebert and Rindfleisch doubt its existence. 



INTERSTITIAL ENDOCARDITIS. 



473 



lished. The pain over the precordium is often relieved by the application 
of a few leeches. The (internal) use of mercury, with the external appli- 
cation of blue ointment to "lessen the plasticity of the blood/'' and even 
the use of iodide of potassium — "for the absorption of the fibrinous exu- 
dation " — are harmful, and the theory of their use has no foundation. A 
single case of recovery from infectious endocarditis has been reported, in 
which the treatment consisted in the use of sulpho-carbolate of sodium and 
inunctions with carbolized oil. 

INTERSTITIAL ENDOCARDITIS. 

Kreizing first traced the relationship between chronic valvular diseases 
of the heart and interstitial endocarditis. 

Morbid Anatomy. — Interstitial (or chronic) endocarditis maybe a sequela 
of the acute, or it may be interstitial from its commencement, and be so in- 
sidiously evolved as to escape notice. Sometimes its lesions are confined to 
the edges or base of the valves ; at others the entire valve may be involved. 

The affected valves may be thickened, indurated, contracted, adherent, 
or degenerated. It is more closely allied to rheumatism, gout, and chronic 
interstitial changes in other organs than either of the other varieties ; 
no part of the endocardium is exempt from interstitial changes, but the 
endocardium over the valves and that at the apex of the left ventricle are 
its favorite sites. The mitral valves may become three or four times thicker 
than normal. Sometimes their functional activity is unaffected even after 
they have undergone extensive pathological changes. White, thickened, 
opaque spots, the results of interstitial endocarditis, are often found irregu- 
larly scattered over the internal wall of the heart cavities. When vegeta- 
tations are developed in interstitial endocarditis, they differ from those of 
the acute form, for they are firmer and less prominent, and rest upon an 
indurated base. In, and underneath, the endocardium there is tissue- 
increase, and fibrin is deposited on any prominence of the endocardium. 
These deposits are of various forms, and may extend for one-half an inch 
or more into adjacent vessels or cavities. They are usually globular or 
wart-like in form, and are situated on the ventricular surface of the aortic, 
and upon the auricular surface of the mitral and tricuspid valves. 

A microscojncal examination of a cross section of an indurated valve 
shows flat cells arranged in irregular layers, having between them a fibrinous 
material, which has in it, here and there, a few elastic fibres. The new 
formation always originates in the layer of fiat cells. These changes are 
best marked in the fibrous zone of the valvular orifices, upon the surfaces of 
the valves, and in the chordae tendinese. After a time the new tissue be- 
comes organized, and contracts, and this contraction is progressive. Gradu- 
ally the rigid valves, whose edges are rounded and hard, are drawn together 
toward their base, and thus assume a puckered appearance. Similar pro- 
cesses in the chordae tendineae cause them to hypertrophy, become rigid and 
shortened. In this way the valves are diminished in depth, and sometimes 
their free edges become approximated to the cardiac walls, so that exten- 
sive valvular insufficiency is the result. This does not always happen ; for 
a thickened cartilaginous valve may have so much fibrinous or papillary 



474 



DISEASES OF THE HEART. 



growth upon it, that the inward current is obstructed, and stenosis results 
without insufficiency. As this thickening and rigidity increase, the mobility 
of the valvular flaps is diminished, and adhesions occur between their 
edges, beginning at their base and extending toward their apex. So ad- 
herent may they become that all evidences of a valvular outline is lost and 
a fibrous diaphragm is stretched across the orifice, having only a small slit 
at its centre, looking and feeling like a button-hole, hence the term 
''button-hole slit" The mitral opening, which normally will admit the 
ends of three fingers, may be so narrowed that the end of the little finger 
will scarcely pass through it, and the aortic opening may not even admit 
a small quill. These retractions and adhesions cause the mitral valves 
with their columns and cords, to assume the form of a perforated cone. 

Long gelatinous vegetations on the aortic valve sometimes form adhesions 
with the aortic walls, and thus a sudden and extensive regurgitation is in- 
duced. Insufficiency and stenosis are often found at the same valvular 
orifice as the result of the valvular thickening, adhesion, and retraction. 
Such changes at the aortic orifice usually occur after middle life, and cause 
more thickening, adhesion, and retraction than those at the mitral valve. 
In children and early adult life, the mitral valves are the most frequent seat 
of interstitial endocarditis. The tendency of this lowly organized tissue is 
to undergo fatty and calcareous changes. The minute patches of fatty de- 
generation in the imperfectly organized tissue underneath the endocardium 
sometimes form atheromatous masses, containing more or less granular 
debris. The endocardium over these patches may be destroyed, or they 
may soften, ulcerate, and cause extensive destruction of the valves. 

A valvular aneurism may form in the same manner as has been described 
in ulcerative endocarditis. The formation of calcareous granules and 
plates is a very frequent termination of interstitial endocarditis. The 
aortic orifice is the most frequent seat of these calcareous degenerations. 
So extensive may this process become that little beads of chalky material 
are seen studding the free edges of the valve and even extending into the 
cardiac cavities. 

When interstitial endocarditis has its seat in the endocardium of the 
heart cavities, it will undergo changes similar to those of the valves, and 
the muscular walls of the heart will become the seat of interstitial changes. 
As a result the walls of the heart become thin and less resistant than nor- 
mal, and depressions occur on its inner surface. The process is a fibrous 
overgrowth, which occurs in spots varying in size from one-half an inch to 
one inch in diameter. When it extends through the entire heart-wall, the 
columns and cords may be so shortened as to cause valvular insufficiency. 
If the cardiac walls yield to the internal blood pressure, a well-defined 
pouch is produced. This condition is called " aneurism of the heart" and 
is usually situated at the apex of the left ventricle ; the pouch may be as 
large as the closed fist, and may communicate with the ventricle by a fun- 
nel-shaped or ring-like aperture. The walls of the sac are firm and rigid, 
the internal surface is generally smooth, but it may be irregular, in which 
case clots adhere to its walls. Cardiac muscular fibres are found in the 
walls of the aneurismal sac. Aneurisms at the base and in the interven- 



CARDIAC MURMURS. 



475 



tricular septum may result from the extension of a valvular aneurism. 
These may destroy the septum and establish a communication between the 
two ventricles. 

Etiology. — As has already been stated, the majority of cases of interstitial 
endocarditis are the sequelaB of the acute, and the affection is more fre- 
quently associated with articular rheumatism than with any other disease. 
"When it occurs with gout, chronic rheumatism, in alcohol drinkers, or 
in the aged, it is interstitial from its onset. 

Symptoms. — There are no positive subjective symptoms of interstitial 
endocarditis. There may be palpitation and a sense of uneasiness, some- 
times amounting to pain, in the pericardium. There may be irregularity 
in the action of the heart ; but all of these when taken together are not 
sufficient for a diagnosis. It can only be determined by the changes it pro- 
duces in the valves and valvular orifices, causing abnormal changes in the 
heart-sounds. 

The physical signs and differential diagnosis are those of the murmurs 
\or valvular disease induced by the chronic interstitial process, and will be 
next considered. 

The prognosis in interstitial endocarditis will depend upon the seat and 
the extent of the valvular lesions which it produces. 

CARDIAC MURMURS THEIR RELATIONS TO VALVULAR DISEASE 

OF THE HEART. 

A cardiac murmur is an adventitious or abnormal sound produced within 
the heart or blood-vessels, either by obstruction to the blood-current, an 
abnormal direction of the blood-current, or a change in the blood constit- 
uents. The study of cardiac murmurs dates from Laennec's discovery of 
auscultation, although forms of valvular diseases had been described by 
Vieussens as early as 1716. Aortic disease was the form first brought to 
notice, from the changes it induced in the radial pulse ; 1 John Hunter, 
Laennec, and Allan Burns were among the pioneers in this branch of in- 
vestigation. 2 

Corvisart was the first to mention the importance of what we call to-day 
the "purring thrill." 3 

Many advocate the " tension theory," viz., that an increase in the ten- 

1 In Virchow's " Handbuch " Meckel's essay of 1756 is given as the first paper on endocardial disease.^ 
Art. by Friedrichs. 

2 The last named supposes " that a reflux current can produce a hissing noise, something like what is 
described as audible palpitation in some diseases of the heart,' 1 1809. 

3 He said : " It probably came from a difficulty experienced by the blood in going through an orifice 
disproportionate to the amount of fluid." Laennec regarded murmurs or " bruits " as due to spasmodic 
contraction of the heart or arteries. Corrigan said that murmurs are "the result of the development of 
currents — the intrinsic collision of the moving liquid." In 1842 Gendrin established the "friction theory " 
(bruits de frottements endocardiaques), and first called attention to the fact that alteration in the con- 
stituents of the blood will produce murmurs audible in arteries of medium calibre. Bouillaud describes 
a murmur as an " exaggeration of the normal bruit caused by blood friction against the segments of the 
heart." Chauveau states that a bruit de souffle is produced by the vibration of a " veine fluide " always 
formed when blood rushes through a part of the circulatory system actually or relatively dilated. This 
veine fluide has its best development in anaemia (then called bruit de diable), for the jugular veins do not 
collapse and the volume of blood in anaemia is diminished. Chau-veau's theory is applicable to anaemic 
murmurs, but not to other cardiac murmurs. It is claimed that valve murmurs are produced by collision 
of the blood particles against one another ; or that either the liquid alone or the liquids and solids con- 
jointly may develop murmurs. 



476 



DISEASES OF THE HEAKT. 



sion and force can so exaggerate a normal sound as to produce a murmur. 
This theory has clinical foundation ; for valve lesions may exist, and the 
blood current and propulsive force may be so feeble that there is no au- 
dible murmur. Spasm of the papillary muscles and chordae tendinese and 
weakening of these structures by fatty degeneration are by some regarded 
as causes of temporary murmurs. 1 The same vibration that produces a 
murmur may produce an endocardial thrill, called the "purring thrill." 
Par more important than the loudness, pitch or quality of a murmur are 
its rhythm, point of maximum intensity, and area of diffusion, all of 
which will be considered in connection with the physical signs of each lesion. 

At the end of a cardiac diastole all the heart cavities are filling ; just 
before the cardiac systole, blood is forced from the lungs and cava? through 
the auricles and ventricles, while the mitral and tricuspid valves are pressed 
against the ventricular walls, thus offering no obstruction to the blood 
current. Should any obstruction exist at either of the auriculo-ventricular 
orifices, the blood while passing through the opening will impinge on such 
obstruction and cause a presystolic murmur. During a cardiac systole, 
the filled ventricles contract and blood is thrown through the arterial 
openings, the flaps of whose valves are pressed against the walls of the 
vessels so that no obstruction is offered to the outgoing current. At the 
same instant, the auriculo-ventricular valves close their orifices, so that 

blood may not flow back into the 
auricles. If the semilunar valves 
obstruct the outgoing current, or 
if the mitral or tricuspid valves do 
not wholly close the auriculo-ven- 
tricular orifices, then, in the one 
case, the blood-current as it passes 
over the obstruction at the semi- 
lunar orifices, will produce a sys- 
tolic murmur, and in the other a 
systolic murmur will be produced 
by the backward current through 
the abnormal opening at the au- 
riculo-ventricular orifices. If the 
pulmonary and aortic system — 

of the valves and cavities. By substituting the '. wards whiph flrp fillpd af thp svsrnlp 

Tri cuspid and Pulmonary for Mitral and Konic, the WmCQ are m,eCl aT tlie SVStOie 

B^ght mart 1 Ulustrate Murmurs occurring in the have back of them a semilunar 

valve that does not completely 
close that end of the circuit, the blood will regurgitate into the ventricles 
during the period of cardiac rest, so that semilunar incompetence causes 
a diastolic murmur. 




Diagram illustrating the mode of -production of Car- 
diac Murmurs in the Left Heart, with the condition 



1 The factors that determine the character of a murmur— its pitch, quality and intensity— are physical, 
as the force with which the jet is propelled, and the physical properties of the media of conveyance ; and 
they are the same as those which determine the quality of other sounds. 



VALVULAR MURMURS. 



477 



Valvular murmurs. 



RHYTHM. 


SITUATION. 


ORIFICE. 


NATURE. 


Systolic, 1 


Basic. 


Aortic. 


Obstructive. 


o 
a 




Pulmonary. 




3 


Apical. 


Mitral. 


Regurgitant. 


4 


( e 


Tricuspid. 




Diastolic, 1 


Basic. 


Aortic. 


<< 


Presystolic, 1 


Apical. 


Mitral. 


Obstructive. 



Pulmonary (diastolic) regurgitant murmurs and tricuspid (presystolic) obstructive mur- 
murs are so rare, clinically, that they may be disregarded. 



The following is the order of relative frequency of cardiac murmurs : 
(1) mitral regurgitation ; (2) aortic obstruction ; (3) aortic regurgita- 
tion ; (4) mitral obstruction ; (5) tricuspid regurgitation ; (6) tricuspid, 
obstruction ; (7) pulmonary obstruction ; and (8) pulmonary regurgita- 
tion. 

The most frequent combinations of murmurs are : (1) aortic obstruction 
and regurgitation; (2) mitral obstruction and regurgitation ; (3) mitral 
obstruction and tricuspid regurgitation ; (4) aortic obstruction and mitral 
regurgitation ; (5) double valvular disease at aortic and mitral orifices (four 
murmurs). 

Having appreciated the existence of a cardiac murmur, it is often very 
difficult to determine its rhythm. This difficulty may be lessened by re- 
membering that the first sound of the heart is synchronous with the carotid 
and radial pulse and the apex-beat, and that it may be wholly replaced by 
a systolic murmur ; the second sound is, however, almost always heard, for 
the pulmonic and aortic valves are rarely diseased at the same time. 

After determining the rhythm, pitch, intensity, and quality of a cardiac 
murmur, we next find the point of its maximum intensity. Murmurs 
arising at the mitral valve are loudest at the apex of the heart, or just above 
it; tricuspid murmurs are loudest over the lower part of the sternum; 
pulmonary murmurs, in the second left intercostal space close to the 
sternum, and aortic murmurs in the second right intercostal space at the 
edge of the sternum. 

Valvular diseases, causing murmurs, consist in a condition of the valves 
allowing either of regurgitation or obstruction. 

Valvular insufficiency results when extensive retraction, perforation, or 
partial detachment of the valves prevents them from completely closing 
their respective orifices ; or when the chordae tendineas have been rupt- 
ured, or calcareous degeneration has made the valves rigid, the backward 
current in such conditions giving rise to a regurgitant murmur. 



DISEASES OF THE HEART. 



When the valves are thickened, retracted, adherent, hypertrophied, or 
degenerated, they obstruct the outward current of blood and give rise to 
obstructive murmurs. 1 Both conditions, viz., stenosis and insufficiency, 

are often found co-existing, but 
rarely to the same extent. The 
lesions which induce these mur- 
murs are acute, when they occur 
during the course of acute endocar- 
ditis, and chronic when they de- 
pend upon the presence of some 
firm tissue, such as connective, 
fibroid, calcareous, or atheromatous 
tissue, which alters the form and 
impairs the function of the valves. 
Both the above varieties may pro- 
duce the same murmurs. 

Since physical signs are here the 
most important factors in diagnosis, 
the normal (physical) relation of 
the heart must be borne in mind: 
the apex of the heart is normally 
felt between the fifth and sixth 
ribs on the left side, about two 
inches below the nipple and one 
inch to its sternal side. The highest part of the base of the heart is on a 
level with the third costal cartilage. The tricuspid orifice is situated at 
the junction of the fourth left costal cartilage with the sternum. The 
mitral orifice is to the left of the tricuspid, immediately behind the left 
border of the sternum, at the junction of the third costal cartilage with 
that bone. The aortic orifice is one-half an inch lower than and to the 
right of the pulmonary orifice, behind the sternum on a level with the third 
interspace. The tricuspid orifice is the most superficial, then the pulmonary, 
next the aortic, and deepest of all the mitral. Banged from above down- 
wards, the pulmonary orifice comes first, then the aortic, then the mitral, 
lastly the tricuspid. 




Fig. 97. 

Diagram showing the Areas of Cardiac Murmurs. 

A. Area of Aortic Murmurs ; M. Mitral ; T. Tri- 
cuspid ; P. Pulmonary. 



AORTIC OBSTRUCTION, OR STENOSIS. 

This is a common cardiac lesion, and is always accompanied by more or 
less hypertrophy of the left ventricle. 

Morbid Anatomy. — The valves will be found to present some or all of the 
changes described in the history of interstitial endocarditis, together with 
degenerative changes due to atheromatous, calcareous, fibroid, fatty, or con- 
nective-tissue metamorphosis; they may be covered with thick, warty, 
irregular excrescences, that cause loud murmurs and yet do not seriously 



1 Some call obstructive murmurs direct ; and regurgitant murmurs indirect, from the current that causes 
the sound. 



AOETIC OBSTRUCTION", OR STENOSIS. 



479 




Fig. 98. 

Vegetations on the Aortic Valves giving 
rise to Aortic Obstruction. 



obstruct the out-going blood-current. Or the aortic orifice may be almost 
completely occluded, and then the extent 
of the lesion is measured more by the re- 
sulting hypertrophy and its effects on the 
systemic circulation, than by the loudness 
or harshness of the murmur. The valves 
are often so rigid that they cannot be 
pressed back, and then they present greater 
obstruction to the outgoing current than 
when vegetations exist ; as the result of 
adhesions, the valves may become fused 
into a mass, so that they project into the 
blood-stream in the form of a funnel, ir- 
regular in shape and studded with calcare- 
ous nodules. The line of attachment of 
the valves to the aorta frequently becomes 
obliterated. 

Aortic stenosis is frequently accompanied 
by atheromatous changes in the aorta, called "Arteritis deformans." As 
a result of aortic stenosis, hypertrophy of the left ventricle occurs, which is 
gradual in its development and called "compensatory" hypertrophy, be- 
cause it is due to the increased force required to propel the blood through 
the constricted orifice. Mitral insufficiency is apt to occur later, either 
from extension of the inflammation from the aortic valves, or from forcible 
pressure of blood upon the ventricular surface of the mitral flaps. Slight 
thickening and roughening of the aortic valves lead to no serious 
results. 

Etiology. — Aortic stenosis is most frequently met in middle and ad- 
vanced life ; the mean age being forty-seven years. It is occasionally 
met with in children under two years of age. It may be the result of 
defective aortic development and perhaps of imperfect development of 
the trachea, causing imperfect expansion of the chest. 1 Interstitial 
endocarditis of rheumatic origin is its most frequent cause. Chorea 
and chronic Bright's disease may cause it. Atheroma or arteritis de- 
formans extending to the valves sometimes gives rise to it. Increased 
aortic tension indirectly causes aortic stenosis. 2 Men suffer from aortic 
stenosis oftener than women, for in them the valves are subject to greater 
tension, and hence non-rheumatic aortic valvular disease is common in 
men and rare in women. Occupations that involve repeated sudden and 
severe muscular effort induce it. In old age, the aortic walls are weak- 
ened, and when aortic disease is met with in the young, it is often the 
result of premature vascular senility. 8 Disease of the aortic valves is 

1 Guy's Hosp. Reports, S. I., vol. vi., p. 235. 

2 The coexistence of cardiac valvular disease and cancer is a remarkable coincidence, possibly with a 
causal relation. 

3 Dr. Allbutt says that in Leeds quite young men have aortic valvular disease ; and Dr. Peacock men- 
tions several cases where it has occurred in young girls who have been placed at service before they were 
fully developed. Corvisart and Virchow both admit the possibility of syphilis being a cause of aortic 
valvular disease, but clinically this is not yet proven. 



480 



DISEASES OF THE HEART. 



oftener non-rheumatic in origin than mitral lesions. It is slower in its 
development, and is more frequently met with in advanced life. 

Symptoms. — The subjective symptoms of aortic stenosis are rarely well 
marked. Although extensive, it may cause no discomfort, for as the ob- 
struction increases, compensatory hypertrophy prevents pulmonary conges- 
tion ; but when this no longer compensates for the obstruction, the arteries 
are inadequately filled, the left auricle cannot empty itself, and consequently 
the pulmonary vessels and the venous system are abnormally full. The 
scanty arterial supply causes pallor of the face, and syncope may occur 
from cerebral anaemia, but these are late symptoms, not usually appearing 
until after the mitral valve has become secondarily involved. The pulse is 
normal in frequency, diminished in volume and fulness, and, as a rule, 
regular in rhythm, though it may be intermittent, compressible, and 
"jerky" in character. Signs of arterial anaemia usually precede those of 
venous engorgement. The sphygmograph gives a slanting or oblique up- 
stroke, showing that the influence of percussion is lost, and the tracings 



and renal vessels are frequently the seat of emboli. The left middle 
cerebral artery is the most common seat of cardiac emboli ; and the left 
lower limb is more subject to embolism from aortic valvular disease than 
the right. Embolism may be due to small auricular or ventricular clots 
that form behind the obstruction ; such clots have occluded the aortic ori- 
fice and caused sudden death. 1 

Physical Signs. — The physical signs of aortic stenosis are usually distinc- 
tive and easily appreciated. 

Inspection shows the area of cardiac impulse to be abnormally increased. 
Very extensive increase of this area is often accompanied by lifting of the 
chest over the precordial region. 

Palpation. — The impulse is felt to be forcible, and may be accompanied 
by a heaving or lifting sensation. The apex is displaced to the left and 
slightly downward. An indistinct thrilling sensation is often imparted to 
the hand during the systole. This systolic fremissement is nothing more 
than an intensified endocardial thrill, and it generally radiates to the ensi- 
form process, being most intense in the second right intercostal space. 

Percussion. — The area of cardiac dulness increases in proportion to the 
displacement of the apex beat to the left. 




may show considerable sep- 
aration between the "percus- 
sion " and "tidal" waves. 
The pulse is rarely slowed. 
There may be slight palpita- 
tion and paroxysmal pain in 
the chest. 



Fig. 99. 

Sphygmographic tracing in a case of Aortic Obstruction, with 
marked separation of the percussion and tidal waves. 



Aortic stenosis is more often 
associated with cerebral em- 
bolism than any other val- 
vular lesion, and the splenic 



1 Path. Tran*., vol. ix., p. 9. 



AORTIC OBSTRUCTION, OR STENOSIS. 



481 



Auscultation. — Aortic obstructive murmurs are loudest and most distinct 
at the second right intercostal space and at the sternal insertion of the third 
left costal cartilage. They are systolic, and oftener accompany, than replace 
the first sound of the heart. The maximum intensity of this murmur is at 
the second sterno-costal articulation of the right side, but it may be heard 
with equal intensity over the whole upper part of the sternum, and may be 
audible at the xiphoid cartilage. It is always a harsh murmur, heard most 
distinctly at the commencement of the systole. In uncomplicated aortic 
stenosis, the aortic second sound may be inaudible ; it is always feeble, but 
the pulmonic second sound is always audible. The area of diffusion of this 
murmur follows the law that a murmur is propagated in the direction of 
the blood-current. It is conveyed along the aorta into the carotids, and 
one of its characteristics is that it is heard in the great vessels of the neck. 
It may be heard in the thoracic and abdominal aorta. When an aortic ob- 
structive murmur is heard at the apex, its intensity is diminished, and 
when heard behind it is most distinct at the left of the third and fourth 
dorsal vertebrae, near their spines, and frequently extends downward along 
the spine in the course of the aorta, but with diminished intensity. It is 
to be noted that a systolic murmur, audible at the base and traceable along 
the ascending arch toward the end of the right clavicle, is by no means 
limited to cases of aortic stenosis, although this lesion always produces a 
murmur with these characteristics. "When the mitral or tricuspid valves 
are thickened or incompetent, or when the myocardium undergoes fatty de- 
generation, this murmur will entirely replace the first sound of the heart. 

Differential Diagnosis. — Aortic obstruction may be mistaken for mitral 
and tricuspid regurgitation, an ancemic druit, or the murmur of a thoracic 
aneurism. Both mitral and tricuspid regurgitation and aortic stenosis pro- 
duce a systolic murmur. The murmur of aortic stenosis is heard with its 
maximum intensity at the third left sterno-costal articulation, and dimin- 
ishes in intensity toward the apex of the heart. The murmur of mitral 
regurgitation is heard loudest at the apex-beat. The murmur of aortic 
stenosis is conveyed into the vessels of the neck ; that of mitral regurgita- 
tion to the left, in the direction of the apex-beat, and is heard behind, be- 
tween the fifth and eighth dorsal vertebrae, at the left of the spine, with 
very nearly the same intensity as at the apex. The pulse in aortic stenosis 
is hard, firm, wiry, but regular ; while in mitral regurgitation it is irregu- 
lar in rhythm and force, but never incompressible, and is easily increased 
in frequency. Gastric, intestinal, renal, hepatic, and bronchial symptoms 
are present in mitral regurgitation, while the subjective symptoms of aortic 
obstruction are cerebral in character. The pulmonic second sound is feeble 
in aortic stenosis, but in mitral regurgitation it is intensified. The mur- 
mur of aortic stenosis is harsh, that of mitral regurgitation soft, and often 
musical. 

Tricuspid regurgitation is accompanied by a systolic murmur which is 
rarely heard above the third rib ; while that of aortic stenosis has its point 
of maximum intensity at the right second sterno-costal articulation. Tri- 
cuspid regurgitation is accompanied by jugular pulsation ; while the mur- 
31 



482 



DISEASES OF THE HEAKT. 



mar of aortic obstruction is heard in the arteries of the neck. 1 The area of 
transmission of tricuspid regurgitant murmurs is not more than two inches 
from the point of their maximum intensity, while aortic stenotic murmurs 
are conveyed into the vessels of the neck. The pulse in tricuspid disease 
is normal ; in aortic stenosis it is hard and wiry. 

Ancemia produces a murmur heard loudest in the carotids and accom- 
panied by a venous hum, which is continuous and best heard on the right 
side of the neck. Thus, in anaemia there are three murmurs : cardiac, 
venous, and arterial. In aortic disease the point of maximum intensity 
and the absence of a "venous hum" will aid in the diagnosis; besides, 
there will be cardiac hypertrophy and an increase in the force of the apex- 
beat, while the impulse is feeble in anaemia. The murmur is soft and 
blowing in anaemia, and harsh in aortic obstruction. The pulse is charac- 
teristic in aortic stenosis, in anaemia it may have a thrill, but is never 
hard and wiry. The etiology and subjective symptoms of these two are 
strikingly dissimilar. 

In thoracic aneurism the dilating impulse on palpation, the normal force 
of the heart-beat, the single and double bruit, and the pjin are all impor- 
tant signs, which are absent in aortic stenosis. 

The prognosis and treatment of "valvular diseases of the heart" will be 
considered at the end of their history. 



AOETIC INSUFFICIENCY, OR REGURGITATION. 

This is an abnormal condition of the aortic valves, which prevents their 
complete closure, and allows a backward current of blood to flow from the 
aorta into the left ventricle during its diastole. It is usually associated 
with more or less aortic stenosis. 
Morbid Anatomy. — In aortic insufficiency, the flaps of the valves may 
be thickened, puckered, or shortened, so that 
they do not meet. If the centre of a valve is 
indurated, it will curl up, either toward the ori- 
fice or back against the aortic wall. In the 
former case, there is insufficiency with great ob- 
struction ; in the latter, insufficiency with only 
slight obstruction. This valvular thickening 
or shortening may be due to endocarditis. In 
some cases, the flaps of the valves may become 
adherent to the walls of the aorta, or a diseased 
valve may be torn or ruptured, which will al- 
low a free opening for the regurgitant blood. 
Valves Following stenosis, little tunnels may form by 




Fig. 100. 
of Aortic Semilunar 



tee m v?ives are™!ick^ the side of the valves and permit of a regurgi- 

enedand curled upward, prevent- -f- flri 4- „ ]irrPT1 f. 
mgthe complete closure of the aor- tclut tuucul 
tic orifice. 



The aortic valves are more lia- 
ble to laceration than any other valves. In 
aortic regurgitation, during a cardiac diastole, 



1 To distinguish hetween intrinsic pulsation of the jugular vein and throbbing of the carotids, press 
lightly on the vein above the clavicle ; this arrests pulsation when due to tricuspid disease, while if due 
to aortic stenosis, the result is negative. 



AOETIC INSUFFICIENCY, OE EEGUEGITATION. 



483 



there is added to the blood, which normally flows from the auricle into 
the ventricle, a regurgitant current from the aorta, and so over-distention 
of the left ventricle results. Thus, after a time, the left ventricle becomes 
permanently dilated. To overcome this distention compensatory hyper- 
trophy takes place. The left heart is often greatly enlarged. As a result, 
the arterial system is over-distended at each cardiac systole. 

The extra ventricular power and the abnormal quantity of blood thrown 
against the arterial walls lead to endarteritis and subsequent atheroma, 
and the degeneration of the vessels predisposes to apoplexy and to aneu- 
rism. Since, normally, aortic recoil fills the coronary vessels, aortic regur- 
gitation must be followed by imperfect blood-supply to the heart, and dila- 
tation again commences at the expense of the walls of the heart, the hyper- 
trophy ceasing to compensate for the increased dilatation. Atrophy of the 
papillary muscles may allow the mitral flaps to pass beyond their normal 
line at the auricles, when there is an increase in blood pressure, and then 
mitral regurgitation and impeded venous circulation wiJl result. Passive 
pulmonary hyperemia may be present ivithout mitral lesions, when the left 
auricle cannot wholly empty itself. 

Etiology. — This is similar to that of aortic stenosis. Rheumatic en- 
docarditis is its chief source ; but it may follow sudden and violent 
muscular effort, atheroma of the aorta or endarteritis. Congenital mal- 
formation, according to Yirchow, is a frequent cause in chlorotic females. 
The atheroma which causes aortic insufficiency is often of gouty origin, 
especially when gouty kidneys coexist or when alcoholismus is associ- 
ated with a gouty diathesis. Dilatation of the aorta at its origin may in- 
duce it. Fagge says only fifty per cent, of the cases of aortic insufficiency 
give a rheumatic history. The violence with which the valves are closed 
during prolonged and violent physical exertion may induce an interstitial 
endocarditis which will lead to it. 

Symptoms. — So long as hypertrophy compensates for the regurgitation, 
there is little or no inconvenience experienced by the patient, even 
though the regurgitation is extensive. When the regurgitant stream is 
small, there is no disturbance of the general health, but in time the hyper- 
trophy induces excessive heart-action during excitement or violent muscu- 
lar effort. The heart-action then becomes labored and the patient is anx- 
ious, nervous and fretful, and knows well that exercise will augment his 
uncomfortable symptoms. The respirations are accelerated with the cardiac 
palpitation ; as the disease advances attacks of headache and vertigo be- 
come more and more prolonged and severe ; the patient complains of muscae 
volitantes, dyspnoea, and giddiness, and is compelled to sleep with his 
head elevated. Palpitation and a visible carotid impulse are now con- 
stantly present. A comparatively frequent symptom is a distinctly par- 
oxysmal shooting or stabbing pain over the heart, in the left shoulder, or 
extending down the left arm. This pain may be accompanied by numb- 
ness and a peculiar whiteness of the skin along the line of pain. In other 
cases, the pain passes from the middle of the sternum down the right arm. 
This pain is increased by excitement, physical exercise, and over-distention 



484 



DISEASES OF THE HEART. 



of the stomach. Sometimes these patients complain of a sickening flutter- 
ing of the heart when the nutrition of the heart walls becomes interfered 
with ; and when mitral insufficiency exists, the systemic veins become over- 
loaded and cyanosis and dropsy result ; the dropsy appears first as oedema 
of the feet, and gradually extends upward until there is general anasarca. 
The cyanosis is increased after slight exertion, and is accompanied by vio- 
lent paroxysms of dyspnoea, carotid pulsation, and puffiness of the face. 

Later in the disease, there is orthopnea, sudden startings in sleep, 
angina pectoris, and there may be albuminuria and enlargement and 
tenderness of the liver. Attacks of syncope at first occur only after active 
exercise ; later, they occur independently, and are very distressing. These 
patients may die at any moment, either when perfectly quiet or when under 
intense excitement ; the danger is greatest, however, during exertion. 

The pulse is the most characteristic subjective symptom, and was first 
accurately described by Sir D. Oorrigan, 1 and is therefore often called "Cor- 
rigan's pulse." He said the disease was indicated by visible pulsation of the 
vessels of the head, neck and upper extremities. On account of the elonga- 
tion of the arteries during their pulsation, and their flexuosity, the pulse is 
of ten called the "piston pulse ;" it is large and distinct, and rapidly pro- 
jected against the finger, and the arterial tension sinks just as quickly to 
a minimum. It may be accompanied by a vibrating jar, on account of which 
it is called the "water-hammer," "jerking,' 7 "splashing," or "col- 
lapsing " pulse. Its characteristics are more apparent when the arm is raised 
above the head ; although slightly infrequent, quick, and jerking, it is 
always regular in rhythm; — the radial impulse is felt a little after the apex- 
beat. As soon as the systemic circulation is overloaded from insufficiency 
of the heart or from secondary mitral insufficiency, the pulse becomes 
feeble, irregular, and sometimes intermittent, but always " jerking." The 
sphygmograph shows a high upstroke and an absence of the dicrotic wave. 

The pulse-tracing of aortic 
regurgitation resembles the 
senile pulse, but a senile pulse 
gives a rounded instead of a 
pointed summit. The pecu- 
liar crochet or beak is very 
noticeable. 2 

Physical Signs. — Inspection 
Fig. 101. reveals an increase in the area 

Sphygmographic tracing in Aortic Regurgitation, showing nT1f l f nrnPl n f f^p nnPY-hpnf 
marked amplitude with absent dicrotic wave. dna lorLe u * LIie apex UCdl, 

which is visible over a wider 
area than in aortic stenosis. The vessels of the neck and upper extremities 
often pulsate ; when compensation ceases to balance the forces in the heart, 
the apex-beat becomes feeble and diffused. Pulsation of the retinal vessels 
has been observed. 3 

1 Edin. Med. Surg. Jour., April, 1832. 

2 Stokes has described a peculiar and characteristic pulsation (steel-hammer pulse) occurring in cases 
of acute rheumatic arthritis, and supervening upon aortic insufficiency. This pulse is abrupt and ener- 
getic as the rebound of a smith's hammer from the anvil ; it is only exhibited, however, in the arteries 
near the affected joints. 

3 Loud. Ophth. Hosp. Rep., Feb., 1873. 




AORTIC INSUFFICIENCY, OR REGURGITATION. 



485 



Palpation. — A heaving, lifting impulse will be appreciated which is 
transmitted over a large area. The apex-beat is displaced down and toward 
the left, sometimes as far as the eighth rib, and two and one-half inches to 
the left of the left nipple. A continuous diastolic thrill is sometimes felt 
over the site of the aortic valves. There may be slight pulsation in the 
scrobiculus cordis. 

Percussion. — The superficial and deep areas of dulness correspond to the 
extent of the cardiac enlargement. As soon as dilatation exceeds hyper- 
trophy, the area of dulness will extend horizontally and slightly upward, 
the apex beating in the axillary line. Dulness may extend six and a half 
inches from right to left and from the third rib to the line of liver dulness. 
Superficial dulness is increased horizontally and to the left. 

Auscultation. — Aortic regurgitation is attended by a diastolic murmur, 
which may take the place of, or immediately follow, the second sound of 
the heart. This murmur has its maximum intensity at the sternal end 
of the second right intercostal space, or at the sternal junction of the third 
rib on the left side. It is transmitted over the sternum and may be loud- 
est at tho xiphoid cartilage and is thence transmitted in the direction of 
the apex. Its area of diffusion is greater than any other cardiac murmur : 
it is not only conducted down the sternum to the apex, but it maybe 
heard at the sides of the chest, along the spinal column, faintly in the 
ascending and transverse arch, in the carotids, and sometimes as far as the 
radial arteries. The murmur is "substitutive" rather than "accompany- 
ing," for the pulmonic second sound is audible at the right base. Incom- 
petency of the posterior segment of the aortic valve induces a murmur 
which is conducted to the apex, while inadequacy of the anterior flaps pro- 
duces a murmur which is conveyed toward the ensiform cartilage ; the 
former murmur would indicate a more favorable prognosis, owing to the 
relationship of the anterior segments to the coronary arteries. When the 
second sound of the heart is distinct, the murmur immediately follows it. 
Some call this a " post-diastolic aortic murmur." 

Although an aortic regurgitative murmur has the greatest area of dif- 
fusion, it is not the loudest murmur ; it is soft, blowing, sometimes rough, 
and frequently musical. It is loudest at the beginning of diastole, gradu- 
ally decreasing in intensity, although it may be " rushing "or " blowing ; " 
this murmur may temporarily disappear during the whole diastole. When 
aortic stenosis coexists there will be a double murmur, audible over a very 
large area, and having its maximum intensity at the right edge of the 
sternum in the second interspace. Systolic and diastolic murmurs may run 
into each other. If mitral occurs with aortic regurgitation, each murmur 
retains its own place of maximum intensity. Barely, when two segments 
of the valve are healthy, a clear aortic second is heard, preceded by a faint 
"reflux " murmur, said to be pre-diastolic in rhythm. 

Aortic murmurs are sometimes so indistinct as to be heard only when the 
patient is in a recumbent posture. A diastolic murmur heard at or below 
the level of the aortic valves, and chiefly audible in the line of the sternum, 
indicates considerable regurgitation. When a diastolic murmur is inaudible 



486 



DISEASES OF THE HEART. 



in the carotids, it is because preceded by a systolic murmur which has its 
maximum intensity in the " aortic area." Such a murmur indicates much 
more obstruction than, regurgitation. When a diastolic murmur is heard 
distinctly in the carotids, and is also preceded by a systolic murmur in 
them, the combination indicates trifling obstruction with considerable in- 
competence. 

Differential Diagnosis. — The diagnosis of aortic regurgitation is generally 
not difficult, as it rests almost exclusively upon the existence or non-existence 
of a diastolic murmur. It may be mistaken for aortic stenosis, mitral ob- 
struction, pericarditis localized over the aorta, aneurism of that portion 
of the aorta immediately above the valves, patency of the ductus arteriosus, 
insufficiency of the pulmonic valves, and occasionally for a rough and in- 
elastic condition of the ascending aorta. 

Mitral obstruction gives a presystolic murmur, while aortic reflux pro- 
duces a diastolic murmur. Mitral stenosis is accompanied by no hyper- 
trophy or dilatation of the left ventricle; whereas these conditions are 
always present in aortic reflux. The quality of a presystolic mitral murmur 
is harsh and rough, and it has a churning, blubbering or grinding character ; 
while aortic reflux has a murmur of low pitch, and a soft, blowing or musi- 
cal character. Mitral stenosis is accompanied by a purring thrill, which is 
absent in aortic regurgitation. The murmur of mitral stenosis is the 
longest of all cardiac murmurs, and is never heard behind ; whereas that 
of aortic regurgitation is heard at the sides of the chest and along the 
spinal column. Finally, mitral stenosis is attended by well-marked pul- 
monary symptoms during active physical exertion, which are rarely pres- 
ent in aortic insufficiency. 

A pericardial friction sound over the aorta has its maximum intensity 
over the seat of its production, and is usually audible during both the 
cardiac systole and diastole. In aortic regurgitation, the character of the 
pulse, the existence of hypertrophy and dilatation of the left ventricle, and 
the carotid pulsation will establish the diagnosis. 

An aneurism at the sinuses of Valsalva is diagnosticated by the history of 
the case, the presence of the murmur over the pulmonary artery, the evi- 
dence of arterial degeneration, the absence of left ventricular dilatation and 
hypertrophy, and by the peculiar jerking pulse. An aneurismal murmur 
is circumscribed, has a booming quality, is usually systolic in rhythm, and 
is never transmitted to the apex of the heart. 

Patency of the ductus arteriosus is a rare condition ; in a case where it 
was diagnosticated 1 the murmur was audible at the left of the sternum, was 
not everywhere continuous with the second sound, was only transmitted 
very feebly to the left, and had a wavy character sufficient of itself to distin- 
guish it from aortic regurgitation. 

Insufficiency of the pulmonic semilunar valves is the rarest of all valvu- 
lar lesions ; the murmur should be diastolic, having its maximum intensity 
in the second intercostal space of the left side, it would be transmitted 
only downward and toward the right apex, and would not be attended 



1 Guy's Hosp. Rep. Series 3, vol. xviii., 1872-3. 



MITRAL STENOSIS. 



48: 



by arterial pulsation, a jerking pulse, or left ventricular dilatation and hy- 
pertrophy. 

A diastolic murmur in the ascending arch due to roughening, rigidity, 
and dilatation of the artery is also rare, while the condition, which some 
say can produce it, is very common. Two cases are recorded in which the 
diagnosis rested upon the character of the pulse, throbbing of the arteries 
and the absence of left ventricular hypertrophy and dilatation. 1 



MITRAL STENOSIS. 

Stenosis or obstruction of the auriculo- ventricular opening of the left 
heart, is due partly to constriction at the base of the mitral valves, and 
partly to adhesion of the valve tips or chordae tendineae. It usually occurs 
as a consequence of rheumatic endocarditis, — rarely of atheromatous degen- 
eration, — and is most likely to occur in endocarditis affecting young persons. 
Usually, insufficiency and stenosis of the mitral orifice occur together, and 
stenosis probably never occurs without some insufficiency. 

Morbid Anatomy. — As a result of acute exudative or interstitial endo- 
carditis, the valves are rendered shorter and narrower, as well as thicker 
and more cartilaginous than normal. These rigid valvular projections not 
only obstruct the flow of blood from the auricle into the ventricle, but 
allow of its regurgitation from the ventricle into the auricle. In mitral 
stenosis, there is not only thickening and contraction of the valves, but 
the valve-tips or the chordae tendineae become adherent and sometimes each 
papillary muscle is changed into a corrugated, cylindrical mass, pierced 
with one or more slits, indicating the chordae of which it was originally 
made up. The wall of the valve, especially toward its free edge, is greatly 
thickened, and these thickened por- 
tions are so dense that they have a dis- 
tinct cartilaginous feel. On the val- 
vular flaps that have undergone this 
sclerotic change calcareous masses are 
very frequently developed, and cal- 
careous nodules are especially liable 
to form when a gouty diathesis exists. 
When the chordae tendineae and pap- 
illary muscles have become adherent, 
the edges of the valves are drawn down 
toward the apex of the heart ; and since 
the flaps are adherent at a greater or less 
distance upward from their base, the 
valve presents a funnel-shaped appear- 
ance with its base looking toward the 
auricle, and its apex toward the ven- 
tricle, whose smaller opening, rarely 
circular, usually resembles a slit whose axis runs with the line which unites 




Fig. 102. 

View of the Mitral Valve in a case of Mitral Ste- 
nosis. The chordse tendinese are chickened and 
shortened, and the edges of the valve are calci- 
fied and drawn downward, giving the funnel- 
shaped appearance. 



1 Bellingham, Dis. 
Cle by Prof. Law. 



of Heart, 1875, p. 152. Also Trans. Path. Society, vol. iii., Mar. 



p. 3. Arti- 



488 DISEASES OF THE HEAET. 



the original segments of the valve. This " button-hole " slit may scarcely 
admit the tip of the little finger, while the normal mitral orifice permits the 
easy introduction of three fingers. Annular (ring-like) stenosis is far more 
common at the mitral than at the aortic orifice. Sometimes the funnel- 
shaped appearance is wanting, and the flaps are stretched horizontally 
across, with a small opening in the centre, like a diaphragm ; looked at 
from the auricle, this slit often appears crescentic. 

In cases of long standing the vegetations may become calcified. If the 

new tissue in the diseased valves undergoes 
fatty change and softens, ulcerative processes 
are set up and the chord se tendinese may 
rupture. On the floor of such ulcers cal- 
careous masses and debris are frequently 
found. Dr. Hayden thinks that all funnel- 
shaped mitral stenosis is the result of primary 
acute inflammation of the valve segments 
with cohesions of their adjacent edges." Out 
of sixty-two cases of mitral stenosis, fifty- 
nine assumed the "button-hole" form and 
three only the funnel shaped. 1 In rare in- 
stances the tendons will adhere to the wall of 
the heart. Adjacent to the valves, the endo- 
cardium will usually be found slightly thick- 
ened. The valves presenting the roughest 
and most irregular surfaces do not give rise 
to the harshest or loudest murmurs. 

The following changes are developed in 
the heart and vessels as a result of mitral 
stenosis. The left ventricle becomes smaller, 
sometimes its walls are thinner than normal. 
The aorta is also small and thin-walled. An 
almost necessary result of mitral stenosis is 
dilatation with subsequent hypertrophy of the left auricle. Sometimes the 
auricular cavity is enormously dilated, and its appendix is elongated and 
curved. Not infrequently the left auricular walls are from one-eighth to 
one-seventh of an inch in thickness. As soon as the auricular hypertrophy 
ceases to be compensatory, the pulmonary circulation becomes obstructed, 
causing tension in, and distention of, the pulmonary vessels. The walls of 
the pulmonary vessels, especially those of the main trunk, are thickened 
and hypertrophied ; they have been found twice the thickness of those of 
the aorta. Although mitral stenosis is a disease of youth, and atheroma 
one of old age, yet it not infrequently happens that, even before the age of 
puberty, atheromatous degeneration occurs in the pulmonary vessels, espe- 
cially in the small branches, as a result of the increased blood tension in 
the pulmonary system. 2 

The passive pulmonary hypergemia which results from the obstructed 

1 Fagge and Hayden. 2 Trans. Path. Society, xvii., p. 90. 




Fig. 103. 



View of the Mitral orifice from the 
Auricle, with calcification of the 
valves and reduction of the opening. 
In the above case the point of the 
little finger was barely admitted 
through the " button-hole " slit. The 
valves are stretched horizontally 
across. 



MITRAL STENOSIS. 



489 



pulmonary circulation may lead to changes which collectively constitute 
drown induration of the lung. Another occasional occurrence directly due 
to extensive mitral stenosis is nodular hemorrhagic infarctions. In some 
instances an extensively dilated left auricle may, by pressing on a bronchus, 
reduce its calibre one-half, and thus interfere with the functional activity of 
the left lung. When the pulmonary hyperemia is extensive, violent physi- 
cal exertion or violent coughing may cause a rupture of one of the larger 
pulmonary vessels, and true pulmonary apoplexy results. Bronchorrhoea is 
a frequent result of the intense hyperemia of the mucous membrane of the 
bronchial tubes which may be produced in mitral stenosis. The lungs are 
alwa} r s so liable to congestion and oedema that any sudden or violent exer- 
cise may cause sudden death. Again, when the above conditions have 
existed for some time, mitral stenosis may lead to dilatation and hyper- 
trophy of the right heart. ' In some rare cases, the tricuspid orifice has 
become slightly insufficient. 

Etiology. — Mitral stenosis is most frequent in the young ; it rarely occurs 
after fifty. Statistics show it to be twice as frequent in females as in males. 
It is not infrequently of congenital origin. Acute rheumatic endocarditis 
is its most frequent cause. In some few instances stenosis results from ex- 
tension of the inflammatory process from the aortic valves. It is a question if 
endocarditis in scarlatina or diphtheria in children ever causes mitral stenosis. 

Symptoms. — The subjective symptoms of mitral stenosis are few. Usually 
after violent exercise there is more or less cardiac palpitation, and this will 
cease as soon as the auricle can empty itself, which is accomplished by the 
patient assuming a recumbent position on the right side, with the head 
slightly elevated. This class of patients are usually pale and anaemic, 
and frequently experience a sharp pain in the region of the apex-beat. The 
pulse is regular and normal in character, so long as the auricular hyper- 
trophy compensates for the auricular dilatation. When the ventricle does 
not receive and discharge its normal quantity of blood with normal regu- 
larity, the pulse becomes small in volume, feeble in force, rapid and irregular 
in rhythm. The sphygmograph exhibits a tracing, sometimes called the 
" mitral pulse," the nature of which is the same as when the ventricle 
throws a greatly diminished blood current into the aorta. 1 The auricular 
systole commences earlier than 
normal on account of the hy- 
pertrophy of the auricle. This 
premature contraction of the 
auricle stimulating ventricular 
contraction, is indicated by a 
second ventricular systole, 
which is much less forcible 
than the first. 

The passive pulmonary hy- 
peremia which attends the ad- 

1 Balfour differs from other authorities in The statement that among the most remarkable subsidiary 
phenomena of mitral stenosis is irregularity of cardiac rhythm which is always present in a greater or less 
degree. 




Fig. 104. 

Sphygmographic tracing in a case of Mitral Stenosis. The line 
of descent is broken by pulsations from premature con- 
traction of the over-filled auricle. 



490 



DISEASES OF THE HEART. 



vanced stages of this form of cardiac disease causes habitual dyspnoea, 
which is exaggerated by physical exertion and by a dry, hacking, " teas- 
ing" cough, which resembles the so-called "nervous" cough. After 
violent or prolonged exertion there may be bronchorrhoea, a pint of glairy, 
watery mucus often being expectorated in a few moments. Severe exercise 
sometimes induces attacks of profuse, watery, blood-stained expectoration, 
indicative of pulmonary congestion and oedema. The exertion of walking 
rapidly against a strong wind will often cause such intense congestion and 
oedema of the lungs in one with extensive mitral stenosis as to induce sud- 
den death. Haemoptysis is not infrequent, small quantities of pure, florid 
blood being expectorated. Orthopncea is a rare symptom, for even in ex- 
tensive and long-standing cases the pulmonary congestion is not constant, 
for the auricle is ordinarily able to empty itself, and only becomes engorged 
during active physical exertion or great excitement. 

Physical Signs. — Inspection. As the left ventricle does not receive its 
normal quantity of blood, the cardiac impulse is feeble. Sometimes it has 
a visible undulating movement. 

Palpation. — On palpation, although the apex-beat is less forcible than 
normal, a distinct purring thrill will be communicated to the hand ; this 
thrill is a constant attendant of mitral stenosis. While mitral stenosis is 
always accompanied by a purring thrill, it should be remembered that a 
purring thrill does not alivays indicate mitral stenosis. It is most distinct 
at the apex-beat, although it may be diffused over the whole precordial 
space. It either continues through the entire diastole, or is only present 
just before the systole. It is sometimes called a "presystolic" thrill. It 
ceases at the apex-beat. 

Percussion. — The increased size of the left auricle may cause an increase 
in the area of cardiac dulness, upward and to the left, at the inner part of 
the second left intercostal space. This increased area of dulness will only 
be recognized on careful percussion during expiration. 

Auscultation. — Mitral stenosis is characterized by a loud "churning," 
"grinding," or "blubbering" presystolic mur?nur ; this murmur is of 
longer duration than any other cardiac murmur, on account of the time re- 
quired for the blood to pass through the narrowed and obstructed orifice. It 
ends with the commencement of the first sound and the apex-beat, being 
synchronous with the purring thrill. The murmur is heard with its maxi- 
mum intensity a little above the apex-beat. It is louder when the patient 
is erect than when in a recumbent posture. When there is great debility 
or just before death, the murmur becomes indistinct. A presystolic mur- 
mur is never present unless there is narrowing of the auriculo- ventricular 
orifice, and then it is seldom, if ever, absent. A prolonged murmur and a 
sharp first sound indicate a "funnel-shaped" stenosis. The pulmonic 
second sound is intensified. When mitral reflux and mitral obstruction co- 
exist, the two murmurs run into each other, constituting a single murmur. 
A mitral obstructive murmur is never soft or musical ; it is usually sepa- 
rated from the first sound by a short interval. In about one-third of all 
cases, the second sound is reduplicated. Pulmonary congestion sufficiently 



MITRAL REGURGITATION". 



491 



accounts for the reduplication. 1 Some regard the length of the pause 
between the murmur and the first sound as a measure of the stenosis : the 
shorter the pause the greater the stenosis. 

Differential Diagnosis. — The diagnosis of mitral stenosis is not difficult : 
it depends upon the existence of two physical signs, the " purring thrill " 
and a loud, long, blubbering presystolic murmur. It may be mistaken for 
pericardial friction, for a prolongated systolic murmur replacing the first 
sound at the apex, and for a pre-diastolic basic murmur transmitted to the 
apex. 

To diagnosticate between local pericarditis and mitral stenosis the same 
methods are employed and the same rules are to be observed as in the diag- 
nosis between aortic murmurs and local pericarditis (q. v.). 

A prolonged systolic apical murmur reaching to the second sound is dis- 
tinguished from a presystolic murmur by its soft and blowing character, 
and its synchronism with the systolic impulse and. carotid pulsation. 

A pre-diastolic murmur is distinguished from a mitral stenotic murmur 
by its progressively diminishing intensity, from the base to the apex, by its 
not being accompanied by hypertrophy of the left ventricle, and by a jerk- 
ing, irregular pulse. 

MITRAL REGURGITATION. 

Eegurgitation at the mitral orifice is due to a condition of the mitra} 
valves which allows the blood to flow back from the left ventricle into the 
left auricle. 

Morbid Anatomy. — The most common lesions are thickening, induration 
and shortening of the mitral valves. In rare instances, regurgitation may 
occur independently of valvular disease, from displacement of one or more 
of the segments of the valve, the result of changes in the papillary muscles, 
chords tendineae, or the ventricular walls. It may also occur in extensive 
anaemia or from relaxation of the papillary muscles and dilatation of the 
left ventricle without a corresponding elongation of the papillary muscles, 
and from rupture of the chordae tendineae. In most instances, however, 
the valves are shortened, thickened, and indurated. In some cases, lime 
salts and large masses of chalky matter are found embedded in the in- 
durated valves. In such cases the surface and edges of the valves are so 
rough and jagged that more or less obstruction accompanies the regurgi- 
tation. All these changes, except calcification, may also occur in the chordae 
tendineae and columnae carneae. The valves may also become adherent to 
the walls of the ventricles, or, as a result of the shrinking and shortening 
of the chordae tendineae, the valve-flaps will not pass back to the plane of 
the orifice. Again, the chordae tendineae may be ruptured so that the 
valves are pressed back into the auricle during the cardiac systole. If the 
chordae tendineae which arc inserted nearest the centre of the valve become 



1 Geigel ascribes it to " non-coincidence in the closure of the valves. " Guttman regards it as originat- 
ing at the stenotic orifice itself. Balfour thinks that thrill and reduplication of the second sound are suf- 
ficient to make a diagnosis in the absence of murmur. 



492 



DISEASES OF THE HEART. 




lengthened, that part of the flap will be bent npon itself, having evidently 
yielded to the blood pressure, and this allows of regurgitation. Sometimes 
when the valves appear perfectly healthy they will 
be found by the application of the " water test " 
to be insufficient. 

The first effect of mitral regurgitation is dilata- 
tion of the left auricle, due to the pressure of the 
c j5 two blood currents during its diastole, bne from 
the lungs, and the other from the left ventricle. 
The dilatation leads to thickening and hypertrophy 
of the left auricular walls ; as a result, the pul- 
monary circulation is impeded. The pulmonary 
vessels enlarge and may undergo degeneration, as a 
result of the continued regurgitant pressure. Passive 
hyperemia of the lungs, with brown or pigment 
induration, is an early pathological sequel of mitral 
regurgitation. The constant interference with the 
return circulation from the lungs, more or less 
fig. ioo. obstructs the outward current of blood to the lungs 

View of the Left Heart in Mitral , . , , . _ . . , , . . . . 

Regurgitation. from the right ventricle. As the obstruction is a 

The auHcuio-ventricuiar valves gradual one, the right ventricle becomes sufficient- 

are thickened ivith calcareous b . 

deposits, as shown at b, b. ly hypertrophied to overcome it, consequently the 

The aortic valves A, A, were J J* ■ • i I j> ±i 

in this case the seat of like de- hypertrophied right ventricle compensates lor the 

mitral regurgitation. 
So long as the hypertrophied right ventricle is able to fully overcome 
the abnormal pressure of the blood in the lungs from the mitral regurgi- 
tation, the patient is comfortable. Sooner or later, however, the compen- 
satory hypertrophy of the right ventricle ceases, and a secondary dilata- 
tion occurs which admits of no compensation. This final dilatation of 
the right ventricle is favored by the myocardial degeneration which occurs 
as a result of defective nutrition of the heart walls ; when this condition is 
reached, the veins throughout the body are placed in a similar condition to 
those in the lungs. This general venous congestion is indicated by passive 
hyperemia of the abdominal viscera and by cyanosis of the surface during 
active physical exercise. The liver is the organ first affected on account 
of its great vascularity, and from the fact that the hepatic veins do not col- 
lapse readily and possess no valves. Thus, the liver becomes enlarged and 
has a stony hardness ; as a result of the obstruction to the emptying of the 
hepatic vein the portal vein is obstructed, and this leads to passive hyper- 
emia of the intestines and stomach, and enlargement of the spleen. The 
impediment to the return of venous blood to the heart causes cerebral con- 
gestion, renal congestion, and, in fact, general systemic venous congestion. 
In addition to these changes, the dilated and hypertrophied left auricle 
throws an abnormal quantity of blood with abnormal force into the left 
ventricle during the diastole, which leads to dilatation of its cavity, and 
necessitates a compensatory hypertrophy of the left ventricular w r alls; this 
hypertrophy increases the force of the reflux current, so that during ex- 



MITEAL REGURGITATION. 



493 



oitement and active physical exertion, pulmonary congestion and oedema 
are liable to occur. 

Etiology. — Mitral regurgitation may occur at any age ; it is especially 
liable in the young to follow rheumatic endocarditis, which causes exten- 
sive valvular retractions aud thickenings. It is not infrequently second- 
ary to changes at the aortic orifice produced either by an extension of endo- 
carditis from the aortic to the mitral valves and their appendages, or by 
the secondary mitral valvulitis excited by the regurgitant blood current 
from the aorta. Mitral insufficiency may also be the result of that enlarge- 
ment of the left auriculo-ventricular orifice which accompanies excessive 
dilatation of the left ventricle. Diseases of the columnae carneae and chor- 
dae tendineae, when their structures are so weakened as to allow the flaps of 
the valves to pass back of the plane of the orifice, will also cause mitral 
insufficiency. Ulcerative endocarditis may also cause it, either by perfora- 
tion and rupture of the valves or by rupture of the chordae tendineae. 

Symptoms. — During the early stage, when the hypertrophy of the right 
ventricle compensates for the regurgitation, there are no rational symp- 
toms which would lead one to suspect its existence ; but when the right 
ventricle is unable to overcome the obstruction to the pulmonary circu- 
lation caused by the regurgitant blood current, there will be more or less 
dyspnoea accompanied by a short, hacking cough with an abundant expec- 
toration of frothy serum. Sometimes the watery expectoration is blood- 
stained. Active physical exertion increases the dyspnoea and causes cardiac 
palpitation. 

In advanced cases, the extremities, face, and lips become blue, the result 
of the interference with the capillary return circulation. The liver becomes 
enlarged and hardened, a condition easily recognized by palpation and per- 
cussion. The patient will complain of a sense of weight and fulness in the 
right hypochondrium, and there will be anorexia, nausea, and a sense of 
oppression in the epigastrium, and sometimes the hepatic circulation be- 
comes so obstructed that the biliary secretion is interfered with and a jaun- 
diced hue of the surface will be added to the cyanotic discoloration, which 
will give to the skin a greenish tint. Headache, dizziness, vertigo, stupor, 
somnolence, and sometimes a peculiar form of delirium of short duration, 
result from the passive cerebral hyperasmia induced by obstruction in the 
superior vena cava. Following the hepatic derangement, are frequent 
attacks of gastric and intestinal catarrh, and evidences of embarrassed renal 
circulation. The urine is diminished in quantity, high colored, and loaded 
with lithates. Sometimes albumen and blood casts are found in it. Fre- 
quently the blood-stained expectoration is accompanied by free haemoptysis ; 
a cough and watery expectoration with occasional dark blood stains are 
usually present as advanced symptoms of mitral regurgitation. Another 
late symptom of mitral regurgitation is dropsy ; it first appears in the lower 
extremities, and gradually extends over the whole body. With the general 
anasarca there is more or less dyspnoea. Late in the disease, pulmonary 
hemorrhagic infarctions may occur. 

The pulse of mitral regurgitation is, at first, regular in force and rhythm ; 



494 



DISEASES OF THE HEAKT. 



later it becomes diminished in volume, irregular in rhythm, and diminished 
in force ; it is never jerking in character. When the heart's action is 

excited, it becomes feeble and com- 
pressible and has a certain tremu- 
lousness. The sphygmographic 
tracing shows great depth and 
amplitude of the diastolic notch. 

Physical Signs. — Inspection. 
The area of the visible cardiac 
impulse is increased, and not in- 
Fig. 106. frequently there is a slight pulsa- 

Sphygmographic tracing in Mitral Regurgitation show- tion, Corresponding in rhvthm 
ing great depth and amplitude of the diastolic notch. 1 , rru 

with the heart beats. The epi- 
gastric pulsation is due to right ventricular hypertrophy, which is a con- 
dition always found with extensive mitral regurgitation. The jugular veins 
appear swollen, especially when the patient is lying down. 

Palpation. — The apex-beat is displaced to the left and is felt lower than 
normal. When the dilatation exceeds the hypertrophy, the apex-beat is 
carried outward and often slightly upward. The impulse is diffused and 
more or less forcible, according as right or left ventricular hypertrophy 
predominates. Palpation sometimes reveals a systolic thrill, which is con- 
fined to the region of the second left intercostal space near the sternum. 
This systolic fremissement is not noticeable when the base of the heart lies 
close to the chest-wall because of retraction of the margin of the left lung. 
A purring tremor, systolic in rhythm, felt most intensely at the apex, and 
becoming feebler the farther the hand is removed from that part, either to 
the right or upward, is invariably due to mitral regurgitation. 2 

Percussion. — Percussion reveals an increase in the area of cardiac dul- 
ness, especially laterally ; it extends both to the left and right of the normal 
line, as well as downward. The area of the superficial as well as of the 
deep-seated dulness will be increased laterally and downward. 

Auscultation. — Mitral insufficiency is attended by a systolic murmur, 
which either completely or partially replaces the first sound of the heart. 
The quality of the murmur is variable, and not in itself distinctive. It is 
usually soft and blowing ; sometimes, toward its end, the murmur will 
assume a distinctly musical character. The first sound of the heart may 
be heard distinctly in the early stages, but later the murmur nearly always 
takes the place of the heart sound. Hence many English writers rightly 
call this murmur "post-systolic" rather than "systolic" in its nascent 
stages. It is heard with its maximum intensity at the apex-beat. Its area 
of diffusion is to the left, on a line corresponding to the apex-beat. It is 
audible at, or near, the inferior angle of the left scapula. It can he heard 
between the lower border of the fifth and the upper border of the eighth 

1 Skoda, Bamberger and Leyden record instances in which inspection showed a double impulse, accom- 
panying, with more or less regularity, each cardiac systole. This only occurs in aggravated cases, and 
arises from non-coincidence of contraction of the ventricles. 

2 Hayden states that " it is exceptional to have a purring thrill with simple mitral reflux.'" I have never 
found it, except in those cases where left ventricular dilatation greatly exceeded the hypertrophy. 




MITE A L REGURGITATION. 



495 



vertebra, at the left of the spine, with nearly the same intensity as at the apex. 
The second" sound of the heart, over the pulmonary valves, is accentuated, 
while at the junction of the third rib with the sternum on the left side, 
both heart sounds are feeble. Skoda first drew attention to exaggeration 
of the second pulmonary arterial sound as a "positive and unerring" indi- 
cation of mitral regurgitation. It is not always present. Whatever 
may be its character, the murmur is generally loudest at its commence- 
ment. 

A loud systolic murmur at the apex, and not heard at the back, is not 
indicative of mitral reflux. If stenosis and regurgitation occur in the same 
individual, they give rise to a combined presystolic and systolic murmur, 
which begins shortly after the second sound of the heart, and continues 
until the second sound commences. The two sounds, although mingling 
to form one murmur, can, in the majority of cases, be readily distinguished 
from each other, for the point of maximum intensity and the very limited 
area of diffusion of a presystolic murmur readily distinguish it from a mi- 
tral systolic, which is audible in the left scapular region. It is important 
to recognize the existence of both these murmurs in estimating the progno- 
sis in any case. 

Differential Diagnosis. — It is usually not difficult to recognize mitral re- 
gurgitation. The seat and rhythm of the murmur and its area of diffusion 
are sufficient to distinguish it from other cardiac murmurs. The character 
of the pulse, the symptoms referable to the right heart, and the pulmonary 
complications will also assist in its diagnosis. It may, however, be mis- 
taken for aortic obstruction, since each gives rise to a systolic murmur, for 
tricuspid regurgitation, and for roughening of the ventricular surface of 
the mitral valve, or of the ventricular wall near the aortic orifice. The di- 
agnosis between mitral regurgitation and aortic stenosis has already been 
considered. 

Mitral and tricuspid insufficiency both produce a systolic murmur ; a 
mitral regurgitant murmur has its maximum intensity at the apex, and is 
conveyed toward the left axillary and scapular regions, while the maximum 
intensity of a tricuspid regurgitant murmur is to the left of the base of the 
xiphoid cartilage, and it is transmitted upward and to the right, — the area 
of transmission establishes the diagnosis. Pulmonary symptoms are prom- 
inent in mitral reflux and absent in tricuspid regurgitation. The pulmo- 
nary second sound is markedly enfeebled in tricuspid regurgitation, and 
markedly intensified in mitral regurgitation. 

Roughening of the ventricular wall gives rise to a murmur which has its 
maximum intensity at the base of the heart, and is transmitted along the 
aortic arch and into the vessels which spring from it in the thorax. The 
vibration of an irregular chorda tendinea stretched across the aortic orifice, 
its extremities being inserted into opposite walls of the ventricle, may pro- 
duce a systolic rvisical murmur, but the line of its transmission will cor- 
respond to that of an aortic obstruction. A systolic mitral murmur, due to a 
sudden rupture of one or a number of the valve-flaps, of the papillary mus- 
cles, or tendons, is a loud, blowing murmur, usually appearing suddenly, 



496 



DISEASES OF THE HEAET. 



which is immediately accompanied by all the urgent symptoms of acute 
pulmonary congestion. 

TRICUSPID STENOSIS. 

This lesion is so rare that there are no rules for its diagnosis. Its morbid 
appearances and etiology are similar to those of pulmonic stenosis. Its 
symptoms would be those due to obstruction to the entire systemic venous 
circulation. The right auricle would be dilated, and there would be vis- 
ceral enlargements in the abdomen, cyanosis of the face and extremities, 
scanty and albuminous urine, hemorrhoidal tumors, headache, dizziness 
and vertigo (due to passive cerebral hyperemia), and general anasarca. The 
few cases recorded are associated with mitral stenosis, with one exception, a 
case of Bertin's. 1 In a case exhibited by Quain, the tricuspid flaps, thick 
and opaque, were united for one-third of their extent. In the other cases, 
the flaps of the valve formed a diaphragm whose central opening admitted 
only the point of one finger. In every recorded case of tricuspid stenosis 
the heart was enlarged. Tricuspid stenosis (as also pulmonic stenosis) may 
be the result of the pressure of a tumor. In all well-authenticated cases, 
the chief symptoms seem to have been extreme lividity, palpitation, and 
dyspnoea. 

Physical Signs. — Inspection reveals general cyanosis. The jugulars are 
turgescent and exhibit presystolic pulsation. This pulsation is sometimes 
the only inconvenience the patient suffers. 

Palpation may discover a venous thrill at the base of the neck. 

Percussion may show the right auricle to be greatly enlarged, and car- 
diac dulness will be increased laterally and toward the right. 

Auscultation. — Tricuspid stenosis should be attended by a presystolic 
murmur whose maximum intensity would be at the lower portion of the 
sternum just above the xiphoid cartilage. This murmur may be propa- 
gated faintly toward the base, but never toward the apex of the heart. It 
is sometimes accompanied by fremitus. Hayden offers the following 
"diagnostic point:" — the murmur of mitral stenosis (without Avhich 
tricuspid stenosis never occurs) is limited to the apex region ; a murmur of 
the same rhythm is produced at the sternum by tricuspid stenosis, "and 
between these two localities there is apointtvhere no murmur can be heard." 

It is unnecessary to consider its differential diagnosis. The lesion 
would be diagnosticated (if at all) by exclusion, and prognosis and treat- 
ment would depend upon the gravity of the accompanying condition. As 
tricuspid stenosis never occurs unless there is extensive mitral obstruction, 
the latter condition is always the predominant one. 

TRICUSPID REGURGITATION. 

This lesion is usually secondary, yet it may be primary. Mitral disease 
is, in nearly every instance, the antecedent condition. 
Morbid Anatomy. — The lesions are similar to those occurring in mitral 



1 Traite. des Mai. du Cceur, Obs. 17. 



TBICUSPID EEGUKGITATIO^. 



497 



insufficiency. The valves are thickened, shrunken and opaque ; the papil- 
lary muscles are shortened and thickened, and the chordae tendineaa under- 
go like changes and are sometimes adherent. The valves, or the columns 
or cords, may rupture ; in either case acute and extensive insufficiency re- 
sults. Acute endocarditis of the right heart is rare in adults, but when it 
occurs the tricuspid valves are its principal and primary seat, on account 
of their anatomical structure and the tension to which they are subject in 
mitral disease. They are rarely the seat of rheumatic or calcareous de- 
generation. Ulcerative endocarditis in the right heart is seldom met with. 1 
Any infection from emboli from the tricuspid flaps will produce their 
secondary effects in the lungs. The first effect of tricuspid regurgitation 
is dilatation of the right auricle ; following this, there will be hypertrophy 
of its walls. The auricular hypertrophy soon ceases to compensate, and 
then venous engorgement occurs. 

As soon as the valves in the subclavian and jugular veins are no longer 
able to resist the regurgitant current, jugular pulsation follows. But, be- 
fore this occurs, the tributaries of the inferior cava and the organs to which 
they are distributed will become greatly engorged, for they have no valves 
to resist the regurgitant current. The inferior cava and the hepatic veins 
sometimes become enormously distended under these circumstances, the 
liver showing the peculiar appearance on section that has gained for it the 
name of nutmeg liver. Following the hepatic changes, the skin as- 
sumes a dingy yellow hue. When this is combined with cyanosis it has a 
peculiar greenish tint, only met with in heart disease. The spleen enlarges 
and hardens ; the mucous membrane of the stomach is congested and 
ecchymotic, and often presents numerous hemorrhagic erosions. Intestinal 
catarrh is subsequently developed, and the general venous congestion with- 
in the abdominal cavity is exhibited by hemorrhoids and ascites. The 
kidneys become congested and stony, and thrombi may form in the femoral 
vein and induce subsequent pulmonary infarctions. 

The stasis in the veins below the diaphragm is accompanied by transu- 
dation of serum, first in the ankles, and thence the dropsy progresses up- 
ward until the patient may finally reach a condition of general anasarca. 
The resulting obstruction to the general systemic circulation may cause 
hypertrophy of the left ventricle, and then we have the rare occurrence of 
disease of the left heart following that of right. Since tricuspid reflux 
has mitral disease for its principal cause, the heart becomes greatly en- 
larged, and a condition of extreme cardiac dilatation and hypertrophy is 
reached. 

Etiology. — The most frequent cause of tricuspid regurgitation is mitral 
stenosis and regurgitation. Tricuspid reflux from primary endocarditis is 
very rare. Any condition of the lungs which will produce hypertrophy 
and dilatation of the right ventricle will lead to it ; it is met with in 
extreme pulmonary emphysema and in cirrhosis of the lung with exten- 
sive chronic bronchitis. Balfour regards chronic bronchitis as its most 



1 Charcot and Vulpian record a case where one of the tricuspid valves was softened and perforated, 
presenting numerous vegetations. Scattered abscesses in the lungs were found in this case. 
32 



498 



DISEASES OF THE HEART. 



frequent cause after mitral stenosis. Any valvular disease in the left heart 
of long duration may lead to it. In all these causes the rationale is the 
same : the abnormal amount of blood in the right ventricle presses with 
undue force against a valve which physiologists regard as normally slightly 
insufficient, and the stress upon the valve flaps and the valvular attach- 
ments is such that endocardial inflammation is excited at the part subject 
to the greatest strain, and valvular insufficiency results. 

Symptoms. — As tricuspid reflux is usually secondary to some other form 
of valvular disease, or to some chronic pulmonary affection, the symp- 
toms during its early stages are vague and masked by those of the 
primary disease. But directly the venous return is markedly impeded, 
a train of symptoms is developed which has its origin in the visceral de- 
rangements. In addition to these symptoms, there may be, in extensive tri- 
cuspid reflux, cardiac palpitation, cardiac dyspnoea, and marked irregularity 
in the force and rhythm of the heart. The liver is enlarged, the skin becomes 
dingy, and there is obstinate constipation and hemorrhoids. The liver is 
rendered liable in such cases to interstitial hepatitis. The spleen is en- 
larged. Venous stasis in the stomach is evinced by dyspepsia, nausea, vom- 
iting, and hsematemesis. The secretion of the kidneys is scanty, dark 
colored, of high specific gravity, often containing albumen and casts. 
Passive cerebral hyperemia is marked by headache, dizziness, vertigo, and 
muscas volitantes ; there is a peculiar mental disturbance which is not 
met with in any other form of heart disease. Placing the patient in 
a horizontal position, after the disease has existed for some time, causes 
the face to become turgid and blue, and if the position be retained, stupor 
and coma may supervene. Jugular and epigastric pulsation are its char- 
acteristic physical signs. A very late symptom is dropsy, which begins at 
the ankles, extending upward until there is general anasarca. It is a no- 
ticeable point, that in the dropsy from tricuspid reflux the genital organs 
sutler slightly, if at all. 

Physical Signs. — Inspection. In extensive tricuspid disease, the area of 
cardiac impulse is increased more than in any other valvular lesion. This 
area sometimes extends from the nipple to the xiphoid cartilage, and it 
may reach as high as the second right intercostal space. There is a visi- 
ble impulse in the jugular veins, more apparent in the right than in the 
left. Sometimes the veins in the face, arms, and hands are seen to pulsate, 
and even the thyroid and mammary veins. 

Palpation. — The apex-beat is indistinct, except in cases where there is 
marked hypertrophy of the left ventricle. Pulsation occurs in the epi- 
gastrium, which maybe due to reflux into the enlarged hepatic veins, or to 
the fact that the dilated and hypertrophied right ventricle so presses on the 
liver, that the impulse is conveyed through the diaphragm with each car- 
diac pulsation. Early in the disease, the impulse in the jugular is con- 
fined to the lower part of the vessel. Beyond this point, the vein rarely 
undulates. Later, a systolic pulsation is felt as high as the angle of the 
jaw, and may be accompanied by distinct, though feeble, presystolic pul- 
sation. The liver may simply undergo systolic depression, chiefly at the 



PULMONIC OBSTRUCTION. 



499 



left lobe ; or the whole liver may pulsate from an impulse coming from an 
enormously dilated vena cava ; or the systolic pulsation of the veins within 
the organ may give rise to a palpable expan so-pulsatory movement. The 
hepatic pulsation is synchronous with the cardiac impulse. In rare 
cases it precedes jugular pulsation. Sometimes pulsation is felt in the 
femoral veins, 1 Sphygmographic tracings of the jugular pulse show it to 
be dicrotic. 

Percussion shows an increase in the area of cardiac dulness to the right 
and upward, sometimes as far as the second intercostal space. 

Auscultation. — The murmur of tricuspid reflux is heard with, or takes 
the place of, the first sound of the heart ; it is superficial, of low pitch, 
blowing, soft, and faint, and is heard with greatest intensity over the lower 
part of the sternum, at its left border between the fourth and. sixth ribs. 
It is rarely audible above the third rib, or to the left of the apex-beat. This 
murmur is transmitted from the region at the base of the xiphoid cartilage, 
upward and to the right, from one to two inches. Sometimes it is heard 
over a very limited area, and then it may be overlooked. 

Differential Diagnosis. — A tricuspid regurgitant murmur may be con- 
founded with an aortic obstructive, pulmonic obstructive, and mitral regur- 
gitant. A tricuspid regurgitant murmur is never audible above the third rib, 
is accompanied by an accentuation of the second sound over the pulmonary 
artery and by jugular and epigastric pulsation, and is heard with maximum 
intensity near the base of the ensiform cartilage. These points are suffi- 
cient to differentiate it from an aortic obstructive murmur. 

The differential diagnosis between it and a mitral regurgitant murmur 
has been given. 

PULMONIC OBSTETJCTIOtf. 

Very little is known of diseases at the pulmonary orifice. Their diagnosis 
is arrived at by exclusion, and they cannot be recognized, except by their 
physical signs. Endocarditis in the right heart is rare, except in intra- 
uterine life. Valvular diseases of the right heart are usually the sequelae 
of valvular disease in the left. The pulmonary artery may become athe- 
romatous, but, even then, disease of the pulmonary valves is rare. Balfour 
believes that constriction of the pulmonary artery may occur at various 
periods of intra-uterine life ; as a rule, the pulmonary valves are subject to 
no lesions except congenital malformations. 

Morbid Anatomy. — Bertin records an instance of pulmonary obstruction 
where the distorted and adherent valves formed a horizontal septum across 
the orifice, which was only one-fourth of an inch wide. A rigid tricuspid 
valve has been found to be the cause of obstruction at the pulmonary ori- 
fice, the pulmonary valves themselves being normal. A few autopsies have 
revealed obstructions at the pulmonary artery caused by aneurisms, tumors 
of the pericardium or of the anterior mediastinum, enlarged bronchial 
glands, or pressure of a solidified lung. The pulmonary artery may be oc- 

1 Guttman thinks epigastric pulsation is due wholly to reflux into the veins of the liver, and not to right 
ventricular pulsation. 



500 



DISEASES OF THE HEART. 



eluded just beyond the valves by a cancerous tumor, and there are exam, 
pies where a phthisical process in the left lung has induced it. A murmur 
indicative of pulmonary obstruction may be produced by a cardiac throm- 
bosis. 

The above statements I place under the head of morbid anatomy of the 
lesion, as they cannot be appreciated nor their pathological significance 
realized during life. Eeasoning from analogy, obstruction at the pulmo- 
nary orifice ought to be followed by compensatory hypertrophy of the right 
ventricle, and accompanied by tricuspid regurgitation and dilatation of the 
right auricle. 1 I have met with only two cases of pulmonic obstructive 
murmurs in which autopsies were obtained. In both cases it was found 
that the murmur had been produced by mediastinal tumors pressing upon 
the pulmonary artery so as to diminish its calibre. 

Etiology, — Pulmonary stenosis is rarely the result of endocarditis or of 
degenerative changes in the pulmonary artery. Bertin states that when ab- 
normal communication between the two sides of the heart has existed, the 
arterial blood may excite endocarditis in the right heart. Syphilis has 
been advanced as a possible cause of degenerations at the pulmonary orifice. 

Symptoms. — The only rational symptoms that have been noted in the few 
recorded cases of pulmonic disease admit of manifold explanations, and no 
one is either constant or diagnostic. In some cases anaemia existed ; in 
others there was cardiac palpitation, dyspnoea, cyanosis, and dropsy, but 
none of these belong exclusively to a pulmonic lesion, nor do they necessa- 
rily depend upon it. 

Physical Signs. — Inspection, palpation, and percussion give negative re- 
sults. Palpation may give a systolic thrill, confined to the second left in- 
tercostal articulation. Such a fremissement results both from roughness 
and contraction of the pulmonic orifice. 

Auscultation. — A systolic murmur is heard with its maximum intensity 
directly over the pulmonic valves ; it is very superficial and consequently 
very distinct, and is limited in its diffusion. It is never heard at the xiphoid 
cartilage, nor along the course of the aorta. If it has an area of diffusion, 
it is toward the left shoulder. The murmur is loud and soft in character, 
sometimes " bellows ; " it is not audible in the vessels of the neck, nor is it 
attended by arterial pulsation. When phthisical consolidation partially oc- 
cludes the pulmonary artery, a loud but soft systolic murmur is heard, 
which is sometimes high-pitched and musical, and which is often entirely 
suspended during a full inspiration. In some few instances, there is a bruit 
de diahle in the jugular veins. 

Differential Diagnosis. — It is possible to confound a pulmonic obstructive 
murmur with a mitral regurgitation which is propagated upward into the 
left auricular appendix. But the area of a mitral regurgitant is also back- 

1 Dr. Ormerod records three cases in which pulmonary obstruction was diagnosticated during life, and 
where the post-mortem proved the accuracy of the diagnosis. Two of these occurred in men under twenty- 
eight, and the other in a woman twenty-one. In two of these cases all the cardiac valves were healthy, 
except the pulmonic. The pulmonic orifice would barely admit a goose quill. Warbnrton Begbie men- 
tions a case (man: aet. 18) in whom reflux and stenosis at the pulmonary orifice coexisted. There were 
four valves, and these were incompetent. All the other valves were normal. Congenital stenosis of the 
infundibulum of the right ventricle is the probable result of foetal myocarditis or syphilis. 



PULMONIC ^REGURGITATION" . 



501 



ward, and by this it could be distinguished from a pulmonic obstruction. 
Beside, in mitral disease the pulse is very different from the pulse of pul- 
monary stenosis. 

Aortic stenosis can hardly be mistaken for pulmonary obstruction, for the 
arterial pulsation, the peculiar pulse, and the transmission of the murmur 
into the arteries of the neck will suffice to discriminate between them. An 
aneurism at the sinus of Valsalva may produce a murmur in the pulmonary 
artery by the pressure which is exerted upon that vessel. It would be im- 
possible to distinguish this murmur from that of a pulmonic stenosis. 

The diagnosis of pulmonary obstruction is usually reached only by ex- 
clusion. 

PULMONIC EEGURGITATION. 

Many doubt the occurrence of this form of valvular lesion. There are 
only a few well authenticated cases, 1 and in them the lesion has been the 
result of injury or congenital defect. The statement 2 that the pulmonary 
valves exhibit a cribriform condition nearly as often as the aortic, is not 
sustained by post-mortem examinations. In one of the cases to which I 
have referred as an example of pulmonary stenosis^ the valves were also in- 
sufficient. In Dr. Begbie's case, where there were four flaps to the valves 
(producing obstruction), marked insufficiency coexisted. The morbid an- 
atomy, etiology, and rational symptoms do not require a separate considera- 
tion. The anatomical conditions are the same as those found in similar 
conditions of the aortic valves ; and the etiology and rational symptoms 
are those of pulmonic stenosis. 

Physical Signs. — Theoretically pulmonic regurgitation should be accompa- 
nied by a diastolic murmur having its maximum intensity over the pulmonic 
valves ; and its area of diffusion should be downward and toward the xiphoid 
cartilage. It should be soft and blowing in character. This murmur is 
rarely heard alone ; it is usually associated with obstruction at the same 
orifice, or with some murmur whose origin is on the left side of the 
heart. Memeyer states that dyspnoea, hemorrhagic infarction, and con- 
sumption of the lungs have followed insufficiency at the pulmonary orifice. 
No other authority mentions such symptoms, while the assignment of val- 
vular disease as a cause of phthisis is absurd. With a pulmonic regurgitant 
murmur there should be, on palpation and percussion, physical evidences of 
hypertrophy and dilatation of the right heart, the rationale of whose pro- 
duction should be identical with that which was considered in aortic re- 
gurgitation. I have never heard a regurgitant pulmonic murmur. 

Differential Diagnosis. — The murmur of pulmonary regurgitation may be 
mistaken for that of aortic regurgitation. The points in connection with 
their differentiation have already been given. The prognosis and treat- 
ment are the same as those of the former lesion. 

Prognosis in Valvular Disease of the Heart.— The duration of life in valvu- 
lar disease of the heart varies greatly. 



i Path. Trans., vol. xvi., p. 74. 



2 Dis. of Heart. Bellingham. 



502 



DISEASES OF THE HEART. 



To establish a basis of comparison, I shall give a resume of eighty-one 
cases, in all of which the diagnosis of valvular disease was confirmed by a 
post-mortem examination. 1 In fourteen cases of different valvular diseases, 
each of which was complicated by cardiac hypertrophy and dilatation, fifty 
per cent, of deaths were directly due to the valvular lesion. In one of 
these, where there was stenosis at both the mitral and tricuspid orifices, 
death was sudden. In fifteen cases in which there was only cardiac hyper- 
trophy, eleven deaths occurred from the heart-lesion, five of which were 
sudden and directly due to the valvular lesion. In six cases in which dilata- 
tion alone existed, four deaths directly resulted from the heart-lesion, and two 
of these were sudden. In not one of fifteen cases of aortic disease did death 
occur directly from the heart-lesion. Of these fifteen cases, sudden death 
occurred in only two. In twelve cases of calcified mitral valve, no death oc- 
curred directly from the heart-lesion ; there were but two sudden deaths, 
both from cerebral apoplexy. The aortic and mitral valves were diseased in 
fourteen cases ; two deaths were due to the heart-lesion, and there were but 
three sudden deaths (uraemia, apoplexy, and croupous laryngitis). The aortic 
and pulmonary valves were involved in three cases, all of which died suddenly, 
and none directly from the heart-lesion. In two instances, the aortic, mi- 
tral and tricuspid were involved, in neither of which sudden death occurred. 
Thus, of eighty-one cases, twenty-four deaths only were directly due to the 
heart-lesion, and of these only eight were sudden. 

From the above cases it seems evident that the prognosis is not bad in 
valvular disease, except when hypertrophy and dilatation coexist, and then 
many complications are liable to occur. In 1870, I had a patient sixty 
years old with extensive aortic reflux, who had had three attacks of pneu- 
monia during the eight years he was under my observation. There was only 
slight cardiac dilatation in this case. 2 

In aortic stenosis, life may be prolonged many years. So long as the 
left ventricular hypertrophy compensates for the stenosis, the prognosis is 
good ; but when it fails, and dilatation begins, cerebral anaemia soon re- 
sults. If violent or prolonged efforts are followed by irregular heart- 
action, sudden death may occur. Hypertrophy and dilatation, syncope, 
cerebral anaemia, vertigo, muscular debility, a very pale face, and an irreg- 
ular pulse render the prognosis unfavorable. Should vegetations be 
suspected, there is danger of cerebral embolism. Complicating (secondary) 
mitral disease renders the prognosis unfavorable. Death results from 
complications, degenerations of the heart, and pulmonary oedema. 

Aortic regurgitation is a graver form of disease than aortic stenosis. Its 
duration is indefinite, as it may give rise to no symptoms until it is far ad- 
vanced. Twenty-one days and five years are the extreme limits recorded. 
In no other valvular disease is sudden death so Halle to occur. Eefer- 
ence to the above cases shows that mitral stenosis ranks nearly equal to it 
in this respect. The shorter and more gushing the murmur, the more ex- 

1 Med. Rec, N. Y., Apr. 1, 1870, p. 66, etc. 

2 Dr. Walshe states that the order of relative gravity of valvular lesion is : Tricuspid reflux, Mitral 
reflux and stenosis, Aortic reflux, Pulmonary stenosis and Aortic stenosis. 



PROGNOSIS IX CARDIAC VALVULAR DISEASE. 



503 



tensive the regurgitation, the effects of which must always be carefully esti- 
mated before a prognosis can be given. Aortic regurgitation is, however, 
more serious in the young than in adults, because in children the changes 
are less atrophic and more inflammatory. In middle life and in those 
who are subjected to great physical or mental strain, the prognosis is un- 
favorable ; if the vessels in these patients show evidences of degeneration, 
apoplexy and cerebral thrombosis are liable to occur. In the very old, I 
have known extreme aortic regurgitation to exist a long time and cause 
little inconvenience. Cyanosis and dropsy and signs of heart failure, dila- 
tation, or degeneration of the walls of the heart, render the prognosis un- 
favorable ; if mitral regurgitation is developed, visceral derangements 
occur and hasten the fatal issue. Sudden valvular incompetence is far 
more dangerous than that which has developed slowly. The prognosis is 
determined more by the condition of the heart walls and the general nutri- 
tion of the patient than by any other elements. When aortic regurgitation 
is complicated by aortic stenosis and mitral regurgitation with marked 
derangement of the general circulation, the prognosis is bad. Death may 
result from embolism, apoplexy, dropsy, pulmonary oedema, sudden cardiac 
insufficiency, or from visceral complications. When the radial impulse is 
felt a little after the apex-beat, it is always important to determine whether 
the heart's action remains regular under mental excitement or violent 
physical exertion ; if it does, the prognosis is good. 

Mitral stenosis admits of no compensation. If extensive, it is always a 
grave disease. The prognosis is estimated by the severity of the thoracic 
symptoms ; if these are greatly increased by physical exertion, the prognosis 
is bad, for pulmonary congestion* and oedema, infarctions and diffused pul- 
monary apoplexy with large extravasations are liable to occur. Statistics 
show that sudden death occurs nearly as often in mitral stenosis as in aortic 
regurgitation. Congenital mitral stenosis is not dangerous, nor does it occa- 
sion inconvenience, for it is always associated with hyperplasia of the arterial 
system. The later in life mitral stenosis occurs, the worse the prognosis. 

Mitral regurgitation, when uncomplicated, gives rise to very little dis- 
turbance of the circulation, because it is generally most fully compensated 
for, and the changes which lead to it are of slow growth and their tendency 
is to remain stationary. Patients with moderate regurgitation suffer little, 
even on exercise. As long as right ventricular hypertrophy compensates, 
there is no dyspnoea. As regards the duration of life, the prognosis m 
mitral reflux is good. When, however, stenosis and regurgitation coexist, 
sudden pulmonary complications are very liable to occur, and the prognosis 
is bad. When signs of right heart failure occur, the prognosis is bad. 
(Edema of the extremities, fluid in serous cavities, cyanosis, dyspnoea, and 
haemoptysis are indications of such failure. Death may result from gen- 
eral anasarca, serous effusions into the pleura?, peritoneum, or pericardium, 
pulmonary oedema and congestion, or from sudden cardiac insufficiency. 

Extensive obstruction or regurgitation at the pulmonic orifice would lead 
to serious results, but w r e have no statistics upon which to base a prog- 
nosis. 



504 



DISEASES OF THE HEART. 



Tricuspid stenosis and obstruction, when associated with mitral dis- 
ease, are very grave lesions, but not so bad as when resulting from chronic 
bronchitis or pulmonary emphysema. When jugular and epigastric pul- 
sation are marked, the changes in the viscera already referred to quickly 
ensue. Walshe says : ' ' Tricuspid regurgitation is the worst of all valvular 
lesions." Patients with tricuspid regurgitation are in constant danger 
from intercurrent attacks of acute pulmonary hyperemia. Tricuspid dis- 
ease leads more rapidly than any other valvular lesion to cyanosis and 
dropsy. 

Treatment of Valvular Diseases of the Heart. — The treatment of aortic 
valvular disease can be summed up in, rest, diet and regimen. Rest must 
be mental as well as physical. The appetite, emotions and passions must 
be under perfect control, hence a sedentary country life is best. Strain- 
ing, especially when the hands are above the head, is to be avoided. The 
nutrition must be kept as perfect as possible to guard against cardiac de- 
generative processes. Sugar, sweet vegetables, and animal fat must be 
sparingly used. The food should consist of nitrogenized material taken 
in quantities that do not interfere with the heart's action. In aortic re- 
gurgitation, patients while sleeping should assume, as nearly as possible, a 
horizontal position, as they thus lower the height of the distending column 
of blood, and relieve both the cardiac circulation and the tendency to pul- 
monary congestion. When defective aortic pressure reacts injuriously on 
the gastric and hepatic secretions, moderate alcoholic stimulation may be 
cautiously employed. The bowels should be daily gently moved. That 
the skin may be active, the body must be warmly clothed. Prolonged ex- 
posure to cold is to be avoided. Warm baths, especially warm sea-baths, 
are beneficial. Medicine is not to be given until the hypertrophy ceases 
to compensate. In aortic reflux with feeble heart-power, tr. digitalis 
and tr. ferri perchlor. are to be given in ten-drop doses, three times a day. 
The iron is especially called for when anaemia is present. Digitalis is 
given as a cardiac tonic, hence small doses only are required. As long as it 
increases the urinary secretion it is safe to continue it. When vertigo and 
syncope are prominent symptoms, quinine and strychnia may be given 
with the digitalis. Should the heart act with violence and rapidity, or 
if there is evidence of high arterial tension, aconite is serviceable. 

In aortic incompetence small doses of arsenic have a stimulating effect, 
when given with digitalis and iron. Iron may disturb the stomach ; arse- 
nic seldom does. Quassia or calumba should always be given with iron. 
When the hepatic or gastric vessels are engorged, three or four leeches 
over the epigastrium or liver, followed by warm anodyne poultices, will 
often afford relief. Large quantities of fluid should never be taken into 
the stomach at one time. Symptoms of angina pectoris with dyspnoea and 
local pain are signs of aortitis, which demands leeches over the sternum 
and small doses of mercury. The treatment of dyspnoea, dropsy, etc., etc., 
will be considered in the treatment of mitral disease. The pain of aortic 
disease may be so severe as to demand an anodyne ; opium by the mouth 
cannot be given, but the sulphate or hydrochlorate of morphia can be 



TKEATME^T OE CAEDIAC VALVULAR DISEASE. 



505 



given hypodermatically. Nitrite of amyl often relieves the angina 
promptly. 1 

The first thing in the treatment of mitral stenosis is to have the patient 
fully understand his exact condition, that he may follow your advice im;- 
plicitly, for the treatment is for the most part in his own hands. As to 
nutrition, the same rules hold as in aortic disease. There must be at least 
one gentle daily evacuation of the bowels. Straining at stool is to be 
avoided. The use of alcohol, strong tea or coffee or tobacco is to be pro- 
hibited. If anaemia exists, give iron one-half hour after meals, gr. x — xx 
of Vailette's mass, two or three times daily for a long period. The pro- 
longed use of the voice is dangerous. Small doses of quinine and strych- 
nia alternating with the iron are advantageous. If there is anorexia, the 
vegetable bitters are to be given. The triple phosphates of iron, quinine 
and strychnine, or small doses of dilute sulphuric acid will improve these 
patients when they show signs of extreme debility. In every case of mitral 
disease there comes a time when pulmonary hyperemia shows failure of 
right cardiac compensation. An adjustment of the heart to the circula- 
tion is now effected by administering digitalis, which should only be given 
when heart failure is marked and is accompanied by pulmonary congestion. 
Half an ounce of the infusion, every two hours for twenty-four or 
forty-eight hours, is often required to overcome the cardiac failure. The 
time will come when digitalis ceases to sustain the heart, hence it should 
be used sparingly and carefully — never continuously. When the pulse is 
rapid, feeble, and irregular, more time and greater force for the ejection of 
blood from the ventricle are demanded. Digitalis meets both indications. 
The pulse becomes regular, full, and forceful. The urine becomes abun- 
dant and normal. Pulmonary engorgement diminishes and commencing 
dropsy slowly disappears. Hayden advises 1 0 drops of chloroform, 15 drops 
of tincture of digitalis, and 1 5 drops of tincture ferri perchloridi, in one 
ounce of water every three hours. When asystolism is present, or sup- 
pression of urine is threatened, digitalis must be given in large doses. In 
most cases of mitral stenosis digitalis is contraindicated. The dropsy of 
advanced mitral reflux may be promptly relieved by pulvis jalapm co. com- 
bined with calomel in sufficient quantity to produce prompt and free cathar- 
sis. Squills, juniper, broom, and cream of tartar act as diuretics in such 
cases. 

In mitral regurgitation a compound of digitalis and nitrous ether acts 
well as a diuretic. Whenever a diuretic is given in heart disease, the loins 
should be cupped or warm poultices applied and the bowels freely purged. 
In copious haemoptysis in cardiac disease, ergotin in full doses hypoder- 
mically may be given. The haemoptysis that accompanies pulmonary apo- 
plexy of heart disease may relieve the dyspnoea ; hence Drs. Dickenson, 
Fagge and other English authorities recommend venesection for relief of 
pulmonary engorgement. Precordial pain accompanying valvular disease 
may be relieved by the application of leeches over the precordial space. 



1 Barlowe and Fagge advise senega and carbonate of ammonia for the less severe effects of aortic regur- 
gitation, which they regard as least amenable to treatment of all cardiac diseases. 



506 



DISEASES OF THE HEART. 



Hyoscyamus, hydrochl orate of morphia, nitrite of amyl, chloroform, and a 
belladonna plaster over the precordium may be employed for the same pur- 
pose. Such pain is the cry of a heart-muscle for higher nutrition. Bleed- 
ing favors dropsy by thinning the blood and by diminishing the heart- 
power ; it should never be practised except in emergencies. 1 When digi- 
talis fails to regulate the circulatory disturbances, its use does harm ; but 
in all cases of mitral disease where this drug has not been used, it is safe to 
say that its administration will give prompt relief. Morphia is the best 
anodyne and hypnotic to be used in mitral disease. 

Hygiene, diet, and exercise are to be the same in pulmonary, as in 
mitral disease, further treatment is solely symptomatic. 

The treatment of tricuspid obstruction depends on the gravity and 
sequelae of the accompanying mitral disease. For tricuspid stenosis never 
occurs till mitral stenosis is excessive, and the latter condition is the pre- 
dominant one. The general treatment is the same as in aortic and mitral 
diseases. The patient should lead a perfectly quiet life in a warm, equa- 
ble climate. When this lesion occurs with mitral disease, digitalis should 
not be omitted, for the drug promotes ventricular contraction, and thus 
relieves the tricuspid pressure. In tricuspid regurgitation with emphysema, 
this drug should be very cautiously given, and its use or omission must 
depend upon the effects produced in each case. If cerebral symptoms are 
exaggerated it must be stopped. Tonics should be given on the same prin- 
ciples as in mitral disease and the same drugs used. A drastic purge or 
taking a few ounces of blood from the arm temporarily relieves the venous 
engorgement. Dropsy and local oedema are treated as in mitral disease. 
For the relief of the gastric, hepatic and intestinal symptoms, which are 
often the most troublesome occurrences in tricuspid regurgitation, I have 
found one or two purgative doses of calomel to act promptly and satisfac- 
torily — in fact, in all cases of heart disease in which there is evidence of 
hepatic hyperemia, an occasional calomel purge will be followed by marked 
relief and improvement. 

Several new drugs have recently been employed in the treatment of car- 
diac diseases. Strophanthus and nitroglycerine are the more important. 
In many cases where a simple cardiac tonic is desired, or when digitalis 
causes gastro-intestinal disturbances, strophanthus will be found valuable. 
It is more prompt in action than digitalis, and thus may be used to initiate 
an action which is to be continued by digitalis. Nitroglycerine, in patients 
who are not affected unpleasantly by its action, may be employed to lower 
arterial tension, and thus relieve a laboring heart. Oonvallaria is at times 
of value, but its action is not constant or permanent, and, like strophan- 
thus, it has little diuretic action. Adonidine relieves many of the distress- 
ing symptoms, but appears to me to act only as a sedative. Caffeine is a 
valuable cardiac stimulant for temporary effects. When digitalis fails or 
cannot be used in cases of cardiac dilatation, spartein sometimes gives 



1 Niemeyer advises arsenic and antimony in mitral valvular disease ; when and why he does not 
say. 



CAKDIAC HYPERTROPHY. 



507 



relief. Its action is quickly obtained, as it is absorbed rapidly and elimi- 
nated with equal rapidity. 

No drug, however, has yet been introduced which supersedes digitalis as 
a cardiac tonic in the early stages of cardiac disease. 



CARDIAC HYPERTROPHY. 

By the term cardiac hypertrophy is meant thickening of the walls of the 
heart by an increase in their muscular tissue. This muscular increase may 
be confined to one portion of the heart, or it may involve the walls of both 
auricles and ventricles. There are three recognized forms of cardiac hyper- 
trophy. 

I. Simple Hypertrophy. — In this form there is an increase in the thick- 
ness of the cardiac walls, the capacity of the cavities remaining normal. 
Simple hypertrophy is usually confined to the left ventricle, and is most fre- 
quently met with in connection with chronic Bright's disease and chronic 
alcoholismus. 

II. Eccentric Hypertrophy. — In this form there is thickening of the walls 
of the heart, with increase in the capacity of its cavities. It is most com- 
monly met in connection with, or occurs as the result of, some valvular 
lesion. 

III. Concentric Hypertrophy. — In this form there is thickening of the 
walls of the heart, with diminution in the size of the cavities. Some 
observers deny its occurrence, and claim that the diminution in the capa- 
city of the cavities is only apparent — that it is the result of violent ven- 
tricular contraction just prior to death. I have never seen any example 
of this form of hypertrophy. 

Morbid Anatomy. — The anatomical changes in cardiac hypertrophy vary 
according to its seat, and sometimes according to the character of the 
hypertrophy. In eccentric hypertrophy there will always be an increase 
in the size of the papillary muscles, and the septum will be thickened, 
which does not necessarily occur in connection with simple hypertrophy. 
The ventricular septum is far less liable to hypertrophy than the rest of 
the ventricular parietes. It is often difficult, even after death, to deter- 
mine the existence of a moderate degree of cardiac hypertrophy, while 
extensive hypertrophy is very readily recognized. 

When cardiac hypertrophy exists, the first thing noticed is a change in 
the shape of the organ, and this change will correspond to the seat of the 
hypertrophy. If the hypertrophy is confined to the left ventricle, either 
simple or eccentric, the heart will assume a more than usual pyriform 
shape, and will become elongated — the right ventricle seems to be a mere 
appendage to the left. On the other hand, hypertrophy of the right ven- 
tricle increases the horizontal measurement of the organ and gives it a 



508 



DISEASES OF THE HEART. 



more oval shape, the apex not being as pointed as in health, since the 
extremities of both ventricles are on the same level. If all the cavities of 
the heart are increased in capacity, and their walls hypertrophied, the 
whole heart will be increased in size, but the change will be most marked 
in its horizontal direction, and the organ will assume a globular shape. 
Sometimes the shape of the organ is not notably changed in general 
hypertrophy. 

Left ventricular hypertrophy occurs of tener than right, and hypertrophy 
of the right auricle much oftener than that of the left. The ventricles 
are hypertrophied oftener than the auricles. In all varieties of hypertro- 
phy the cardiac walls are stiff, so that when the cavities are opened and 
the blood has been removed from them, they do not collapse. The sub- 
stance of an hypertrophied left ventricle can generally be torn with ease, 
while an hypertrophied right ventricle is tough and leathery. The color 
of the muscular tissue is redder than normal ; there is an increase in the 
number of the muscular fibres, which differ in no way in their anatomical 
structure from those of normal heart muscle. Occasionally there is an 
increase in the size of the cardiac muscular fibres. 1 There may be more 
or less increase of connective-tissue between the muscular bundles ; and 
Dr. Quain stated that this may be so excessive as to be a "false hyper- 
trophy." Sometimes there are accumulations of fusiform involuntary 
fibres which have not as yet developed into the higher state of striped 
fibres. 

There is no limit to cardiac hypertrophy. The heart may reach such a 
degree of enlargement as to weigh forty ounces more than in its normal 
state (" cor bovinum"). After the hypertrophy reaches a certain point 
there is dilatation, preceding and accompanying which is fatty degenera- 
tion, which first occurs in the more recently formed muscular fibres. An 
increase in the number or size of the muscular fibres of the heart walls 
causes a corresponding increase in the heart power. The walls of the hy- 
pertrophied heart vary in thickness according to the cause of the hyper- 
trophy. The walls of the left ventricle may become an inch and a half 
or even two inches thick, while those of the right ventricle rarely reach 
an inch in thickness. The auricles are seldom more than double their 
normal thickness. The columnse carnese of the right ventricle are more 
liable to hypertrophy than the walls. Sometimes the walls of a cavity are 
thinned at one point while they are hypertrophied at another. The heavier 
a heart becomes, the deeper does it lie in the thoracic cavity ; the dia- 
phragm is pushed down, and the heart inclines more to the left of the 
thorax. 

Etiology. — In general terms cardiac hypertrophy is caused by over- 
work ; for some reason the cardiac walls are called upon to perform 



1 Cornil and Ranvier state that " it is not yet known whether hypertrophy is entirely due to increase m 
size of the muscle-fibres, or to a new formation of these fibres. The phenomena of development of new 
muscle-fibres have never been observed, so that the former hypothesis seems the more probable." 



CAEDIAC HYPERTROPHY. 



509 



more than their normal amount of labor, and an increase in the number 
of their muscular fibres necessarily follows. Whenever the function 
of the heart is permanently or repeatedly overtaxed, or when the resist- 
ance which it should normally encounter is increased, hypertrophy of 
its walls is the result. The modes by which it is directly induced are as 
follows : 

(1) Dilatation of the Cavities of the Heart. — Under certain circumstances 
dilatation of one or all of the cavities of the heart takes place during its dia- 
stole, and they receive more than their normal quantity of blood. A certain 
degree of force is required to discharge the normal quantity of blood ; if 
there is more than the usual amount, an abnormal degree of force is required 
to expel it. This demand for increased heart power is supplied by an in- 
crease of muscular fibres in the heart walls, — the hypertrophy is developed 
in proportion to the increase of force required. This is the cause of those 
forms of cardiac hypertrophy which occur in connection with valvular 
insufficiency. Under these circumstances the hypertrophy is always eccen- 
tric, and is not due so much to the valvular lesions as to the dilatation of 
the heart cavities which occurs as a result of these lesions. The order is, 
first, dilatation, then hypertrophy to compensate for the dilatation. Dila- 
tation is developed during cardiac diastole ; hypertrophy during cardiac 
systole. 

(2) Mechanical Obstruction. — Of those causes which originate in the 
heart, aortic stenosis gives rise to hypertrophy of the left ventricle ; mitral 
stenosis to hypertrophy of the left auricle ; pulmonic disease to hypertro- 
phy of the right ventricle ; and tricuspid stenosis to hypertrophy of the 
right auricle. In the list of mechanical causes are included all those dis- 
eases of the arteries which diminish their elasticity. The walls of the 
large arteries may lose their elasticity from atheromatous degeneration, or 
they may be constricted or dilated, and thus offer obstruction to the blood 
current. An aneurismal tumor may have developed sufficiently to obstruct 
the current of blood, 1 or some tumor may press upon and diminish the 
calibre of the aorta ; under such circumstances a more than normal 
amount of work will be imposed upon the left ventricle, and simple car- 
diac hypertrophy will be developed as the result. Twisting of the thorax 
and deformities of the spine, thorax, etc., may act in the same way. Again, 
obstruction to the pulmonary circulation will give rise to hypertrophy of 
the walls of the right ventricle ; in many instances dilatation will occur 
prior to the hypertrophy, but in quite a large number of cases direct 
hypertrophy of the right ventricular walls will occur as the result of 
obstruction to the pulmonary circulation, Such obstruction may be devel- 
oped in connection with pulmonary emphysema, fibroid and compressed 
lung, chronic pleurisy, asthma, hydrothorax, and other chronic diseases 
which interfere with the circulation of blood through the lungs. It does 



1 But this is rare : Axel Key has shown that aneurism of the aorta alone is not productive of left ven- 
tricular hypertrophy, since it does not lead to increase in the arterial tension. 



510 



DISEASES OF THE HEAKT. 



not occur in the early stage of pulmonary phthisis, for the pulmonary cir- 
culation is not obstructed until the advanced stage of the disease. Hyper- 
trophy of the left ventricle may also result from interference with the 
general capillary circulation. 

Simple hypertrophy of the ' cardiac walls is one of the most constant 
attendants of Bright' s disease. 

The relations between cardiac hypertrophy, arterial and renal disease 
are exceedingly complex. It is "known that the changes of general arterial 
capillary fibrosis induce an increased arterial tension which causes hyper- 
trophy of the heart, and that a similar cardiac condition is a constant 
attendant of all forms of chronic Bright's disease. The. theory that the 
renal obstruction alone is responsible for the hypertrophy is now aban- 
doned, and two distinct conditions are recognized. In one the renal 
change is cirrhotic and part of a systemic condition, developed in a patient 
of fibroid diathesis. In such cases the vascular changes causing increased 
arterial tension and cardiac hypertrophy are organic and permanent. In 
the other cases the renal changes are parenchymatous, and the vascular 
contraction is arterial, and due primarily to contraction of the muscular 
coat, through a sympathetic nervous stimulus, that is intended to produce 
increase of arterial tension for the sake of its diuretic action. It is claimed 
that this reflex vasomotor contraction may result in hypertrophy of the 
muscular coats of the arteries. In chronic alcoholismus, rheumatic hyper- 
inosis, or any other condition which interferes with the systemic capil- 
lary circulation, more or less extensive simple cardiac hypertrophy of the 
left ventricle is developed. 

Anything which increases for any length of time the rapidity and force 
of the heart's contraction may produce cardiac hypertrophy. Among this 
class of causes may be included excessive and prolonged muscular exercise, 
esjoecially in young subjects, and in soldiers who are on the march. Emo- 
tional conditions that produce cardiac palpitation, prolonged mental ex- 
citement, the immoderate use of strong coffee or alcohol, are causes of car- 
diac hypertrophy. These are styled " nervous" causes (Quain) ; and to 
this class probably belong those cases occurring in Graves's or Basedow's 
disease. Pericarditis is not infrequently a cause of cardiac hypertrophy, 
either by inducing softening and dilatation of the ventricles, or by the 
obstruction which is offered to the heart's action by the adhesions between 
its two surfaces. The heart becomes hypertrophied in pregnancy, but 
returns again to normal after delivery. Sometimes no cause can be found 
for cardiac hypertrophy. 

Symptoms. — The valvular lesions, arterial changes, or capillary obstruc- 
tions which are associated with cardiac hypertrophy modify, or to a greater 
or less extent obscure, the phenomena which attend the hypertrophy. Total 
eccentric hypertrophy usually cannot be detected except by a physical ex- 
ploration of the chest. There are, however, certain subjective symptoms 
which are important and which will aid in its diagnosis. The direct effect 
of general hypertrophy of the heart is to cause an abnormal fulness of the 



CARDIAC HYPERTROPHY. 



511 



arteries and a lack of blood in the veins. The pulse is full and strong, and 
is bounding in character ; the face is easily flushed, the eyes somewhat 
prominent and brilliant, and there is carotid pulsation. The respiration is 
not usually disturbed until the heart becomes so increased in size as to give 
rise to pressure upon the adjacent lung-tissue and upon the diaphragm ; 
then the patient will have a sense of fulness about the chest, and with that 
sense of fulness there will be more or less uneasiness in the epigastrium, 
and the stomach digestion may be more or less interfered with. If dyspnoea 
is present it is due to the pressure of the enlarged heart rather than to any 
change in the lung-tissue. In eccentric hypertrophy with dilatation, more 
especially when the right cavities are affected, pulmonary oedema and con- 
gestion are usually present, and then there is marked dyspnoea. 

In simple hypertrophy there is often a dry irritating cough ; and in young 
fleshy females it has a wheezing character. In right heart enlargements the 
cough is often distressing. This class of patients when excited are very apt 
to complain of cardiac palpitation. The heart's action is often irregular 
and intermittent. In almost all cases there is some cerebral hyperemia, 
consequently it will be found that in those who are the subjects of eccen- 
tric cardiac hypertrophy alcoholic stimulants, nervous excitement, and 
active physical exercise will cause headache, vertigo, ringing in the ears and 
bright spots or flashes before the eyes. In left hypertrophy, haemoptysis is 
common and comes on suddenly. Rupture of the bronchial arteries may 
occur. 1 Cerebral apoplexy may at any time occur, when the arteries are 
predisposed to, or have already developed small aneurisms. In fact, the 
majority of cerebral apoplexies which occur in young subjects are as- 
sociated with cardiac hypertrophy. It is now well established that there 
is a close connection between atheroma of the arteries and cardiac hyper- 
trophy. Some observers claim that the cardiac hypertrophy is secondary 
to the arterial changes ; but it is a fact of every-day observation that hyper- 
trophy from valvular changes will give rise to atheromatous changes in the 
arteries for reasons which have already been fully considered in connection 
with the history of valvular diseases. The steps of the change are, first, 
cardiac hypertrophy ; second, endarteritis ; and, lastly, atheroma. The 
general symptoms considered in connection with its physical signs render 
its diagnosis easy. 

Physical Signs. — The physical signs of cardiac hypertrophy will vary with 
the seat and extent of the hypertrophy. When it is general, upon inspec- 
tion it will be noticed that although the heart's action is regular there is an 
increased area of impulse, and that there is a motion with each cardiac 
pulsation over and even beyond the precordial space. In children there 
is often bulging of the precordial space. 

In right ventricular hypertrophy, inspection may reveal a rounded 
smoothness of the epigastrium, with, perhaps, some bulging of the ensi- 



1 Niemeyer states that epistaxis is not infrequent. When the right heart is bypertrophied melaena or 
haematemesis may be produced from obstructed hepatic circulation. 



512 



DISEASES OF THE HEART. 




A. Right ventricle ; B. Left ventricle ; C. Eight au- 
ricle; D. Left auricle; E. Aorta; F. Pulmonary 
artery ; G. Second cartilage ; H. H. Dotted lines 
showing limit of hypertrophy of the ventricle. 



form and lower left costal carti- 
lages. The apex-beat may be dif- 
fused, extending toward the ensi- 
form cartilage. 

On palpation the cardiac area is 
abnormally increased, and the im- 
pulse has a heaving, lifting char- 
acter. The shock of an hyper- 
trophied heart may be perceptible 
over the whole precordial space, 
and in cases of extensive hyper- 
trophy the head of the listener is 
often lifted by the shock. When 
the right ventricle is the seat of 
the hypertrophy, it may cause a 
strong epigastric impulse. When 
the left ventricle is the seat of the 

hypertrophy the apex-beat is felt Diagram moating tlfe PhyLl Signs in Hypertrophy 

farther to the left than normal, 
sometimes three inches below, and 
three or four inches to the left of 
the normal position. 

On percussion, in general cardiac hypertrophy, the normal area of 

cardiac dulness, both deep-seated 
and superficial, will be increased 
to the right, left and downward. 
The dulness is increased upward 
only when the auricles are not only 
hypertrophied but also dilated. If 
the hypertrophy is confined to the 
right ventricle the area of dulness 
may extend considerably to the 
right of the sternum, sometimes 
reaching an inch or more beyond 
the right sternal edge, and extends 
loiver down than normal. While if 
/ \ ^^T^/l the hypertrophy is confined to the 

V^?/ / \ left side of the heart, the area of 

dulness may extend considerably 
beyond the left nipple. The area 
of superficial dulness will also be 
increased. In eccentric hypertrophy 
of the left ventricle, the superficial 
area of dulness will be increased to the left ; when the same condi- 
tion of hypertrophy is present in the right ventricle, the superficial area 
of dulness will be increased to the right and downward. 

On auscultation, the first sound of the heart, if not accompanied by a 




Fig. 108. 

Diagram Illustrating the Physical Si?ns in Hyper 
trophy of the Right Venticle. 
A, A. Limit of hypertrophy. 



CARDIAC HYPERTROPHY. 



513 



murmur, is dull, muffled, and prolonged, and in some cases greatly in- 
creased in intensity. The post-systolic silence is shortened. If the hyper- 
trophy is confined to the left ventricle, the second sound heard oyer the 
aortic orifice is increased in intensity ; if the right ventricle is hyper- 
trophied the second sound over the pulmonic orifice will be increased in 
intensity. In hypertrophy of the right ventricle the first sound is more 
distinct" and more superficial than normal, and the second sound is not 
infrequently reduplicated. In extensive hypertrophy both sounds of the 
heart often have a metallic ring. There is a diminution or an entire ab- 
sence of the respiratory murmur over the normal precordial region. When 
extensive pulmonary emphysema exists, although the heart may be very 
much increased in size, the increase in the volume of the lungs will prevent 
appreciation of the increased force in the apex-beat, and the heart-sounds 
will be diminished rather than increased in intensity. It may, however, 
be assumed that when extensive pulmonary emphysema is present and is 
attended by venous pulsation in the neck, there is hypertrophy and dilata- 
tion of the right ventricle. 

Differential Diagnosis.— Cardiac hypertrophy may be confounded with 
cardiac dilatation, thoracic aneurism, mediastinal tumors, consolidation 
of lung-tissue surrounding the heart, and displacement of the heart. Under 
certain circumstances pleuritic effusion may be confounded with cardiac 
hypertrophy. The differential diagnosis of the first four conditions can 
be better considered in connection with cardiac dilatation. 

Displacement of the (normal) heart may be distinguished from hyper- 
trophy by there being no increase in the area of dulness, no change in 
character or intensity of heart-sounds, and no " heaving " impulse. Be- 
sides, certain subjective symptoms, especially those of cerebral hyperemia, 
are marked in cardiac hypertrophy and absent in displacement. 

Prognosis. — Cardiac hypertrophy admits of a more favorable prognosis 
than any other cardiac affection. In almost all instances it is compensa- 
tory ; the urgent symptoms of some other cardiac affection are relieved by 
it and life is prolonged. Simple cardiac hypertrophy, unless the result of 
aortic stenosis, may exist for years without the occurrence of any danger- 
ous or very troublesome symptoms. Slight hypertrophy of the left ventri- 
cle is very common in those who have led an active life, and have been 
compelled to perform active and prolonged physical labor ; the hyper- 
trophy is no more than is required to maintain an equilibrium in tho cir- 
culation, and in no way interferes with duration of life. In the young and 
in athletes, if the cause be removed, the prognosis is very favorable. The 
patient should not be made aware of the presence of such hypertrophy, for 
although there is no danger attending it, a knowledge of the fact may 
greatly alarm him. When there is not only hypertrophy but also degen- 
eration of the hypertrophied walls, the result of imperfect nutrition, the 
prognosis is very unfavorable. 

The prognosis in hypertrophy of the right ventricle is not as favorable as 
in hypertrophy of the left, because it must inevitably be accompanied by 

considerable pulmonary obstruction, and consequently is rapidly progres- 
33 



514 



DISEASES OF THE HEAKT. 



sive. In Bright's disease, or when there is disease of the arterial coats, the 
prognosis is unfavorable. The prognosis in any case of cardiac hyper- 
trophy depends upon the cause of the hypertrophy, and upon the kind of 
valvular or other cardiac lesion coexisting. 

Treatment. — Although cardiac hypertrophy cannot be removed, still, 
much can be done to arrest its development by removing the causes which 
produce it, or by rendering them inoperative. Patients with cardiac hy- 
pertrophy must especially avoid alcoholic stimulants, immoderate eating, 
active and prolonged physical exercise and mental excitement. All those 
conditions which interfere with the general circulation must, if possible, 
be removed. This embraces interference with the abdominal circulation, 
as well as with the pulmonary and systemic. Straining at stool and con- 
stipation should be avoided by daily keeping the bowels freely moved. This 
condition of the bowels should be maintained chiefly by habits of life and 
regulation of diet, cathartics being resorted to only in exceptional cases. 
As little liquid as possible should be taken into the stomach. Any symp- 
toms of cerebral hyperemia must be immediately relieved by those means 
which diminish the force of the heart's action. When the pulse is full and 
strong and there are evidences of cerebral hyperemia, it has been the prac- 
tice of some to bleed, but this treatment is contraindicated, for the pres- 
ence of anaemia greatly aggravates the dangers arising from cardiac hyper- 
trophy, since it increases irritability and excitability of the heart. The 
symptoms must be very urgent to warrant venesection. 

Of all the remedial agents which diminish the force of the heart's action, 
I have found aconite the best. When given in full doses it is more reliable 
than any other means. From two to three drops of Fleming's tincture of 
the root may be administered every three or four hours. No drug that I 
have used so fully and promptly relieves the vertigo and other painful sen- 
sations that attend cardiac hypertrophy. Hydrocyanic acid, belladonna, 
and conium are used, but are inferior to aconite. Whenever the dilatation 
of the cavities exceeds the hypertrophy of the cardiac walls, aconite does 
harm. 

Digitalis is contraindicated, unless there is evidence of heart insuffi- 
ciency. When digitalis is administered in chronic Bright's disease, although 
hypertrophy of the left ventricle is one of its constant attendants, failure 
in the renal secretion indicates the advent of degenerative changes in the 
cardiac muscle and heart failure. In such cases, the heart, although 
hypertrophied, is not able to overcome the obstruction to the circulation 
in the small arteries and capillaries, and the tonic effect of the digitalis 
raises the heart-power to the point where the obstruction is overcome and 
the equilibrium of the circulation established. Acetate of lead and vera- 
trum viride are much thought of by many American authorities. For 
painful palpitation, wild cherry bark is the best drug. Morphine is sel- 
dom of service. 



CARDIAC DILATATION. 



515 



CARDIAC DILATATION. 

By the term cardiac dilatation is understood a condition of the heart in 
which there is an increase in the capacity of its cavities, with relative 
diminution of its contractile power. There are three forms : — 

I. Simple Cardiac Dilatation, in which the capacity of the heart-cavities 
is increased without any marked change in the cardiac walls. Such a con- 
dition is apt to occur during convalescence from any disease in which there 
has been great impairment of nutrition, such as typhoid fever. 

II. Hypertrophic Cardiac Dilatation. —In this form there is increase in 
the capacity of the heart-cavities and increase in the thickness of the 
heart-walls ; but the relative contractile power of the heart may be dimin- 
ished as the result of a degeneration following eccentric hypertrophy, or 
independent of any hypertrophy of the cardiac walls. 

III. Atrophic Cardiac Dilatation. — In this form the capacity of the heart- 
cavities is markedly increased, and the cardiac walls are thinner than nor- 
mal. Sometimes the ventricular walls are not more than two or 
three lines thick, and the auricular walls may become so thinned that 
they will present the appearance of a simple membrane. Under these 
circumstances the contractile power of the heart is almost lost. Anatom- 
ically, as well as clinically, the significance of cardiac dilatation is in pro- 
portion to the excess of the capacity of the cavities over the thickness of 
the cardiac walls. A cardiac cavity may be very much increased in capac- 
ity, but so long as there is an increase in the muscular power of its walls 
sufficient to meet the demand for the increased work they are called upon 
to perform, there will be little or no disturbance of the general circulation. 
Eccentric hypertrophy and hypertrophic dilatation approach each other 
very closely, and it is often very difficult to draw the line between them. 

Morbid Anatomy. — One or all of the heart cavities may be the seat of 
dilatation. The shape of the heart is changed according to the cavity 
which is the seat of the dilatation. If the dilatation is confined to the 
right ventricle, the heart will be increased in breadth and the apex may 
appear bifid ; while if the dilatation affects mainly, or only, the left ven- 
tricle the heart will be elongated. Dilatation occurs most frequently in 
the auricles, and thinning of the cardiac walls is most commonly met 
with here ; next the right ventricle and last of all the left ventricle is the 
seat of dilatation. When all the cavities are dilated the entire organ is 
increased in size and assumes a globular shape. When the ventricles are * 
excessively dilated, the trabecule are sometimes reduced to the condition 
of fleshy tendinous cords. When the walls of the left ventricle are very 
much thinned they collapse when the ventricle is cut into. It is a question 
whether dilatation ever exists without some hypertrophy. The hypertro- 
phy is apt to be overlooked, for the walls of the dilated cavities seem to 
be of normal thickness. 

The structural changes which take place in the muscular tissue of the 
walls of the dilated cavities vary with the morbid process which precedes 



516 



DISEASES OF THE HEART. 



and attends the dilatation. When it results from pericarditis or myocar- 
ditis there are serous infiltration and granular degeneration of the muscu- 
lar fibres ; when it is the result of fatty metamorphosis the muscular fibres 
undergo fatty degeneration. In hypertrophic dilatation it is often impossi- 
ble, even by a microscopic examination, to determine the exact changes 
which the muscular fibres undergo ; the abnormal state of the muscular 
fibres can only be determined by the other evidences of feeble heart power. 

A heart distended with blood and relaxed by putrefaction may, on first 
view, be mistaken for a dilated heart. The distinctive marks of a heart 
softened by the putrefaction processes are its extreme softness, its satura- 
tion with the coloring-matter of the blood, and the evidences of decompo- 
sition in other parts of the body. 

Etiology. — The causes of cardiac dilatation may act by disturbing either 
one or more of the elements determining cardiac action. They are : 

I. The muscular power of the heart. 

II. The amount of ivork required, or the cardiac vascular tension. 
III. The cardiac innervation. 

I. The contractile power of the heart may be weakened by any of the 
causes of defective nutrition, as anaemia, deficient food, disturbances in 
the digestive organs, etc. The physiological decline of the nutritive pro- 
cesses in old age results in a similar condition. In these cases the heart 
muscle is not necessarily degenerated, but either atrophies or simply loses 
its normal power without obvious change in its elements. "When thus 
weakened, the normal cardiac tension during diastole as well as systole may 
stretch the muscle and result in dilatation. Degenerations of the cardiac 
muscle are prominent causes of decrease in its power ; so that all causes 
inducing fatty, fibroid, or other degenerations are secondarily causes of 
dilatation. 

Prominent among these are the myocardial inflammatory changes asso- 
ciated with pericarditis and endocarditis. Retention and accumulation of 
excrementitious matter in all forms of Bright's disease is j)eculiarly liable 
to cause cardiac degeneration and dilatation, while the perversion of the 
nutrient elements of the blood, and the presence of poisonous compounds 
developed in the course of the specific diseases, as typhoid and the other 
eruptive fevers, diphtheria, septicaemia, and phthisis, are direct causes of 
those degenerative changes which precede dilatation. That form of dila- 
tation which follows atheroma of the aorta or coronary arteries is also pre- 
, ceded by degeneration. 

II. Any increase in the amount of force demanded in the heart to main- 
tain the circulation results directly in dilatation only when that demand is 
sudden and extreme. Rupture of a valvular leaf or the immediate increase 
of vascular tension attendant upon some supreme muscular effort may 
induce acute dilatation in a heart possessing but little reserve power. 

The more common and gradually developed obstructions to the circu- 
lation found in valvular stenosis, atheroma, capillary fibrosis, the arterial 
contraction of parenchymatous nephritis, or the compression of large ves- 



CAKDIAC DILATATION. 



517 



sels by new growths, induce primarily hypertrophy, which passes into dila- 
tation only when the nutritive processes are no longer able to keep pace 
with the demand for new tissue and the repair of the old. In these con- 
ditions dilatation may supervene either with or without precedent degene- 
ration of the muscle. Emphysema, pulmonary compression, fibroid disease, 
and like conditions of the lung, are to be included under this head as 
affecting the right heart. 

Increase of intracardiac tension during diastole, caused by valvular 
insufficiency, produces cardiac dilatation or increase in the capacity of the 
cardiac cavities ; but when slowly developed, the dilatation is so immedi- 
ately followed by compensatory hypertrophy, unless the muscle is weak- 
ened, that the direct result of aorbic and other regurgitant lesions were 
better regarded pathologically as what it is clinically — eccentric hypertro- 
phy rather than hypertrophic dilatation. 

It becomes dilatation when cardiac failure supervenes even in the small- 
est degree. 

III. Dilatation is less frequently to be attributed to disturbances in the 
nerve supply. All forms of excess in the use of narcotics, as tea, coffee, 
tobacco, opium, chloral, etc., or excesses in venery, and even prolonged and 
intense mental strain and anxiety, may so disturb the nervous mechanism 
of the heart as to allow of dilatation under even the normal vascular ten- 
sion. The nervous condition known as Graves's disease, and some other 
lesions of the vasomotor system, may also be the cause of cardiac dila- 
tation. It is evident that a single cause of those enumerated is seldom 
responsible for the cardiac condition. In most cases some form of degen- 
eration is associated with overstrain or a valvular lesion. 

Symptoms. — The symptoms that attend the development of cardiac dila- 
tation will depend upon the character and seat of the dilatation. In simple 
cardiac dilatation the heart walls are of normal power, but the capacity of 
the cavities is increased, and the amount of blood to be expelled with each 
cardiac pulsation is greater than normal ; consequently there is labored 
action of the heart (often so great as to be mistaken for the action of an 
hypertrophied heart), yet the force of the heart's action does not increase, 
and therefore we have a feebleness of the radial pulse. The rhythm of 
the heart's action will not be disturbed. In that form termed atrophic 
dilatation there is a very different state of affairs. The heart cavities are 
not only dilated, but the walls of the cavities are thinner than normal ; the 
heart power is insufficient for the expulsion of the blood from its cavities, and 
as a result there is a labored action, and the heart, on account of the increased 
amount of labor, staggers in its action, the arteries are imperfectly filled 
with blood, the veins become over-distended, the rhythm of the "heart's 
action is disturbed, and the radial pulse becomes markedly feeble and inter- 
mitting. These latter points are of special importance as affecting the 
question of prognosis, for if a patient has all the symptoms of cardiac 
Cii.atation without an irregular and intermitting pulse, the prognosis is com- 
$38£ative]y good, The same disturbance of the circulation occurs in that 



518 



DISEASES OF THE HEART, 



form of dilatation which is developed from the degeneration of eccentric 
hypertrophy. 

The first and perhaps the most constant symptom which is common to 
all varieties of cardiac dilatation, is cardiac palpitation. At times this 
palpitation is very distressing. There is almost constantly a sense of pain- 
ful pulsation in the region of the heart. The patient complains of weight, 
oppression, or uneasiness in the cardiac region, with a sense of fluttering 
and a tendency to sighing respiration. Yery soon after the palpitation has 
manifested itself, the patient will begin to suffer from dyspnoea on slight 
exertion; when he is perfectly quiet he suffers very little. As the irreg- 
ularity of the heart's action and the palpitation increase, the patient's 
countenance assumes a pale, languid, anxious expression, with more or less 
livid ity of the lips. The extremities are habitually cold. On excitement, 
or active physical exertion, the entire face and neck become livid ; the 
pulse, which is usually regular, for a time becomes irregular and inter- 
mittent. In this condition patients often live some time in comparative 
comfort; but they are conscious not only of a loss of physical, but also of 
mental power, and they are troubled with dyspeptic symptoms and a sense 
of fulness about the epigastrium. Vomiting is not infrequently a trouble- 
some symptom. 

As the cardiac dilatation reaches a point at which there is constant car- 
diac insufficiency, the patient suffers constant dyspnoea, which becomes 
severe on slight exertion ; the cardiac palpitation is always present, and 
often accompanied by attacks of syncope. The countenance assumes a still 
more anxious expression, and the lips are always livid; the pulse is 
constantly irregular and intermitting. With these symptoms there will 
be scantiness of urine, which will contain albumen and perhaps blood ; the 
feet and ankles become cedematous, the oedema generally extending up- 
ward until the patient is in a state of general anasarca. The breathing 
becomes very difficult, so much so that the patient is unable to lie down, 
but is obliged to sit with his head inclined forward and resting on some 
firm support ; he is unable to utter more than a single word at a time. The 
respirations may be thirty or forty per minute, and panting and noisy in 
character. Cough and expectoration are not uncommon; haemoptysis may 
occur, and in some cases pulmonary infarctions form. Petechial extravasa- 
tions not infrequently occur, especially in dilatation of the right heart. 
The extremities become cold and blue ; the mind wanders, the skin as- 
sumes a yellow tinge, and the patient dies from general anasarca with pul- 
monary oedema or from urinary suppression. During the advanced stage 
of this affection violent paroxysms of dyspnoea sometimes occur, in some 
cases of which it seems as though the patient must die, yet they are rarely 
immediately fatal, but the patient passes from them into a state of coma 
and, later, dies unconscious. There is always danger from sudden syncope, 
which may prove immediately fatal. 

Although the general symptoms vary greatly in different cases, the 
physical signs are very distinctive. 

Physical Signs. — Upon inspection it will be noticed that the area of the 
cardiac impulse is increased ; but it is so indistinct that it will be difficult to 



CARDIAC DILATATION. 



519 



determine (by inspection) the exact point where the apex of the heart strikes 
the walls of the chest. This is especially the case if the chest walls are cov- 
ered with adipose tissue, or are at all oedematous. Epigastric pulsation oc- 
curs in dilatation of the right ventricle. In persons with thin chest-walls, 
there will sometimes be noticed an undulating motion over the whole of the 
precordial space. Successive beats strike the chest-wall at different points, 
and cause the undulatory motion. 

Upon palpation, dilatation can readily be distinguished from hypertro- 
phy by the feebleness of the cardiac impulse. Although it can sometimes 
be felt as far to the left as the axillary line, yet there is an absence of the 
lifting, forcible impulse which attends cardiac hypertrophy. It is often 
difficult to determine the exact point of its maximum intensity, but it wil] 
be accompanied by an undulating motion, wanting in power. Sometimes 
a purring thrill may be obtained. 

Percussion shows a greatly increased area of lateral dulness. The area 
will be increased to the right if the right side of the heart is dilated, and 
it may extend to the right nipple. If the left side of the heart is the seat 
of the dilatation, the area of dulness will be increased to the left, and it 
may extend well into the axillary space. In general dilatation the shape 
of the increased precordial area will be oval. This point is of importance 
in the differential diagnosis between cardiac dilatation and pericardial effu- 
sion. The area of the superficial cardiac dulness is not increased in the same 
proportion as the deep-seated, as is the case in cardiac hypertrophy. Di- 
lated auricles are recognized by an upward increase in the area of dulness, 
even to the first rib. When the jugular veins are .permanently dilated and 
knotted, the existence of dilatation of the right auricle will not be difficult 
to determine. 

Auscultation. — The sounds of a dilated heart are short, abrupt, and fee-* 
ble ; the second sound is often inaudible at the apex, and the two sounds are 
of very nearly equal duration and character, so that it is very often difficult 
to distinguish them. Eeduplication of the first sound sometimes occurs. 
A systolic murmur generally accompanies dilatation ; many authorities re- 
gard its production as possible without attendant valvular lesion, from 
tardy and incomplete contraction of the ventricle. Whenever a cardiac 
murmur has existed prior to the development of the dilatation, the rhythm 
of the murmur is lost as the dilatation develops^ and it becomes simply a 
confused murmuring sound. This condition has been denominated asys- 
tolism. It is a condition in which it is impossible to determine whether 
the murmur is synchronous with the first or second heart-sound ; pauses or 
intermissions occur at irregular intervals, which are of more frequent oc- 
currence during exercise than when the patient is quiet. When the asys- 
tolic condition is present, the prognosis is very unfavorable, independent of 
the general condition of the patient ; under such conditions the patient is 
liable to die suddenly. Asystolism is generally accompanied by a diffused 
cardiac impulse, which is peculiar, and readily appreciated by the ear as 
it rests over the precordial space. The respiratory murmur is diminished 
in intensity over the whole of the upper portion of the left lung. 

Differential Diagnosis. — The diagnosis of dilatation of the heart rests 



520 



DISEASES OF THE HEAKT. 



mainly on the following conditions : — feeble heart action, undulating im- 
pulse, indistinctness of apex-beat, lateral increase in the area of percussion 
dulness, very nearly square in its outline ; short, abrupt, and feeble heart 
sounds that strikingly resemble each other, and a feeble, irregular and in- 
termitting pulse, accompanied by the general symptoms of systemic and 
pulmonary obstruction and congestion. 

The differential diagnosis between cardiac hypertrophy and cardiac dila- 
tation is never difficult. The heart sounds are intensified in hypertrophy 
and feeble in dilatation. In both cases there is an increased area of apex- 
beat, but in hypertrophy it is distinct and forcible, in dilatation it is feeble, 
diffused and indistinct. The fact that an individual has had cardiac hyper- 
trophy with all its attendant symptoms, but now has a tired expression of 
countenance, livid lips, and loss of physical vigor, daily becoming more and 
more marked, and accompanied, it may be, by oedema of the feet, shows that 
cardiac hypertrophy is giving place to cardiac dilatation. The pulse is full, 
strong and bounding in hypertrophy, and weak and feeble in dilatation. 
The first sound is dull, muffled, prolonged, and intensified in hypertrophy ; 
while it is indistinct and resembles the second sound in dilatation. The 
face is flushed in hypertrophy ; pale, livid and anxious in dilatation. The 
presence of distended, irregular, turgid jugular veins tells very positively of 
dilatation of the right auricle ; and pulsation in the jugulars, with feeble 
heart action and increase in the area of cardiac dulness to the right, indi- 
cates dilatation of the right ventricle associated with tricuspid regurgitation. 
At the same time there will be hepatic, renal, and cerebral disturbance. 

The differential diagnosis between enlargement of the heart (whether from 
dilatation of its cavities or hypertrophy of its walls) and thoracic tumors is 
sometimes difficult. One very reliable differential sign is the direction of 
the increased area of percussion dulness ; thoracic aneurisms and medias- 
tinal tumors always enlarge upward and to the right or left, while in car- 
diac enlargement the area of dulness is increased laterally and downward. 
In aneurism there is a dilating impulse, vibratory thrill, dysphagia, pain 
in the dorsal spine and the peculiar aneurismal " bruit/' 

Consolidation of lung-tissue in the region of the heart may give rise to 
some of the signs of cardiac enlargement, but the other attending physical 
signs of pulmonary consolidation will distinguish between the dulness on 
percussion thus produced and the increased area of dulness due to cardiac 
enlargements. The character of the first sound of the heart, the pulse, the 
shape of the dulness and the presence or absence of pulmonary or bronchial 
symptoms will aid in the diagnosis. 

Prognosis. — The prognosis in cardiac dilatation is always bad, and the 
danger to life is increased in proportion to the excess of the capacity of the 
cavities over the thickness of their walls. Feebleness of the general mus- 
cular system and impoverishment of the blood increase the danger. The 
presence of disease of the kidney, or other disease of the heart, renders 
the prognosis in dilatation very grave. If patients have been subject to 
paroxysms of dyspnoea and attacks of, syncope, the prognosis is especially 
bad, for then there is danger of sudden death. Whenever dropsy exists, 
the prognosis is immediately unfavorable ; under such conditions few 



CARDIAC DILATATION. 



521 



patients, even with the best of care, live more than eighteen months ; the 
majority die within a year. In those cases in which the pulse is regular 
or only becomes irregular after violent physical exertion, the prognosis is 
comparatively good ; much can be done to relieve symptoms and prolong 
life. When general anasarca exists and the patient is no longer able to 
assume the recumbent posture, relief may be given, but it will only be 
temporary. 

Treatment. — Cardiac dilatation is incurable. Even the good effects of 
palliative measures are temporary. There are, however, two important 
things to be accomplished. First, the nutrition of the body must be 
maintained at its highest point. Second, all irregular or violent action of 
the heart must be prevented. 

To accomplish the first result, the diet must be most nutritious and 
taken in small quantities and at short intervals, An exclusive milk diet 
will often be found most advantageous ; stimulants must only be taken in 
small quantities and with the food. When symptoms of anaemia are pres- 
ent, iron may be administered with the food ; as a rule it is always safe 
to administer iron daily to a patient with dilated heart. Strychnia and 
arsenic may be administered alternately with iron. The greatest amount 
of fresh air and the best hygienic surroundings should be secured. 

To accomplish the second result, this class of patients must be placed 
under strict rules in regard to exercise. They should never allow them- 
selves to be placed in such circumstances as to render sudden and violent 
exertion necessary, for a single violent physical strain may jeopardize life. 
Flannel should be worn next the skin. A dry, bracing air generally best 
agrees with this class of patients. As regards the medicinal agents to be 
employed, each case must be studied by itself. All discharges that are 
exhausting must be arrested. If hyperemia of the liver and of other 
abdominal viscera exists, it must be relieved by the administration of small 
doses of mercury combined with rhubarb and soda ; excessive purgation 
is not admissible, but a daily movement of the bowels without exhausting 
is important. When there is loss of appetite and impaired digestion, vege- 
table tonics and mineral acids are indicated. 

Those remedial agents which have a direct effect upon the heart itself 
are important. The most serviceable of this class of remedies is digi- 
talis. It may always be administered in full doses, so long as the amount 
of urine passed is increased. Often when the feet become cedeinatous and 
the patient cyanotic, it has a wonderful effect, entirely removing for a time 
all unpleasant symptoms. When the heart's action becomes regular, the 
digitalis may be given in smaller closes, but the small doses must be con- 
tinued for a long time. If, after a time, the heart's action cannot be con- 
trolled by the digitalis, strophanthus, convallaria, or spartein may some- 
times be employed with advantage. Belladonna and opium may be given 
to tranquillize the excited heart, but they should only be resorted to 
when the digitahs has been thoroughly tested and has failed. In the use 
of digitalis the same restriction is to be observed which was described in 
connection with the treatment of other cardiac diseases — that is, it should 
never be used indiscriminately. It is always desirable to postpone its use 



522 



DISEASES OF THE HEART. 



as long as possible. Should the heart become nervously excited during 
the administration of the digitalis, as it often does, the various antispas- 
modic remedies may be employed. Should cough be persistent, morphine 
may be given. Paroxysms of dyspnoea may be temporarily relieved by 
ether, nitrite of amyl, and dry cupping along the spine. 

During the slow progress of a chronic case of cardiac dilatation, a great 
variety of measures may be indicated and afford temporary relief ; still, 
our chief reliance will always be upon digitalis and iron, combined with 
the most nutritious diet and absolute rest. Ammonia and the diffusible 
stimulants are rarely of service. 



MYOCAKUITIS. 



(Carditis.) 



Myocarditis, or carditis, is an inflammation of the muscular structure of 
the heart ; it may be acute or chronic. The chronic form is attended by 
fibroid changes, general or local. It is met with most frequently in con- 
nection with peri- or endocarditis. 

Morbid Anatomy. — The diseased process consists in changes which take 
place either in the primi tive bundles of muscular fibre or in the connective- 
tissue. Both are usually involved, but when the muscular structure alone 
is attacked, it is called parenchymatous myocarditis. When the change 
primarily affects the connective- tissue it is called interstitial myocarditis. 1 
Although these two varieties may not be determined during life, they are 

very readily recognized after death. 
As a rule, the layers of myocardium 
just beneath the peri- and endocardium 
are primarily and chiefly affected. The 
change may have its seat in any portion 
of the muscular tissue of the heart ; 
the portion most frequently affected is 
the left ventricle. The first change 
noticed is one in color ; at first, the 
muscle is a dark red, later it assumes 
a grayish, mottled, opaque, buff color, 
and finally it changes to a dark green. 

The microscopical appearances will 
vary with the stage of the inflamma- 
tion. At first the primitive bundles 
are large, opaque, and swollen from 
infiltration of serum ; their striae be- 
come indistinct, and there is nuclear 
proliferation. Later the fibrillae rupt- 
ure and break down into a finely 
granular detritus ; then the muscular 
fibre is replaced by connective-tissue, or the degenerative process goes on 




Fig. 109. 
Section of Acute Myocarditis. 
A. Longitudinal section slw?ving granular muscle- 
fibres, obliteration of stria?, and prominence of 
nuclei. 

At B ike section includes some fasiculi cut ob- 
liquely and transversely. The connective -tissue 
infiltration may be noted at C> C. x 500. 



1 Coruil and Kanvier deny the existence of Virchow's parenchymatous myocarditis, p. 296. 



MYOCARDITIS. 



523 



until there is a breaking down of tissue and the formation of abscesses. 
When a large amount of the muscular tissue of the ventricular wall is 
replaced by new connective-tissue formations, the power of resistance of 
the ventricular wall is diminished, so that during the ventricular diastole 
the new connective-tissue is liable to become gradually and slowly stretched, 
and finally it gives rise to aneurism of the heart. This is the manner in 
whioh aneurisms of the heart are most commonly formed. Calcareous 
matter may also be deposited in the newly formed connective-tissue, and 
then calcareous developments will take place in the walls of the aneurism. 

When the inflammatory process terminates in the formation of an abscess 
the molecular degeneration replaces more and more the muscular fibres, 
until finally there are formed swollen yellow-white masses (abscesses) sur- 
rounded by red ecchymotic and boggy embryonic tissue, which gives, on 
section, a small quantity of various colored puriform material consisting of 
pus and muscular debris. Sometimes the whole cardiac tissue is infiltrated 
with pus. This form is not met with except in pyaemia and low forms of 
fever. Abscesses from acute local myocarditis are small ; they may burst ex- 
ternally into the pericardium or one of the heart cavities. As a result of 
this gradual destruction of muscular tissue, rupture of the heart may take 
place with or without abscesses, and at the post-mortem the pericardium 
will be distended with blood. Pycemic abscesses are very small and multi- 
ple, they may project from either surface of the heart, and the surround- 
ing muscular tissue may be either fatty or granular ; bacteria are often 
present. There may be emboli in the coronary arteries that serve as foci 
for the pysernic abscesses. 

Etiology. — The causes of myocarditis, endocarditis, and pericarditis are 
almost identical. Rheumatism, the most frequent cause of pericardial and 
endocardial inflammation, is a frequent cause of myocarditis. It is main- 
tained by some that endocarditis and pericarditis never occur unless they 
are associated with some myocarditis ; but in most cases, the myocarditis is 
so slight that it little affects the diagnosis or prognosis. Myocarditis may 
be the result of embolism or degeneration of the coronary arteries. It oc- 
curs in connection with all septic dieases, such as pyaemia, septicaemia, 
typhus, typhoid fevers, and acute ulcerative endocarditis. When it occurs 
with pyaemia it generally terminates in abscess ; when it occurs with 
rheumatism, it usually terminates in connective-tissue formation, especially 
at the apex of the left ventricle. 

Rheumatic myocarditis may be independent of either peri- or endo-car- 
ditis. It most frequently occurs in males before the twenty-fifth year. 
Sometimes no cause can be discovered. Occasionally it has its starting- 
point in syphilitic connective-tissue changes. Prolonged high temperature 
and exposure to cold are mentioned as possible exciting causes. 

Symptoms. — There are no distinctive symptoms of myocarditis. In a 
large majority of instances it is impossible to positively determine its ex- 
istence during life. A rapid, feeble, compressible, and irregular pulse, 
coming on suddenly in the course of an acute endocarditis or pericarditis, 
is its most reliable symptom. Restlessness and urgent dyspnoea are com- 



524 



DISEASES OE THE HEAKT. 



mon. The face is anxious and cyanotic, there is great restlessness, anxi- 
ety, and sometimes delirium. The principal symptoms which should lead 
one to suspect its existence, are attacks of cardiac palpitation, a feeble, ir- 
regular, intermitting pulse, syncope on slight exertion, and all the phe- 
nomena of heart failure ; if these come on suddenly in one who is suffer- 
ing from some severe septic disease there is reason to suspect myocarditis. 

There are no physical signs except those common to all conditions of 
heart failure, though at first the heart action is violent. The heart sounds 
are at first short and sharp, and then feeble. If, however, the myocarditis 
has terminated in connective-tissue formations, and aneurism of the ven- 
tricular wall has occurred it may be recognized by a change in the shape 
of the heart. 

The area of precordial dulness will be increased upward and toward the 
left shoulder, rather more than when there is cardiac hypertrophy or dila- 
tation. The diagnosis of myocarditis can only be conjectural. When ab- 
scess of the heart occurs as a termination of myocarditis, it will probably 
go unrecognized until the post-mortem. But the sudden occurrence of a 
murmur indicative of rupture of a portion of the wall or of a valve, along 
with restlessness, delirium, and rigors, may cause one to suspect it. 

Differential Diagnosis. — The existence or non-existence of a murmur 
alone enables us to distinguish endo- and peri- from myo-carditis. In chil- 
dren it may be mistaken for acute meningitis. 

Prognosis. — General myocarditis must of necessity prove fatal ; circum- 
scribed myocarditis may be recovered from. The present state of our clin- 
ical knowledge of the disease admits only of a speculative prognosis, based 
rather on our knowledge of its pathological lesions than on any symptoms 
to which these changes may give rise. Extensive connective-tissue for- 
mations, frequently found in the cardiac walls, give evidence that circum- 
scribed myocarditis is frequently recovered from. But the extent and stage 
at which recovery is possible and the symptoms which indicate fatal termi- 
nation are still undetermined. It lasts from a few hours to a few days, 
death occurring from asthenia, heart failure, rupture, aneurism, haemo- 
pericardium, embolism, and secondary septicaemia. 

Treatment. — If myocarditis is suspected in the course of an endocarditis 
or pericarditis, the plan of treatment will not be materially changed. It is 
essentially the same as that already indicated for the management of those 
affections. Great care should be exercised not to overtax the heart. This 
class of patients should never be allowed to go up-stairs or take active ex- 
ercise until some time after convalescence. Warmth to the extremities is 
of service, as it tends to equalize the circulation, and thus relieve and pre- 
vent cardiac strain. It is probable that many cases of fatty heart are the 
sequelae of myocarditis. 

Palpitation is an indication for the moderate use of alcoholic stimulants. 
Digitalis and ammonia should be very cautiously given. Not infrequently 
septic and fever patients, after violent physical exertion during convales- 
cence, die suddenly ; death under such circumstances may be the result of 
overtaxing a heart weakened by myocarditis. Besides absolute rest and 



FIBROID DISEASE OF THE HEART. 



525 



sustaining measures, all that can be done for these patients is to relieve 
unpleasant symptoms. 

FIBROID DISEASE OF THE HEART. 

(Chronic Myocarditis.) 

As has been stated, acute inflammation of the myocardium ends in ab- 
scess or in connective- tissue formation. When fibroid tissue replaces part 
of the muscular structure of the heart, we have a fibroid heart, or what 
some call "connective-tissue hypertrophy," a condition analogous to what 
Grull and Sutton call arterio-capillary fibrosis. 

Morbid Anatomy, — The walls of the ventricle are oftenest involved ; 
there may be distinct patches of fibroid tissue or there may be patches just 
under the endo- or peri-cardium, radiating from which are bands of fibrous 
tissue which insinuate themselves into the deeper muscular structure. 
A " fibroid patch " is most frequently found near the apex of the left ven- 
tricle. When it is a continuation of endo- or pericarditis the new tissue 
blends imperceptibly from the lining or covering membranes into the mus- 
cular structure of the heart. The tissue is dense, firm, inelastic, and 
gray-white in color. Sometimes it has a glistening blue or even green ap- 
pearance ; the form of the masses is variable : sometimes they are little 
spherical projections into some one of the cardiac cavities, and, again, they 
bulge out into the pericardial sac. They may be dots, streaks, bundles, 
or islands. ^The hard tissue interferes materially with the movements of 
the heart. Aneurism, dilatation, and annular constriction within one of 
the cavities not infrequently result from interstitial myocarditis. The 
aneurismal dilatations sometimes contain thrombi. 

In "connective-tissue 99 hypertrophy the heart is enlarged, the weight in- 
creased, and the walls are firm, tough, and leathery. The color varies from 
a pale pink to a deep purple. Gummy tumors are not infrequently found 
along with fibroid (syphilitic) patches. Under the microscope the muscu- 
lar tissue is seen atrophied, granular, or fatty ; in some places it has entirely 
disappeared. The apices of the papillary muscles are not infrequently in- 
volved in the same process. 

Etiology. — All the causes of acute myocarditis are causes of chronic myo- 
carditis. Eheumatism and syphilis are its most frequent causes. In the 
latter case the fibroid mass is called a "syphilitic patch," but histologically 
it is identical with non-specific developments. Arterial fibrosis and cir- 
rhotic kidney seem to be associated with its development. It occurs oftenest 
in males who are past middle life. In many instances no cause can be made 
out. It has been regarded by some as part of a " senile " change. 1 

Symptoms. — In limited or in slight general fibrosis there are no symptoms. 
Slight precordial pain, palpitation on exertion or excitement, dyspnoea on 
active exercise, small and sometimes irregular pulse, and later dropsy and 
visceral complications are frequent accompaniments of fibroid disease of the 



J Long continued congestion of the heart, Jenner states, may lead to its induration. 



526 



DISEASES OF THE HEAET. 



heart. 1 Should fibrosis of the columnar carneae induce insufficiency on ac- 
count of shortening of the papillary muscles, then there will be a systolic 
murmur. But a murmur is usually evidence of the non-existence of fibro- 
sis. The heart sounds may be sharp and short, resembling the sounds 
"tick tack." The patients emaciate and are very feeble. In connective- 
tissue hypertrophy, the physical signs are in nowise different from those 
of ordinary hypertrophy. 2 

Differential Diagnosis. — The subjective symptoms of chronic endocardi- 
tis simulate fatty degeneration of the heart. The etiology will aid in estab- 
lishing a diagnosis, which can never be positive. 

Prognosis. — The disease is not immediately fatal, though it is incurable 
and sooner or later causes death. Its course is chronic, but sudden death 
is possible at any moment, and a very common ending, being more common 
than in any other form of cardiac degeneration. Dropsy and congestion 
and oedema of the lungs are common complications. 

Treatment. — To relieve symptoms and aid nutrition is all that can be 
done unless syphilis be a cause, and then anti-syphilitics often cause 
marked improvement. They should be administered tentatively in all 
cases and the results carefully watched. Digitalis is of doubtful efficacy ; 
a restricted diet is an important part of the treatment. 



FATTY DEGENEKATION OF THE HEAET. 



This is a common form of cardiac degeneration. It may be circum- 
scribed or diffused. When circumscribed it has a local cause. There are 
two distinct morbid processes connected with fatty degeneration of the 
heart. 

I. Fatty degeneration of the primitive muscular fibre, termed " Quain's 

fatty degeneration." 

II. Fatty accumulation on the surface 
and in the substance of the heart so as 
w \ , , k W^^^J^ ^° interfere with its functions. 

Morbid Anatomy.— In true fatty de- 
generation the first change noticed is 
that the primitive muscular fibres lose 
their nuclei, their striss disappear, and 
they become completely granular. This 
granular material at first presents the 
jj £ ^ \ \ 5 M^yH * V\ appearance of albuminous matter ; soon, 

however, the sarcous substance gives 
place to fat granules and to oil globules, 
which are arranged in rows, and event- 
ually entirely obliterate the muscle 
The degenerated fibres are of 

All 




Fig. 110. 

Teased Fibres from the Heart in Fatty De 
generation. 

The fatty chanqe is seen in varying degr ' __ 

from the granular condition A, to the com- fibres. 
plete obliteration of the muscle fibres by fat . , . & n 

globules, b. x 4oo. the same size as the normal fibres 



1 Ruhle, who has made a careful study of this disease (and considers it as far more frequent and less 
often diagnosticated than acute myocarditis) regards the irregularity and variability of the pulse, occurring 
at any moment during the day, as being most characteristic. 

2 Hyde Salter's case was marked by epistaxis and haemoptysis. 



FATTY DEGENERATION OF THE HEART. 



527 



the fibres are not involved. The muscular tissue assumes a yellow, buff, 01 
dirty brown color, and loses its power of resistance, sometimes tearing like 
paper and readily breaking down under pressure. The heart in most 
instances is dilated ; it may be hypertrophied. When a fatty heart is 
hypertrophied it is friable, not flabby. The coronary arteries may be 
atheromatous, calcified, obliterated, or normal; when the degeneration 
occurs secondarily to muscular hypertrophy, the coronary circulation is 
more or less obstructed and the fatty changes are local. Its most frequent 
seat is in the left ventricle, and is most marked in the columnae carnese and 
m the inner wall of the heart. 

In fatty infiltration there is simply an increase of fat in the areolar 
tissue of the heart ; this fat does not interfere with the function of the mus- 
cular fibres except by its pressure. 1 If the fatty accumulation is extensive, 
it may cause atrophy of the muscular fibres. Fatty degeneration may 
cause death by so weakening the walls of the heart that rupture will take 
place, or by so weakening the contractile power of the heart as to render 
it incapable of performing its function. 2 Fatty infiltration may diminish 
the heart-power, but it rarely, if ever, either directly 
or indirectly causes death. 

Etiology. — All the causes of fatty degeneration of the 
muscular fibres of the heart are as yet undetermined. 
It is evident, however, that anything which interferes 
with the nutrition of the heart tends to fatty degenera- 
tion of its walls ; it is essentially a disease of middle and 
advanced life ; it comes on with senile decay. 3 It is 
often a prominent sign of the marasmus which comes 
on in Bright's disease, chronic alcoholismus (especially 
when combined with syphilis), gout, phthisis, cancer, Fatty infiltration, 
etc.; when developed in this connection it never reaches A p }r^ n %/t rd vmtHde, 
a point where it seriously interferes with the action of teamed and showing the 

1 . J infiltration of J at, B, 

the heart. In quite a large proportion of cases, fatty wuh\twphy%f is S 
degeneration of the heart is the result of mal-nutri- heart fibres, a. x 400. 
tion from some interference with the supply of blood through the coronary 
arteries. Such interference may arise from atheroma or calcification of the 
coronary vessels, embolic obstruction, external compression from pericar- 
dial thickenings, or impairment of the aortic recoil ; it is met with in con- 
nection with phosphorus poisoning, changes in the heart in specific 
fevers, acute yellow atrophy, etc. The same degenerative tendency which 
manifests itself in other tissues of the body, due to constitutional condi- 
tions, either hereditary or acquired, predisposes to it. 

Fatty infiltration of the heart occurs as a part of general obesity, which 
so frequently develops after persons have passed middle life. It is quite 
frequently met with in connection with chronic alcoholismus. Sedentary 
habits increase the liability to its development. 

1 Normally there is more or less fat in the auriculo-ventricular grooves. 

2 One-half the cases of true fatty degeneration end in rupture of the heart. Partial rupture called 
"cardiac apoplexy " is common; aneurism is not uncommon, and the weakened columnae carneas per- 
mit of valvular insufficiency. 

9 Hence the French call it " senile cardiac softening." 




528 



DISEASES OF THE HEART. 



Symptoms. — Moderate fatty degeneration of the heart will go unrecog- 
nized ; sudden death has occurred from this cause when there was no sus- 
picion of its existence. As a rule, the progress of the disease is very gradual 
and insidious, and most of the symptoms which attend its development are 
due to heart-insufficiency. Persons who are subjects of fatty heart cannot 
undergo active physical exertion for any length of time, without complete 
exhaustion ; their skin is of a pale, "pasty" yellow color, at times more or 
less livid. Their extremities are cold and oedema is not uncommon, espe- 
cially in old age ; digestion is feeble ; they perspire profusely on slight ex- 
ertion ; they suffer from paroxysms of dyspnoea after physical exercise. 
" Uneasy " feelings and pain about the heart, and sudden suffocating palpita- 
tion of the heart are not infrequent. During these paroxysms the liver 
enlarges, the respiration is feeble and irregular, often sighing in its charac- 
ter ; " Cheyne-Stokes' breathing" is present in some cases, and is regarded 
as an important symptom. The cardiac insufficiency is progressive. The 
tissues become flabby ; there are evidences of arterial degeneration ; the 
arcus senilis is often present. The temper is irritable ; there is habit- 
ual depression of spirits, disturbance of vision, failure of memory, giddi- 
ness and vertigo ; sudden cerebral anaemia may occur during excitement, 
inducing syncope or epileptiform attacks. Frequent attacks of fainting in 
one who has the symptoms of fatty heart are always alarming. The pulse 
is peculiar : it is always feeble, although it apparently varies in force ; it 
may be perfectly regular in rhythm while the patient is quiet, yet on slight 
exertion it becomes greatly accelerated and irregular both in force and 
rhythm. It may be very rapid for some minutes, then suddenly it becomes 
irregular, not beating more than thirty or forty times in a minute ; — this 
is very characteristic. 

In an advanced stage of the disease, in addition to cerebral symptoms al- 
ready referred to, patients sometimes get into a condition which bears a 
striking resemblance to a state of anaesthesia. Attacks of angina pectoris 
sometimes occur in connection with fatty heart. Fatty infiltration of the 
heart gives rise to no functional disturbance of the organ, and is not at- 
tended by any unpleasant or dangerous phenomena. Should atrophy of 
the muscular substance of the heart, from pressure of the fatty accumula- 
tion, occur (which seldom happens), the attending symptoms and results 
differ in no respect from those already detailed as attendants of fatty de- 
generation of its muscular fibres. 

Physical Signs. — The physical signs of fatty heart are few and not diag- 
nostic. 

On inspection, the apex-beat will be indistinct. 

On palpation, no impulse will be detected over the precordial space, or it 
will only be perceptible when the body is bent forward. If the fatty meta- 
morphosis has occurred in an hypertrophied heart, there will be "an undulat- 
ing motion similar to that which accompanies excessive cardiac dilatation. 

On percussion, the area of precordial dulness, both superficial and deep, 
is usually increased. If hypertrophy and dilatation exist it may be very 
greatly increased. 



AMYLOID DEGENERATION. 



529 



Upon auscultation, the muscular element of the first sound will be indis- 
tinct or absent. The valvular element is " toneless/' and is followed by an 
unusually long period of silence. 

Differential Diagnosis. — Fatty heart may be confounded with other cardiac 
degenerations. The differential diagnosis between cardiac dilatation and 
fatty heart is always difficult. In both there may be a feeble, irregular pulse, 
vertigo, ringing in the ears, and attacks of syncope. A dilated heart occu- 
pies an abnormal space in the thoracic cavity, and consequently gives rise to 
an abnormal area of cardiac dulness ; the area of a fatty heart does not ex- 
ceed the normal area. The muscular element of the first sound may be 
feeble in dilatation, but it is never absent, as in fatty heart. Cerebral symp- 
toms, and Cheyne-Stokes' breathing are marked symptoms in fatty heart and 
absent in dilatation. If fatty degeneration accompanies cardiac dilatation, 
there will be a greater disturbance of the heart's action than in fatty degen- 
eration icithout dilatation. 

Prognosis. — The prognosis is always unfavorable ; its tendency is steadily 
to advance. 1 Individuals with fatty heart may live for years, but when the 
disease reaches an advanced stage, life is very uncertain ; a fatal termina- 
tion may occur suddenly from syncope, 2 from rupture of the heart, coma, 
or as the result of cerebral anaemia ; it may also terminate slowly by asthenia, 
which is usually attended by dropsy. 

Treatment. — There is no plan of treatment that can restore the degener- 
ated muscular fibres. The principal thing is, to improve or rather increase 
the tissue-making power of the blood ; to this end, iron, cod-liver oil, 
and strychnine may be given in connection with a good nutritious diet, fresh 
air, and physical exercise which must never be sufficient to cause dyspnoea 
or any irregularity in the heart's action. All active or violent physical 
exercise and excitement must be avoided ; the life of the patient must be 
that of an invalid. If alcoholic stimulants have been used habitually or 
to excess, they must be stopped. By avoiding everything that may stimu- 
late the heart's action, and by strict observance of all the laws of hygiene, 
life may be prolonged. Digitalis does harm. 

In fatty infiltration the only treatment which seems to be of any ser- 
vice is to restrict the diet to animal food and place the patient under a sys- 
tematic physical training, so as to diminish or remove fatty accumulations 
in other parts of the body. It is upon this principle that Oertel's treat- 
ment by mountain-climbing is based. All the excreting organs must be 
active, so as to relieve the heart as much as possible. Quain says that 
galvanism applied from the back of the neck to the precordium, by the 
interrupted current, has been found useful. 

AMYLOID DEGENERATION. 

Amyloid or waxy degeneration of the heart is rare. 

Morbid Anatomy. — This form of cardiac degeneration is never met with 
except in connection with similar changes in other organs of the body, and 
is due to a constitutional cause ; it consists in the formation of a shining 

1 Rindfleisch states that "new fibrillse can be formed from cell-elements remaining within the sarco* 
lemma." 

2 Quain says death is sudden in fatty heart in the proportion of five to one to any other mode of death. 



530 



DISEASES OF THE HEART. 



homogeneous substance in the primitive muscular fibres, which gives the 
reaction of amyloid material. It is most frequently found in the walls of 
the right ventricle, causing its cut surface to present the characteristic 
appearance of waxy metamorphosis. The primary changes take place in 
the connective-tissue surrounding the muscle-bundles ; it is often associated 
with syphilitic gummata. 

Etiology. — Waxy degeneration of the walls of the heart is due to those 
causes which produce similar degeneration in the other organs and tissues 
of the body ; among these causes syphilis stands first. 

Symptoms.— There are no special symptoms attending it, except those 
which are indicative of cardiac failure. Its existence can only be suspected, 
never positively determined. If the signs of cardiac failure, with waxy de- 
generation of other organs, as the spleen and liver, are present in an indi- 
vidual who has never been the subject of rheumatism or any valvular dis- 
ease, but who has a syphilitic history, there is good reason to suspect waxy 
degeneration of the heart. 

Treatment. — There are no special indications different from the treatment 
of waxy degenerations in other organs. 

PARENCHYMATOUS DEGENERATION OF THE HEART. 

Parenchymatous or granular degeneration, or "cloudy swelling" is that 
variety usually met with in acute (specific) diseases attended by high tem- 
perature. 

Morbid Anatomy .—The whole heart is soft, flabby, friable, and of a dirty 
red-yellow, clouded appearance. It may be slightly enlarged. The peri- 
cardium is dull, clouded, ecchymotic and somewhat cedematous. Under 
the microscope the muscle-fibres are swollen, some of them rupture, and 
they all have a granular appearance, which disappears on the addition of 
acetic acid. The striations are very indistinct. 

Etiology.— Parenchymatous degeneration of the heart is caused by exten- 
sive blood-poisoning with or without high temperature. 

Symptoms. — Its symptoms are obscured by those that attend the causa- 
tive disease. The heart impulse is feeble, the apex-beat is indistinct. The 
first sound gradually disappears and the second sound becomes indistinct. 
Violent palpitations are often present. 

The Diagnosis is made by the character of the pulse and the indistinct 
apex-beat, common in the course of any acute febrile disease. 

The Prognosis depends on the conditions under which it occurs. If in 
the course of any acute specific fever, signs of heart-failure come on, the 
prognosis is very bad . 

Its Treatment consists in the prompt and judicious administration of 
stimulants. 

PIGMENTARY DEGENERATION OF THE HEART. 

Pigment granules are found in the cardiac muscle-fibres in nearly every 
case of chronic valvular disease. In atrophy of the heart pigmentation is 



ATEOPHY OF THE HEART. 



531 



especially marked, and the particles lie near the axis of the fibres. Pig- 
mentation also occurs in cases of long-standing jaundice. In melanosis we 
find a pigmentary infiltration of the heart differing from the above by the 
black color of the granules, by their seat being in the connective-tissue 
and in the muscular-tissue at the same time, and by their localization in 
points and circumscribed spots. 

This condition has no clinical importance. 



ATEOPHY OF THE HEAET. 

Atrophy is a diminution in the size and weight of the heart. When 
the term eccentric atrophy is used a condition of simple dilatation is indi- 
cated. Atrophy may be confined to the walls of one cavity, or it may in- 
volve the walls of all the cavities of the heart. 

Morbid Anatomy. — Some writers describe atrophy of the heart under the 
head of simple, concentric, and eccentric ; but these terms are hardly nec- 
essary, as all cases of true cardiac atrophy are concentric ; that is, are ac- 
companied by diminution in the capacity of its cavities. In some cases, 
wasting of the cardiac muscles is attended by inter-muscular connective-* 
tissue increase ; in such cases there will be no decrease in the size of the 
heart, but a marked diminution in its contractile power. There may be a 
decrease in size and number of the muscular fibres. The pericardium is 
puckered and opaque. The coronary vessels are tortuous and prominent. 
When fatty or fibroid changes have induced by (pressure) atrophy of the 
heart-muscles, the term "yellow atrophy "has been given to it. Senile 
("brown") atrophy is due to extensive pigmentation. There may be no 
histological change in the muscular fibres, or they may undergo fatty de- 
generation. 

Etiology. — Any chronic exhausting disease, as phthisis, syphilis, can- 
cer, or any disease that is accompanied by wasting of the general muscular 
system, may produce atrophy of the heart. It is frequently met with in the 
very aged. Atrophy of the heart may result from the pressure of extensive 
chronic pericardial effusion. Mediastinal growths may also cause it, by 
their pressure. Fibrous thickening of the pericardium, causing constric- 
tion of the coronary arteries, as well as atheroma and thrombosis of these 
vessels, may cause partial or complete cardiac atrophy. Abnormally small 
hearts are not infrequently congenital, and are associated with imperfect 
vascular and sexual development. 

Symptoms. — Cardiac atrophy is usually attended by no special symptoms, 
as it is rarely met with except in connection with wasting of the muscles of 
the general system. It is difficult to decide whether the symptoms indi- 
cating enfeebled circulation depend upon loss of heart-power or upon gen- 
eral muscular feebleness. The existence of that form of cardiac atrophy 
which is met with in the aged cannot be positively determined during 
life. That form which results from local interference with the nutrition 
of the heart is attended by symptoms similar to those of fatty heart. In 



532 



DISEASES OP THE HEART. 



"both forms, the heart's impulse is feeble and its sounds indistinct, and the 
apex-beat is to the right of and aboye its normal position. 

Prognosis. — The prognosis depends upon the cause and extent of the 
atrophy. In extensive atrophy attended by fatty degeneration, and in 
atrophy depending upon the pressure of a pericardial effusion, the progno- 
sis is unfavorable ; the atrophy of old age is not attended by any special 
danger to life. 

Treatment. — All that can be done in this disease is to avoid excessive 
physical exertion and mental excitement. The food must be nutritious 
and wine may be indulged in rather freely. Iron, which is so serviceable 
in other cardiac affections attended by enfeebled nutrition and failure of 
heart-power, will be found of service in this condition. 

RUPTURE OF THE HEART, 

Rupture of the heart rarely if ever occurs, unless preceded by degenerative 
changes in the heart walls. The seat of the rupture is usually in the left 
ventricle, and it may be single or multiple. The fissure generally runs par- 
allel to the fasciculi of the heart fibres — it may be partial at first, and 
complete some time after. Complete rupture may vary in size from two 
inches to an opening only large enough to admit a probe ; ecchymoses are 
usually found around the rent ; fluid blood and large coagula distend the 
pericardium ; the rupture usually takes place from within outward, and 
occurs or commences during the cardiac systole. 

Etiology. — Rupture of the heart may follow atrophy, cardiac aneurism, 
abscess, hemorrhagic softening, fatty and other degenerations of the cardiac 
walls ; its immediate cause is usually some violent physical effort or mental 
excitement. If it occurs during sleep, or when the individual is quiet, 
there is reason to believe that it commenced some time before it became 
complete, and that this apparently sudden rupture is only its com- 
pletion. It is rare before forty and occurs usually after the sixtieth 
year. 

Symptoms. — If the rupture is complete the patient's hand is suddenly car- 
ried to the chest, a few convulsive twitches occur, and unconsciousness and 
death immediately follow. If the rupture is partial, the symptoms are 
those of collapse : — rapid, feeble pulse, restlessness, faintness, pallor, cold 
skin, vomiting, dyspnoea, and perhaps convulsions ; death may not occur 
for several hours. Rupture of the heart sometimes occurs in connection 
with a paroxysm of precordial pain resembling angina pectoris. 

Prognosis. — Death is certain ; nothing can avert it. In seventy-five per 
cent, it is sudden. 

Treatment.-— Necessarily this can only be palliative. Stimulants and nar- 
cotics may be given to afford temporary relief, 

CARDIAC THROMBOSIS. 

At nearly every autopsy there will be found a dark red clot of blood in 
the right heart, or in the auricles. This clot will be most firm in those 



CARDIAC THROMBOSIS. 



533 



who die of chronic disease ; it will be more or less adherent to the cardiac 
walls and the trabecule and may extend like a cord into the vessels. In 
phthisis they are usually very firm ; in anaemia they are jelly-like and pale ; 
in leukaemia they are soft, creamy and puriform. In the exanthemata they 
are very soft, and when an acute disease runs a very short sharp course 
there is often no clot. At one time these clots are entirely composed of 
fibrin, and are of a pale straw-color ; at another time they contain red 
globules, and are of a dark red color. The.coagulum is not infrequently 
whitish at its upper portion, and deep red at its lower, according to the 
position of the body. These clots are formed during the last hours of life, 
and immediately after death. They have no pathological significance. 
They are often called passive coagula. 

Morbid Anatomy. — In true cardiac thrombosis coagula are formed in the 
heart-cavities, either a short time before death, or they may have existed 
for years. They vary in size from a pin's head to a walnut, and may fill 
the greater part of one of the heart-cavities. If they are of small size and 
firmly adherent to the valves or chordae tendineae, they are called vegetations. 
If they are of large size, they are called thrombi, and form in any of the 
heart-cavities ; they are more or less firmly adherent to the endocardium. 
Their projecting portion is smooth and globular. In those diseased con- 
ditions which interfere with the free circulation of the blood through the 
heart, thrombi usually form in such portions of the heart-cavities as 
are farthest removed from the active blood-currents. The constitution of 
these thrombi varies; sometimes they are firm, dry and of a whitish color, 
composed of exsanguinated fibrin ; at other times they have a globular 
outline, are firmly attached to the endocardium, and have the constitution 
of cysts. 

Cardiac thrombi may remain permanently attached to the endocardium, 
or they may become separated from it in masses of considerable size, or in 
minute particles, giving rise either to embolism or septic infection ; they 
may be detached, and, as " fibrinous balls," lie free in the auricular 
cavities. 1 

Etiology.— All cardiac thrombi originate in coagulation of the blood. In 
some instances the coagulation is rapid and the coagula are of large size ; 
in others, the coagulation is slow, and the coagula are of small size. The 
conditions which favor these coagulations are, first, obstruction to the pas- 
sage of blood through the heart ; second, abnormal changes in the compo- 
sition of the blood ; and third, inflammatory changes in the interior of the 
heart. Obstruction to the passage of blood through the heart may be due 
to valvular lesions, cardiac dilatation, or feebleness of the contractile power 
of the heart, inherent, or from degenerations. The thrombi in the latter 
case are called marantic thrombi. The condition of the blood which 
favors its coagulation, is that which we find in acute inflammation, 
rheumatism, Bright's disease, and certain acute infectious diseases, as 



1 According to the theory of Schmidt, the formation of true or cardiac thrombi is due to condensation 
of the fibrogenic substance of the blood in contact with an inflamed wall. Hence results a slow coagula- 
tion and one that does not include the red corpuscles. 



534 



DISEASES OF THE HEART. 



hemorrhagic variola and puerperal fever. Phosphorus poisoning causes it. 
Coagulation in endocarditis is due to the roughening of the endocardial 
surface produced by the inflammation. 

Symptoms.— The symptoms of cardiac thrombosis in its gravest form are 
urgent. At the moment of coagulation, the heart's action becomes fre- 
quent and irregular, the pulse is small, weak, and irregular in force and 
rhythm. Partial syncope, with restlessness and jactitation are combined 
with symptoms of more or less complete pulmonary obstruction. Dyspnoea 
is intense, there is active delirium, convulsions, and finally a fatal coma. 
Pulmonary congestion, infarction and oedema occur. Life is rarely pro- 
longed beyond the third day. 

In less grave forms, the symptoms are not so urgent. The dyspnoea is 
slight, the cyanosis is not extreme, the jugular veins are but slightly dis- 
tended, the respiration is somewhat hurried, and the pulse is increased in 
frequency, is intermittent and irregular ; the symptoms are those of ad- 
vanced heart disease. Where the coagula are of small size, and the coagu- 
lation takes place slowly, there will be few, if any, subjective symptoms to 
indicate their presence, and life may not be seriously endangered ; these 
latter cases, however, are rather cases of vegetations forming on the valves 
and chordae tendineae, than true cardiac thrombosis. The dislodgment of 
a large piece of a thrombus en masse may block up a valvular orifice com- 
pletely, and thus cause sudden death. Arterial embolism results from 
breaking off of small pieces, and there may be subsequent well-marked 
pyaemic symptoms. 

Physical Signs. — Inspection and palpation show irregularity in the cardiac 
impulse. The area of cardiac percussion dulness is increased to the right 
of the sternum. 

On auscultation, there is marked irregularity in the heart-sounds. 
New murmurs are developed, or, if murmurs existed prior to the occurrence 
of the thrombosis, they are increased in intensity. The most common 
murmur is that indicative of obstruction at the right auricuio-ventricular 
or at the pulmonic orifice, having its maximum intensity at the xiphoid 
cartilage and being conveyed to the left of the sternum. Occasionally 
there will be a murmur indicating obstruction in the left ventricle. If the 
coagula are of small size, the murmurs are similar to those which accom- 
pany endocarditis. 

Differential Diagnosis. — The symptoms of sudden shock to the heart, and 
the systemic effects of sudden intra-cardiac obstruction, taken in connection 
with the sudden development of a loud cardiac murmur evidently origi- 
nating on the right side of the heart are sufficient to lead one to suspect 
the existence of cardiac thrombosis. The only condition which is liable to 
be mistaken for it is the rupturing of a valve, or of one of the cliordm 
tendineae from ulcerative endocarditis. I know of no means by which a 
differential diagnosis can be made between them until some time after the 
occurrence. 

Prognosis. — It is unfavorable in all cases of extensive cardiac throm- 
bosis. If the coagula are small, it is possible for them to disappear after a 



ANEURISM OF THE HEART. 



535 



time, or to become changed into vegetations ; but large cardiac thrombi 
destroy life, sometimes in twelve hours, and at other times life may be pro- 
longed for two or three days. 

Treatment. — Theoretically, the alkaline carbonates have the power of ar- 
resting or preventing the formation of cardiac thrombi, hence some give ses- 
quicarbonate of ammonia in endocarditis and pneumonia, to prevent the 
formation of heart-clots, which they believe to be very frequently the cause 
of sudden death in these diseases. There is no positive evidence in favor 
cf, or against this theory. Bleeding, and every agent which has a tendency 
to enfeeble the heart-power must be avoided. Absolute quiet must be in- 
sisted upon and digitalis and opium may be administered in small doses. 
Alcoholic stimulants must be given with great care, and only to prevent 
collapse. Formerly many described cardiac thrombosis as " polypi " and 
polypoid growths in the heart. 

AltfETJKISM OF THE HEAET. 

Aneurisms of the heart may be fusiform, sacculated, or globular, and 
they are usually situated in the wall of the left ventricle near its apex. 1 
They may be single or multiple, and if multiple, open separately or in com- 
mon. Sometimes cardiac aneurism looks like an elongated sac winding 
around the aorta. 

Morbid Anatomy. — In most instances, cardiac aneurisms form slowly, 
and are the result of inflammatory processes in the endocardium and myo- 
cardium. These processes (as I have already stated) may convert a small 
or large portion of the muscular wall of the ventricle into fibrous tissue. 
The portion so charged yields to the internal blood pressure, and a cir- 
cumscribed pouch or sac is formed which communicates with the heart- 
cavity by an opening which may be very narrow, or may be the largest 
part of the sac. The neck is hard, often cartilaginous, and may be smooth 
or jagged. As these pouches increase in size, their walls become thinner 
and sometimes rupture ; they may undergo calcification. The wall consists 
mainly of fibrous tissue with endocardium internally and pericardium ex- 
ternally. 2 Adherent pericardium usually strengthens the sac, which varies 
in thickness from that of a sheet of paper to a quarter of an inch. These 
sacs may be partially or completely filled with fibrin, fluid blood, or blood- 
clots. Aneurisms of the inter-ventricular septum, and at the base, usually 
result from the extension of a " valvular aneurism." The heart is usually 
enlarged. 

Etiology. — Among the causes of aneurism of the heart may be included 
endocardial, pericardial, and myocardial inflammations, the different forms 
of degeneration, fibroid changes, and tuberculous and syphilitic new 
growths. Rare before twenty, it seems to become more frequent as age 
advances. Males suffer twice as frequently as females. 

Symptoms. — The symptoms of this affection are obscure. There is noth- 



1 In Quain's 56 cases, 52 were in the left ventricle. 
8 The cells are flat and arranged parallel to the surface of the aneurism on account of pressure. 



536 



DISEASES OF THE HEART. 



ing in its clinical history which distinguishes it from other diseases of the 
ventricular walls. In some instances every known symptom of cardiac dis- 
ease is present. 

The physical signs are equally unsatisfactory and unintelligible. 1 The 
physical signs of chronic pericarditis, endocarditis, hypertrophy, and dila- 
tation are sometimes all present. In twenty per cent, of cases murmurs 
exist that replace the heart sounds. 

Prognosis. — Sudden death may occur from rupture of the heart into the 
pericardium, or the patient may be worn out by the attendants of cardiac 
dilatation. 

Treatment. — It has no special treatment. Those means advised for the 
relief of cardiac dilatation will be found most serviceable. 

NEW FORMATIONS IN THE HEART. 

Morbid growths, or new formations in the walls of the heart have no 
clinical importance, and I shall only enumerate them. 

Cancer of the heart, as a primary affection, is exceedingly rare ; while 
cancerous nodules in the walls or on the surface of the heart, in connec- 
tion with general cancerous infection, occasionally occur. It is apt to be 
associated with cancer of the lungs, or mediastinum. Under these circum- 
stances, the disease usually manifests itself in the form of small circum- 
scribed medullary or melanotic tumors, which are developed either in the 
heart walls or under the pericardium or endocardium. The surfaces of the 
heart rather than the substance of the myocardium are affected, and the 
right heart suffers oftener than the left, although the cancer nodules are 
nearly always multiple. Encephaloid is the form most frequently met with, 
and epithelioma is the rarest. When cancer of the heart is the result of 
extension of cancer from the neighboring parts, large portions of the heart 
may become transformed into cancerous tissue. Its existence cannot be 
recognized during life ; it is of interest only pathologically. In a few cases 
local pain, anginal symptoms, murmurs and symptoms generally indica- 
tive of heart disease have led to suspicion of cancer of the heart when evi- 
dences of cancer existed elsewhere. 

Tubercle is found in the heart only in connection with acute general tu- 
berculosis; then it develops in the connective-tissue. Its existence cannot 
be recognized during life. Both gray miliary and yellow cheesy masses are 
found at the post-mortem. They are usually situated near the pericardium. 

Fibroma, lymphoma, lipoma, sarcoma, and myoma are rare forms of cir- 
cumscribed tumors found in the cardiac walls, or under the endocardium 
or pericardium. Their existence cannot be determined during life. 

Parasites. — The heart may be the seat of parasites. The echinococcus, 
the cysticercus, and entozoa have all been found in the heart-walls, and 
have been known to lead to their rupture, causing death. Three and one- 
half per cent, of the cases of hydatid disease occur in the heart. 2 They 



1 Extensive dulness down and to the left accompanied by a feeble impulse may cause one to suspect it 

2 Cobbold states that hydatid cysts in the heart are commonly multiple. 



CARDIAC XEUROSES. 



537 



project into the pericardium or into the heart-cavities as cystic tumors. The 
sac may rupture in either direction, giving rise to embolism or to pericar- 
ditis, usually with hsemopericardium. 

True cysts, containing serum or grumous fluid, are very rarely found 
in the heart-walls. All of these developments have the effect of depress- 
ing or interfering with the heart's action, but their diagnosis in most cases 
cannot be made. 

TUBERCULOSIS OF THE PERICARDIUM. 

Tuberculosis of the pericardium is only met with in connection with 
acute general miliary tuberculosis. Unless the tubercular development 
takes place only a short time previous to death, it will give rise to pericar- 
ditis. Its presence may be suspected from the existence of the pericarditis 
in connection with the symptoms of general tuberculosis. In these cases 
tubercles may develop in the layer of fibrinous exudation or be in the vis- 
ceral membrane itself. Hemorrhage is common when the neoplasm is ac- 
companied by pericarditis. 

CAXCER OF THE PERICARDIUM. 

The pericardium may be the seat of cancer, but the cancerous develop- 
ment is nearly always secondary to cancerous developments in other parts 
of the body. It may comport itself (as to pseudo-membrane and exuda- 
tion) precisely like tubercle in the pericardium. More frequent than either 
is the formation of tuberculous or cancerous masses in the lung or medi- 
astinum, which by pressure and nearness to the pericardium excite fatal 
pericarditis, by some called cancerous or tuberculous pericarditis. 

CARDIAC NEUROSES. 

The two prominent neuroses of the heart are nervous palpitation and 
angina pectoris. Both are functional disorders. 

Nervous Cardiac Palpitation. — As has already been stated, cardiac pal- 
pitation is a very common symptom of organic disease of the heart. A 
purely nervous cardiac palpitation may occur independently of organic 
heart disease. It comes on suddenly, and is generally intermittent. Indeed, 
all cardiac neuroses have a paroxysmal character. 

Morbid Anatomy. — There are no known anatomical changes either in the 
heart, or in its nerve-supply, which can be regarded as the constant causes 
or concomitants of cardiac palpitation. 

Etiology. — The direct cause of this affection is over-stimulation of the 
cardiac muscle, or the excitability from functional derangement of the vagus 
or cardiac ganglia, which is either induced by direct or reflex causes. Violent 
physical exercise, or indulgence in intoxicating liquors will accelerate the 
circulation and give rise to a form of cardiac palpitation, which ceases as 
soon as the cause is removed. Blows on the epigastrium cause it. Adults 
with contracted chests, and young persons about the time of puberty, whose 



538 



DISEASES OF THE HEAKT. 



growth has been rapid, often complain of palpitation. In these cases it 
seems to be caused by the narrowness of the chest, which interferes with the 
free play of the heart. Palpitation is a very frequent symptom in states of 
debility or anaemia. Under this head are included sexual excesses, chlo- 
rosis, enervating habits, diabetes, and all acute infectious diseases that are 
attended by extensive nutritive disturbances, as typhoid fever, scurvy, 
etc. 

Cardiac palpitation is of frequent occurrence in persons with what is 
called a nervous temperament, induced by late hours, the habitual use of 
strong tea and coffee, the inordinate use of tobacco, derangements of the 
digestive organs, sudden shock or fright, chorea, etc. The excessive habit- 
ual use of aconite and digitalis is known to have caused it. Cardiac palpi- 
tation is frequently met with in those with a gouty diathesis and chronic 
diease of the liver, accompanied by dyspeptic symptoms which are attended 
by flatulence. It is more common in women than in men, and often seems 
distinctly allied to hysteria. 

Symptoms. — In a perfectly healthy subject with a well-formed chest, the 
cardiac impulse is so slight that the motion is not perceptible, unless the 
hand be applied to the precordial space. Whenever a person becomes 
sensible of the beating of his own heart, he may be said to have cardiac 
palpitation ; by the term is understood an unnaturally strong cardiac im- 
pulse accompanied by an unnaturally rapid action of the heart, which may 
be irregular or intermitting. Sometimes there is a loss of three or four 
beats which causes a sense of oppression or even of impending death. It 
may be accompanied by a choking, paroxysmal, " fluttering " sensation. 
In some cases the impulse communicates a quick shock to the chest walls ; 
in other cases the impulse is prolonged and heaving in character, and in 
others is weaker and almost imperceptible. The heart-sounds may be so 
increased in intensity as to be audible to the patient when he lies on his 
left side. There may be precordial pain, but usually it only amounts to 
precordial "anxiety." The carotids throb ; the heart may beat from thirty 
to one hundred beats in a minute ; the impulse and sounds increase and 
diminish at the same time ; the fits of palpitation may come on suddenly, 
and be of short duration, or they may come on gradually, and be protracted 
and severe. Murmurs are usually due to the accompanying anaemia. Ke- 
duplication of the second sound is quite characteristic. Sometimes there 
is extreme dyspnoea and headache, vertigo and ringing in the ears, and 
photophobia. The mind may be bewildered and the patient may stagger, 
yet no paralysis or vertigo exists. The respirations are irregular or op- 
pressed, with dyspnoea and a short, dry cough. 

Differential Diagnosis. — To distinguish between cardiac palpitation inde- 
pendent of organic disease of the heart, and cardiac palpitation depending 
upon organic cardiac disease, is of the greatest importance. Cardiac palpi- 
tation independent of cardiac disease comes on suddenly, and is not con- 
stant, whereas organic cardiac palpitation comes on slowly and is persistent. 
In functional palpitation, all the physical signs of organic cardiac disease 
are absent. Persons free from organic heart disease complain more fre- 



AKGINA PECTORIS. 



539 



quently of palpitation than those who are the subjects of organic disease ; 
palpitation of organic heart disease is increased by exercise. 

Prognosis. — In cardiac palpitation independent of organic heart disease, 
the prognosis is always good ; although it may cause the patient great un- 
easiness, it never destroys life. 

Treatment. — In each case of cardiac palpitation it is important to find out 
and, if possible, remove its cause. Anaemic subjects should take iron in 
large doses for a long period. In hysterical palpitation all uterine derange- 
ments must be relieved. If the excessive use of alcoholic stimulants, to- 
bacco, strong tea or colfee, is the cause, it must be stopped. Occurring in 
a gouty subject, those means which have been found to relieve gouty mani- 
festations must be employed. Those in whom no special cause can be 
found, should be directed to sponge the surface of tlje body night and 
morning in cold water, exercise moderately in the open air, and live on a 
nutritious diet. 

During the attacks, relief will usually be obtained by the administration 
of some of the more reliable nervines and diffusible stimulants. Narcotics 
generally do harm. Digitalis should never be given in purely nervous car- 
diac palpitation. Ether, ammonia, chloral hydrate, and the bromides are 
occasionally useful ; sometimes camphor, assafcetida, musk and valerian are 
serviceable as anti-spasmodics. A very important element in the successful 
management of an attack of nervous cardiac palpitation, is the positive 
assurance of the medical attendant that there is no danger attending the 
paroxysm, and that there is no disease of the heart. 

ANGINA PECTORIS. 

Angina pectoris is a neurosis of the heart due to organic changes in its 
structure or to diseases involving its nerve supply ; strictly speaking, it is a 
symptom or a collection of symptoms of organic cardiac disease. It has no 
special morbid anatomy. 

Etiology. — There is no form of cardiac or aortic disease with which angina 
pectoris has not been found associated, and there is no form with which it 
is invariably or even generally present. Inherited, nervous or "neuralgic" 
tendencies predispose to it ; eighty per cent, of cases occur after the fortieth 
year. Gout, albuminuria, diabetes, and certain hepatic diseases are often 
associated with it. Trousseau dwells on the relationship between angina 
pectoris and epilepsy. There are, however, two forms of heart disease with 
which it is especially liable to occur : — obstruction to the coronary circula- 
tion, and fatty degeneration of the heart. 

The other diseased states with which it is liable to occur are, insufficiency 
of the aortic valves, with a rigid dilated state of the ascending portion of 
the arch of the aorta, combined with dilatation of the left ventricle. When 
these conditions exist, angina pectoris will not occur unless the heart's 
action is suddenly disturbed, or its movements impeded by some mechanical 
cause. 

Symptoms. — The symptoms which attend an attack of angina pectoris are 



540 



DISEASES OF THE HEART. 



quite characteristic. The patient is suddenly seized with an intense ago- 
nizing pain in the precordial region (usually commencing on a level with the 
xiphoid cartilage) extending through the back and along the left arm 
This pain is of a stabbing or lancinating character and produces a sensa- 
tion of impending suffocation — a feeling as though death was near at 
hand. There may be true laryngeal pain. At the commencement of 
this pain the countenance becomes deadly pale and is expressive of ex- 
treme anxiety and suffering ; the surface is covered with a cold perspira- 
tion, the pulse falters, and may be almost imperceptible, the respiration is 
short and hurried, the face livid, and the patient is unable to lie down or 
even to move, for the least motion aggravates his sufferings. His conscious- 
ness is undisturbed, and his spinal as well as his cerebral functions are un- 
affected, but there may be slight wandering as the attack passes off. Not 
infrequently the rhythm of the heart's action is undisturbed and the patient 
does not even experience palpitation. Sometimes the action of the heart is 
so much deranged that syncope or even sudden death occurs. The pulse 
may be slow and feeble or markedly irregular. Usually after the paroxysm 
has continued for a few moments, or at the longest an hour, it gradually 
subsides. The attack may come on during sleep. 

At first, there are long intervals between these attacks, but after a time 
they become frequent. Between the attacks the general health may be un- 
impaired. 

Differential Diagnosis. — Angina pectoris may be confounded with spas- 
modic asthma, hysteria, intercostal neuralgia, myalgia, and the first stage 
of acute pleurisy. 

Although the phenomena attending a paroxysm of angina pectoris may 
bear a striking resemblance to those of spasmodic asthma, a physical ex- 
amination of the chest will detect the presence or absence of the 
characteristic physical signs of the asthma, and thus lead to a correct 
diagnosis. 

The intermitting and irregular character of the pulse in angina pectoris 
will distinguish it from an hysterical paroxysm. 

In intercostal neuralgia, the duration of the attack, the points of tender- 
ness, the direction of the pain, and the absence of cardiac disturbance, will 
distinguish it from angina pectoris. 

Myalgia and acute pleurisy may simulate angina pectoris. In each, 
acute pain and catching breath are present ; but the condition of the circu- 
lation, taken in connection with the locality of the pain and the physical 
signs of pleurisy, will generally decide the question. 

Prognosis.— The prognosis in angina pectoris is necessarily unfavorable. 
Sometimes the first attack proves fatal ; in more instances the second or 
third, while in many more, perhaps in the majority of instances, the 
patient at irregular intervals experiences a succession of attacks, each 
paroxysm being more severe than the previous one, until finally, after a 
period extending from one to six or eight years, an attack occurs in which 
the heart's action is arrested and death ensues. The later attacks are excited 
by trivial causes, or apparently come on spontaneously. The tendency of 



HYDROPERICARDIUM. 



541 



angina pectoris associated with organic disease of the heart is to grow 
steadily worse, and terminate in death within a year. 

Treatment. — During an attack, means should be employed to alleviate or 
arrest the paroxysm ; during the interval the exciting cause should be re- 
moved or its predisposing power diminished. It is doubtful whether there 
are any remedial agents that have the power to arrest or very greatly relieve 
a paroxysm. Diffusible stimulants, sedatives, and anti-spasmodics have all 
been employed, but so far as my experience goes they have no power to 
alleviate or arrest the paroxysm. Eest, and the free administration of 
digitalis, are of the greatest service. Chloroform should not be used. An 
emetic for an overloaded stomach, or hot foot baths, etc., when cold causes 
a paroxysm, are often advantageous. Quain and many others advocate the 
nitrite of amyl, TTt v — vi, inhaled from the handkerchief ; nitro-glycerine 
(1-100 TTt a dose) is very useful, and hypodermatics of morphine may be 
given in conjunction with it. It is well for those who suffer from angina 
to carry constantly either the nitrite of amyl pearls or the nitro-glycerine 
tablets. 

During the interval all violent emotions and all active physical exercise 
must be avoided. Indigestion, or flatulence, when present, should be 
relieved by careful attention to the diet. The only medicinal remedies 
which I have found of service in delaying and rendering less severe 
the paroxysm of angina pectoris are iron, strychnine, and arsenic ; these 
should be administered daily in small doses. Phosphorus and zinc are 
useful in " nervous temperaments." When angina pectoris is associated 
with fatty heart, the rules given for the management of the latter disease 
should be observed. Quain states that a continuous current, the + pole 
on the sternum and the — pole on the lower vertebras, has often produced 
marked amelioration of anginal paroxysms. Trousseau strongly advises 
belladonna given continuously in small doses, on the ground of the analogy 
of the affection to epilepsy. 

HYDEOPERICARDIUM. 

(Dropsy of the Pericardium.) 

Hydropericardium is a sero-albuminous effusion into the pericardial 
sac, non-inflammatory in character, and when absorbed leaves no trace 
behind it. It is often very abundant and a source of great discomfort to 
the patient, but rarely directly causes death. The effect of such fluid 
effusions is to embarrass the action of the heart, while the heart-fibre be- 
comes pale and is easily torn, the result of the serous infiltration. Six, 
seven, or more ounces of fluid are usually found, of a yellow, green, red, 
or red-brown color. Thirty- three per cent, of albumen is usually present, 
and a small amount of fibrinous matter that coagulates on exposure to the 
air. 

Etiology. — Non-inflammatory effusions into the pericardium occur most 
frequently in connection with renal and cardiac diseases. In that form of 



542 



DISEASES OF THE HEART. 



renal disease which complicates scarlatina, it is especially liable to occur, 
and under such circumstances it is passive in character and is soon reab- 
sorbed on the restoration of the renal function. When it occurs in chronic 
forms of Bright's disease, it is more serious and obstinate. When it ac- 
companies chronic cardiac disease it is the result of the general venous 
congestion, and its pressure greatly embarrasses the already enfeebled 
heart. It may result from any disease where there is, from physical causes, 
a tendency to serous transudation into the cavities of the body. 

Symptoms. — The symptoms and the physical signs which attend such 
effusions do not materially differ from those already detailed as marking 
the stage of fluid effusion in pericarditis, except that there is entire ab- 
sence of any febrile disturbance. There is no friction sound present at 
any time during the progress of the effusion. It is an early symptom 
when due to heart or lung disease ; and occurs late when due to splenic, 
hepatic, or renal disease. It occurs very late in the tuberculous and can- 
cerous cachexias 

Prognosis. — In chronic Bright's disease and in advanced cardiac disease, 
it is usually the precursor, although it can scarcely be called the cause of 
death. In other conditions the prognosis will depend upon the circum- 
stances which attend its development. 

Treatment. — In the treatment we must be guided by the peculiarities of 
each case. All the measures recommended for the treatment of hydro- 
thorax may be employed in the treatment of hydropericardium. To find 
out and remove its cause is of the greatest importance ; in other words, 
treat the diseased condition which gives rise to, or permits the effusion. 
Only in scarlatinal albuminuria is the accumulation so sudden that para- 
centesis may be demanded. 

PNEUMOPERICARDIUM. 

Pneumopericardium, or air in the pericardial sac, is the result either of 
a perforating wound of the thorax, or the perforation of the pericardial 
sac by an ulcerative process and the admission of air from some organ 
naturally containing it — stomach, intestine, lung, or oesophagus ; or to the 
putrefaction of an exudation. 

The diagnosis of this accident rests on the tympanitic percussion sound 
over the pericardial space, and the tinkling, splashing, or metallic sound 
heard directly over the heart. With the exception of those cases which 
are of traumatic origin, this accident rapidly proves fatal ; 80 per cent, 
die in non-traumatic and 50 per cent, in traumatic cases. Its treatment is 
altogether symptomatic. 

HiEMOPERICARDIUM. 
Haemopericardium, 1 or blood in the pericardial sac, may be of trau- 



1 Hjemopericardium is non-inflammatory, 
name hemorrhagic pericarditis is applied. 



Blood may fill the sac when inflammation exists ; then the 



SYPHILITIC DISEASE OF THE HEART. 



543 



matic origin, or may result from rupture of the heart, or, far more fre- 
quently, the pericardium becomes distended with blood from the rupture 
of one of those small aortic aneurisms which develop on that portion of 
the aorta included within the pericardial sac. Unless of traumatic origin, 
it rapidly proves fatal, and will be found at the autopsy of many cases of 
sudden death. When of traumatic origin, the effused blood is not often 
absorbed. 

SYPHILITIC DISEASE OF THE HEART. 

There may be two manifestations of syphilis in the heart, — the fibroid 
patch and the gummy tumor or gumma. 

Morbid Anatomy. — Pale, yellow, gummy masses are found, usually inti- 
mately blended with the cardiac substance, but often projecting as nodules 
from its surface. At first they are elastic, firm, homogeneous, often very 
hard ; later they soften and become cheesy. They may become fluid and 
open inward and give rise to cardiac aneurism. As a rule the cheesy prod- 
ucts are absorbed and a puckered, fibrous scar remains at their site. Some- 
times the gummata — which are nearly always multiple — appear as " infil- 
trations " or "deposits." They may occur in any portion of the heart. 
When the outer zone of a gumma undergoes development into fibroid tissue, 
the caseous portion remains as a compact mass. Bruce regards this as an 
intermediate form between the fibroid patch and the true gumma or 
" syphiloma." The myocardial vessels are not infrequently the seat of 
(syphilitic) endarteritis obliterans, giving rise to infarctions in the wall of 
the heart ; and the pericardium is commonly found adherent. 

Etiology. — Fibroid patches and gummata arise both from congenital and 
acquired syphilis. 

Symptoms. — Symptoms of cerebral or visceral syphilis may and often do 
mask those of the cardiac affection. Should the puckered fibroid tissue nar- 
row or distort any part of the heart, or involve the valves to such an extent 
as to cause obstruction or allow of regurgitation, then a murmur — differing 
in no respect from other murmurs — will be the chief symptom. Syncope, 
infrequent pulse, palpitation, dyspnoea, choking, and many other symptoms 
of heart disease have occurred in the few recorded cases of syphilis of the 
heart. 

The diagnosis rests mainly on the exclusion of all other forms of heart 
disease, and the evidences of syphilis, hereditary or acquired, in the indi- 
vidual. 

The prognosis would be more favorable than, probably, with any other 
similar condition, on account of its amenability to treatment, which, of 
course, is purely anti-syphilitic. 



544 



DISEASES OF THE HEART, 



Basedow's disease. 

{Exophthalmic Goitre.) 

Basedow's or Graves' disease is an affection in which there is enlargement 
and hyperemia of the thyroid body, protrusion of the eyeballs, cardiac pal- 
pitation, and anaemia. It is closely allied to functional cardiac diseases. 

Morbid Anatomy. — It is attended by no constant morbid lesions. The en- 
largement of the thyroid body is due to a dilatation of its vessels. The 
protrusion of the eyeball is caused by dilatation of the vessels behind the 
globe ; both of these changes appear simultaneously with derangement of 
the circulation, and cardiac palpitation. There are many circumstances 
which render it probable that the enlargement of the vessels is due to some 
vasa-motor disturbance which allows of their passive dilatation in the neck, 
the thyroid body, and the orbit ; at the same time it causes an excited 
action of the heart. The thyroid body may be filled with cysts or be the 
seat of hyperplasia. Atheroma of the ophthalmic arteries has been 
found. 

Etiology. — It rarely occurs in males. It is met with in women between 
twenty and thirty years of age. A " neuropathic tendency " is usually 
strongly marked. Menstrual derangements attended by violent mental 
emotions of various kinds often precede its development. 

Symptoms. — This disease may come on suddenly or slowly ; if it develops 
slowly, the patient will at times for a long period complain of severe attacks 
of cardiac palpitation, and pulsation in the arteries, gradually these attacks 
of palpitation will become more frequent and severe, the eyes will become 
slightly prominent and staring, and after a time they may become so promi- 
nent that the lids will not cover them. Occasionally the insertion of the 
recti muscles can be seen. The protrusion is often greatly increased under 
excitement. The attacks of cardiac palpitation grow more severe, the thyroid 
gland visibly enlarges, and the eyes become lustrous and projecting. 1 On 
casting the eye down, the eyelids follow but slowly; — this gives a peculiar 
look to the patient. Vision is not usually disturbed, but there may be 
slight loss of co-ordination. In proportion as the eyes bulge the eye- 
lashes and eyebrows fall out. Diplopia, traceable to paresis of the right 
trochlearis has been noted. Profuse lachrymation is not uncommon. 
Exophthalmus is often more marked on one side than the other, and is 
then apt to be attended by enlargement of the thyroid body on the opposite 
side. 

The thyroid gland usually enlarges slowly ; the patient's attention is first 
attracted to it on account of a continued pulsation of the lower part of the 
neck. It is usually unequally enlarged, is soft, elastic, and at first pul- 
sates, due to the dilatation of the vessels in the gland ; after a time there 
is increase of tissue, and blowing sounds are audible over the enlargement. 



1 Eulenberg regards increased development of fat in the cellular tissue of the orbit, as, in part, the 
eduse of the bulging v.f the eyeballs. 



BASEDOW'S DISEASE. 545 

There may be a change in the pitch of the voice, perhaps from pressure of 
the enlarged gland on the recurrent laryngeal nerve. Sometimes the voice 
is hoarse or entirely lost. There is always danger from pressure of the en- 
larged thyroid gland upon the trachea. The cardiac palpitations are rapid 
and irregular, the pulse-rate varying from one hundred to one hundred and 
forty per minute. The heart-sounds are loud, and a soft, systolic bellows- 
murmur may be heard at the base and in the large arteries. There may 
be a distinct thrill. The carotids may be dilated. The circulation is rapid, 
the veins filling rapidly, and the pulsation of the small arteries is felt by 
the patient. Mental emotion and violent physical exertion bring on attacks 
of palpitation, which may be so violent as to produce a visible enlarge- 
ment of the precordia with every beat. Stimulation of the accelerator 
nerves of the heart probably causes the palpitation. 1 

Debility, anaemia, indigestion, anorexia, and diarrhoea may be present dur- 
ing the whole course of the disease. Insomnia, amenorrhoea, and hysterical 
symptoms are very frequently observed in nervous females. In a few instances 
the temperature is often elevated to 103° F., and followed by profuse sweats. 

Differential Diagnosis. — When the three classical symptoms are present 
in a female, viz., bulging of the eyeballs, cardiac palpitation, and enlarge- 
ment of the thyroid, a mistake in the diagnosis will scarcely occur. Von 
Graefe makes a diagnosis on the " want of harmony between the move- 
ment of the eye and its lid." 

Cystic goitre is not accompanied by exophthalmus, nor by paroxysmal en- 
largements. The thyroid in Basedow's is far more elastic than in cystic goitre. 

The lustrous appearance of the eye suffices to diagnosticate it from prom- 
inence due to heart disease {e.g., hypertrophy), which latter would give 
evidence of organic changes. 

Local orbital or cranial causes of exophthalmus are excluded by the 
absence of squint and other k cerebral symptoms. 

Prognosis. — This must always be guarded. The younger the subject, 
the more favorable the prognosis. It may increase for months, remain 
stationary for a year or two, and then gradually decline, but not wholly 
disappear. In some instances its course has been acute and rapid. Recov- 
ery occurs in from four to five per cent, of cases. Great improvement has 
occurred in from thirty to forty-five per cent, of cases. It does not directly 
cause death, but intercurrent affections are generally ill-borne and fatal. 
Any heart disease (organic), great anaemia, or evidence of the "neuro- 
pathic disposition," renders the prognosis unfavorable. Pregnancy is said 
to have a favorable influence. 2 Death may occur from valvular disease of 
the heart, pulmonary tuberculosis, gangrene of the extremities, pulmonary 
apoplexy, or oedema. 

Treatment. — The first remedies proposed in the treatment of this affec- 
tion were quinine and iron, and their use is still followed by the best re- 

1 Friedrich's ingenious theory is that, i he vaso-motor nerves being paralyzed, dilatation of the coro- 
nary artery follows, and hence there is increased excitement in the ganglia of the heart. 

2 Trousseau and Corliea. 

35 



546 



DISEASES OF THE HEART. 



salts. Traube gives them alternately, five grains of quinine one day, and 
ten grains of iron, in the form of Vallett's mass, the following day. Ar- 
senic does harm. Iodine is condemned by some and recommended by 
others. It has been claimed that belladonna, hydrocyanic acid, and ergot 
tranquillize the heart. Galvanization of the cervical sympathetic dimin- 
ishes the exophthalmus and lowers the pulse-rate : it is to-day the favor- 
ite plan of treatment with many. Hydropathic treatment is highly 
praised by some French authorities. It seems to me important that in all 
cases, and especially when chlorotic conditions are present, hepatic stimu- 
lation form an important part of the treatment, and that the diet be re- 
stricted to meat and milk as far as possible. 



CHRONIC ENDARTERITIS. 



547 



DISEASES OF THE BLOOD-VESSELS. 

Under this head will be considered the following diseases of the arteries 
and veins. 

DISEASES OF THE ARTERIES. 

I. Acute Endarteritis. V. Arterio-capillary Fibrosis. 

II. Chronic Endarteritis, or "Ath- VI. Syphilis of Arteries. 

eroma" VII. Atrophy, Hypertrophy, Dilata- 

III. Periarteritis. Hon, Narrowing. 

IV. Degenerations : Fatty, Waxy, and Calcareous. 

DISEASES OF THE VEINS. 

I. Acute and Chronic Phlebitis. II. Dilatation of the Veins. 
III. Embolism and Thrombosis. 

ACUTE ENDARTERITIS . 

Acute endarteritis is an inflammation of the tunica intima, which is 
formed of endothelium lying on longitudinally arranged elastic tissue. As 
an isolated lesion it is rare. 

Morbid Anatomy. — Along some vessel, chiefly the aorta, numerous ele- 
vated round patches are seen projecting from the internal layer. They are 
red, opalescent, soft, and elastic (" gelatinous patches of the aorta "). The 
elevated patches are made up of embryonic cells arranged in parallel lines. 
These patches may undergo ulceration. Fibrin may form on their surface 
and inclose either the white blood corpuscles or the proliferated and free 
elements of the diseased surface. Pus formations and gangrene may result. 
The middle coat is not extensively involved, but a periarteritis nearly al- 
ways occurs. The whole vessel becomes friable. Emboli form, and coagu- 
lation may result in arterial thrombosis. 

Etiology. — Wounds, emboli, extension of inflammation from without, and 
irritation from a hard vegetation may cause it. Acute aortitis is usually of 
rheumatic origin. A purulent aortitis is described by some as occurring in 
septic conditions. 

Symptoms. — There are no special symptoms by which it can be distin- 
guished. When coagula are formed thrombi result, and then the symptoms 
will be those of thrombosis complicated by pyaemia. 

CHRONIC ENDARTERITIS. 

Atheroma, or endarteritis deformans, is a common disease. 

Morbid Anatomy. — It is an inflammation of the internal coat, with thick- 
ening in patches, the thickening being due to multiplication of the cellu- 
lar elements ; — granular fatty degeneration of these elements and of the 
middle coat follows, and a yellow atheromatous focus is produced, separated 



548 



DISEASES OF THE BLOOD-VESSELS . 



from the blood current by a thin tense pellicle. As the atheromatous 
changes take place, the centre of the patch contains a putty-like mass 



of cholesterin crystals, fat granules, 




and crystals of fatty acid. When 
there is little or no fatty 
change in the patches, the 
process is called " sclero- 
sis," and they are then 
stained dark brown. When 
these processes progress 
slowly, calcareous granules 
infiltrate the tunica intima, 
and, later, form thin, fria- 
ble calcareous plates just 
underneath an internal pel- 
licle. The vessels above 
the heart in the thorax are 
most frequently affected ; 
they become enlarged, ir- 
regular, and friable. When 
the stiffened internal coat 
breaks, chinks are formed 
which fill with blood and 
later become melanotic. In 
the aorta the middle coat 



Fig. 112. 

Chronic Endarteritis : Atheroma. 
Magnified View of a Small Artery, partly diagrammatic. 

A. Endothelium of artery, cells turned inward. — B. Intima thrown, 

into folds by C, the elastic lamina. — D. Muscular coat {tunica often disappears COimect- 

media).—E. Adventitia. iff 

F. Swollen and proliferating intima. lVC-tlSSUe taklllP* its place t 

G. Irregular spaces containing calcareous, granular, and fatty mat- ° 7 

ter. destruction 01 the middle 

H. Elastic lamina, limiting the degenerative process. , . ,, , „ 

I. Lumen of the vessel encroached vpon one side only. COat IS the Only Cause 01 

spontaneous aneurism of 
the aorta. The external coat finally assumes the histological characters of 
the altered internal coat. After the aorta, the cerebral, coronary, and 
splenic vessels and those of the lower extremity may become involved. In 
the small vessels, narrowing and stenosis are the results of chronic arteritis. 
Cardiac hypertrophy is a common result of the rigidity and inelasticity of 
the aorta and its branches. 

Etiology. — Atheroma or arterial sclerosis is a disease of advanced life. 
Men are far oftener affected than women. It is predisposed to by gout, 
rheumatism, syphilis, Bright's disease, lead poisoning, and especially by 
alcoholismus. Over-strain of the vessel is often its immediate cause. It 
is said sometimes to be an extension from the endocardium into the 
aorta. 

Symptoms. — Nearly all its symptoms are the mechanical results of rigidity 
of the artery. The left ventricle is hypertrophied. The peripheral arteries 
are enlarged, lengthened, and tortuous, and an irregular outline is readily 
felt along their course. The pulse is feeble, sometimes imperceptible ; 
the sphygmograph shows a short up-stroke and a flat summit (pulsus tar- 
dus). The extremities are cold and parts may become gangrenous (senile 



PERIARTERITIS. 



549 



gangrene). Apoplexy may occur, and some ascribe epilepsy and senile de- 
mentia to atheromatous arteries. The different organs atrophy, the skin 
becomes dry, and the lungs are frequently emphysematous. Dissecting 
aneurisms may be induced after a rupture of an atheromatous abscess; 
persistent anasarca of the legs in old men is often due to calcified 
arteries. 

Differential Diagnosis. — Aortitis sometimes gives rise to symptoms that . 
can establish a diagnosis. These are acute substernal pain with oppres- 
sion, palpitation, quick and feeble pulse. With these symptoms may be 
associated a hard systolic murmur, originating at the seat of inflam- 
mation, and transmitted to a distant point of the aorta. Paroxysms of 
pain like angina pectoris are sometimes marked. 

Prognosis. — It is a condition which cannot be cured. 

Its treatment is altogether hygienic. 

PERIARTERITIS. 

In periarteritis the adventitia and very soon the surrounding cellular tis- 
sue are hyperaemic, swollen and infiltrated with cells. The external coat 
becomes homogeneous and gelatinous. The process terminates either in 
connective-tissue or pus formation. In purulent infiltration of the exter- 
nal coat the intima is not affected ; but should the middle coat become 
involved pus may open into the blood current and an aneurism is liable to 
be formed. 

Etiology. — Periarteritis occurs from wounds, extension of inflammation 
from adjacent parts, or during the course of pyaemia. 1 Periarteritis is the 
first step in the formation of those miliary aneurisms occurring in the 
cerebral vessels, and which are always found preceding cerebral hemor- 
rhages. 

Fatty degeneration, apart from atheroma, is rare. It occurs chiefly in 
the aorta. In the internal coat the fat granules occur in flat layers, and 
in the middle coat they are found between the fibres, and when very 
abundant the muscular elements cannot be distinguished. Sometimes the 
endothelium alone is involved, and it may desquamate, laying bare the 
tunica intima. This is said to accompany erysipelas and relapsing fever. 

Calcification of the arteries, independent of atheroma, is even rarer than 
fatty degeneration. 

Amyloid degeneration occurs in the small arteries, especially in the renal 
glomeruli, but also in those of the spleen, liver, intestines and lymph glands. 
Its causes, gross and microscopical appearances, tests, etc., are fully dis- 
cussed under chronic Bright's disease. 

Cancer only attacks the adventitia. 

Tuberculous granules often stud the external coat of the small arteries. 
Syphilitic disease of the arteries chiefly attacks the cerebral vessels. Great 
thickening and nodose swellings are due to gummatous material infiltrating 

JKussmaul and Maier describe a periarteritis nodosa which, is usually fatal, and Gull and Sutton have 
called the hyaline fibroid appearance of the external coat of the arterioles arterio-capillary fibrosis. 



550 



DISEASES OF THE BLOOD-VESSELS. 



the outer coats. The walls are opaque and the lumen is considerably 
diminished. Later, cellular growths occur in the internal coat. Throm- 
bosis and cerebral softening are often the result. This neoplastic formation 
has been called arterioma. When such a condition is suspected, mercury 
and iodide of potash are to be given. 

General dilatation of arteries may be due to atony or paralysis of their 
.muscular coat, or to atheroma or degeneration of their walls. The aorta 
and the pulmonary arteries are those most frequently involved. Some- 
times the aorta and its branches are the seat of congenital uniform stenosis. 
This occurs in females chiefly, and is associated with other malformations. 
The symptoms are a small pulse, frequent palpitation, cold extremities, 
tendency to syncope, and menorrhagia. Gastric ulcers are common. The 
aorta may be contracted and nearly obliterated at its junction with the 
ductus arteriosus. 

GENERAL ARTERIAL FIBROSIS. 

Dr. Bright, and most pathologists since his time, noticed that the granu- 
lar contracted kidney — the " small red kidney " of the English writers — was 
usually associated with morbid changes in other organs, and it was gen- 
erally held that, under these circumstances, the kidney was the organ 
primarily affected, and that the other changes were the result of the cachexia 
produced thereby. 

In 1872 Sir William W. Gull and William Henry Sutton 1 denied the cor- 
rectness of this latter opinion, and claimed that all the morbid changes, 
those found in the kidney, as well as those of the other organs, were 
equally dependent upon a fibroid degeneration of the walls of the smaller 
arterioles and capillaries. To this degeneration they gave the Yi&mearterio- 
capillary fibrosis, and while admitting that it commonly began in the kid- 
neys, they claimed that there was evidence of its primary appearance in 
other organs, and also of its occasional localization elsewhere, to the entire 
exclusion of the kidney. The morbid changes peculiar to this condition 
have long been recognized by pathologists, as have also the corresponding 
clinical facts, but the connection between them was not understood. It 
is this connection, this grouping together, with a more detailed knowledge 
of the minute changes, that constitutes the present theory. Although 
the description of the pathological changes, as given by Gull and Sutton, 
has been shown to be incorrect, their comprehensive explanation of a gen- 
eral arterial disease, as distinct from any renal disease, is fully accepted. 

Dr. George Johnson and others have shown that an hypertrophy of the 
arterial muscular coats may produce similar symptoms as the fibroid change, 
and an acceptable explanation has been given by Oonheim of the relations 
which such muscular hypertrophy bears to renal disease. While these arte- 
rial changes are thus most frequently associated with some form of nephri- 
tis, they may be primary, and not involve the kidney in any marked degree. 

Morbid Anatomy. — Two distinct pathological processes must be recog- 
nized as producing those changes and symptoms which are characteristic 



1 Medico-Chirurg. Transactions, 1872. 



GENERAL ARTERIAL FIBROSIS. 



551 



id high arterial tension. In the first the changes consist in a general 
increase in the amount of fibroid tissue throughout the body, especially 
marked in the excretory organs, together with hypertrophy of the left and 
dilatation of the right ventricle. The increase of fibrous tissue usually 
begins in the outer coat of the smallest arteries, and spreads thence through 
the connective-tissue stroma of the organ involved. The inner coat is also 
sometimes much swollen, granular, and thickened. In the capillaries the 
new tissue is granular and without any fibroid appearance. According to 
Gull and Sutton the muscular coat of the artery is atrophied. The result 
of these changes is to diminish the calibre and destroy the elasticity of 
the vessels. This alteration in the vessels is the primary and essential 
morbid process ; by its reaction upon the heart, and by its spreading to 
the adjoining tissues, it produces the following secondary changes. By 
the formation and retraction of 
new connective-tissue, especially 
in the kidneys, gastro-intestinal 
tract, and skin, these organs di- 
minish in size and lose more or 
less of their granular epithelial 
elements. 

The lungs are firm, with promi- 
nent bronchi, and often show 
well-marked vesicular emphyse- 
ma. There is atheroma of the 
aorta and of the cardiac valves, 
opacity of the arachnoid, and in- 
crease in the amount of the sub- 
arachnoid liquid. 

Although the renal changes are 
not necessarily associated con- 
ditions, they are so frequently 
developed, late or soon, as to be 
considered a complication if not 
part of the disease. 

The kidneys are small, red, 
and granular, with adherent cap- 
sules, and with small cysts scattered through them. This condition of the 
kidney must be distinguished from the mixed or yellow granular kidney, 
which, according to this theory, is either a large white kidney that has 
shrunk and become granular, or else is the consequence of an attack of 
acute parenchymatous nephritis supervening upon the chronic interstitial 
change. The microscopical appearance of the kidney is such as will be 
described in interstitial nephritis. There is increase of intertubular con- 
nective-tissue, especially around the Malpighian bodies, and in and around 
the walls of the minute arteries. 

The hypertrophy of the heart, which is found so constantly in connec- 
tion with these changes, is readily explained. The heart is called upon for 
greater effort, in order to overcome the obstruction to the blood-current 




Fig. 113. 

Section from the Cortex of a Kidney in general arterial 
fibrosis, show ing two Glomeruli. 

A. Capsule of a Malpighian body thickened icith lamin- 

ated connective issue. 

B. Vascular tuft degenerated into a fibrous nodule. 

C. Capsule of another Malpighian body, with fibrous 

thickening, smaller in amount than at A. 

D. Vascular tv'fi, adherent to capsule, with round cell 

infiltration. 

E. Nucleated fibrous tissue surrounding the atrophied 

glomeruli, x 300. 



562 



DISEASES OF THE BLOOD- VESSELS. 



created by the change in the arterioles and capillaries, and, as in the case 
of other muscles, it increases in size and strength to meet the additional 
demands. The increase of arterial pressure is also felt within the heart, 
and ultimately produces the other changes seen upon the valves — changes 
which are found at the points subjected to great pressure. 

This explanation is in harmony with the following facts observed by Gull, 
and Sutton : hypertrophy of the left ventricle existed in all cases in which 
the vessels were generally thickened by the hyalin- fibroid change, and its 
degree varied directly with the degree or the extent of the change. They 
argue that it is due not to renal disease, but to the morbid changes in the 
vessels, because (1) it is often absent in cases of large white kidney, in lar- 
daceous disease, and in scrofulous pyelitis, with almost complete destruc- 
tion of the organ ; (2) whenever hypertrophy of the heart coexisted with 
large white kidney, the hyalm-fibroid change was also present ; and (3) 
hypertrophy is found at a very early period of the kidney affection when 
the excretory function is not greatly altered. 

The other pathological processes which produce a similar clinical picture 
of high arterial tension and hypertrophied heart associated with renal dis- 
ease, are, according to Dr. George Johnson, found in an hypertrophy of the 
muscular coats of the smaller arteries and arterioles. It seems well estab- 
lished that such an hypertrophy occurs, but the explanation of its cause 
offered by Dr. Johnson, that the hypertrophy was intended to decrease the 
arterial calibre, and thus shut out irritating blood from the organs, does 
not seem tenable. 

This muscular hypertrophy is found especially in connection with paren- 
chymatous forms of renal disease, and Conheim's explanation appears the 
most probable. 

He claims that functional activity in the kidney varies directly with the 
arterial tension and blood-flow. "When part of the renal parenchyma 
becomes inactive through disease, an increased arterial tension is a neces- 
sary condition for the extra activity demanded of the unaffected portions, 
in order that the sum total of the renal secretion may not be diminished. 
To produce this, an increase of cardiac activity is necessary, which results 
in cardiac hypertrophy. In order, then, that the augmentation of cardiac 
activity may not disturb the circulation in organs requiring no change in 
their vascular conditions, but may be concentrated upon the kidney, a gen- 
eral contraction of all the arteries is necessary — a contraction which shall 
vary with the varied requirements of the several parts. Such contraction 
can be accomplished only through the muscular coats of the vessels under 
the control of the sympathetic system. Its persistence results in hyper- 
trophy of the muscular coats. 

Although these changes are pathologically and etiologically entirely dis- 
tinct from an arterial fibrosis, clinically they can not always be distin- 
guished, and we are able to recognize only high arterial tension and its 
results. 

Etiology. — The exciting cause of the fibroid change is usually some form 
of blood-poisoning, either temporary or chronic, such as gout, alcoholism, 
pregnancy, scarlet fever, lead poisoning, and certain forms of dyspepsia, 



GENERAL ARTERIAL FIBROSIS. 



553 



mai-assimilation and functional disorders of the liver, which act by produc- 
ing first a functional and then an organic increase of the arterial tension. 

Aside from these direct causes, however, we recognize a fibroid diathesis 
vhich influences all inflammatory processes. Under its influence causes 
which would otherwise be inoperative produce extensive fibroid degene- 
ration. The exciting cause of the muscular hypertrophy would be found, 
according to the theory given, in defective renal function — a defect which 
may be relative or absolute, inherited or acquired, and be present with or 
without renal disease. 

Symptoms. — The symptoms vary with the organ chiefly affected and the 
period of the disease, The first in order of time, and the one upon which 
Mahomed places the most reliance as a means of diagnosis, is the increase of 
arterial tension, recognized by the pulse, or, better, by the sphygmograph. 
During this stage, if the pressure has increased rapidly, dropsy and albu- 
minuria may be present, but ordinarily these two symptoms denote accom- 
panying epithelial change in the kidney, or an exacerbation in the progress 
of the disease. Albuminuria is not itself a symptom of arterial fibrosis; 
on the contrary, the affection may run its course without the appearance 
of this symptom. In such cases the vascular changes have involved other 
organs, and have left the kidney unchanged or but slightly affected ; such 
patients die with symptoms of pulmonary or gastro-intestinal troubles, or 
of cerebral hemorrhage or aneurism. 

The condition begins as a diathesis in early life, gaining ground every 
year, and betraying itself by the pulse, pulmonary emphysema, or dyspep- 
sia, and if at any time a serious exacerbation occurs, death may be caused 
with symptoms referable more directly to the heart or kidneys. 

Diagnosis. — The diagnosis, therefore, is to be made mainly by a consid- 
eration of the character of the pulse, and it is claimed that heretofore, in 
the majority of cases, the disease has passed unrecognized, 1 the diagnosis 
being made only when the kidneys were sufficiently involved to give rise to 
albuminuria. The important point, therefore, is to recognize the condition 
of high arterial tension. The sphygmograph alone can always do this with 
certainty, but careful examination of the heart and pulse will usually suf- 
fice. The pulse of high pressure has been variously described as hard, 
cord-like, persistent, long, or slow. The most constant and characteristic 
quality is that designated as persistent or slow (not infrequent). The 
artery feels full under the finger during diastole as well as systole of the 
heart, and its systolic expansion is prolonged, — the so-called pulsus tardus, 
shown on the sphygmograph by a prolongation of the elevation of the 
trace. The heart signs of high arterial pressure are a long or reduplicated 
first sound heard over the inter-yentricular septum, and an accentuated 
second sound. 

The following conclusions, taken from Gull and Sutton's first paper and 
Mahomed's last upon the subject, present the points m convenient form. 

1 Mahomed says : li How often patients are allowed to die— nay, more, even killed— when their hearts 
are failing from the terrible arterial pressure they can no longer .overcome. Their flagging, over-taxed 
ventricles dilate : the wretched, feeble, laboring pulse is thought to mean weakness which requires stimu- 
lation, its persistence (indicating over-distention) is passed unnoticed, and the struggling heart, failing at 
last in its work, stops, and the patient dies for want of a lancet or purge.'" 



554 



DISEASES OF THE BLOOD-VESSELS. 



There is a disease characterized by hyalin-fibroid formation in the arteri- 
oles and capillaries, attended with atrophy of the adjacent tissues. This 
morbid change in the vessels is the primary and essential condition of the 
morbid state called arterio-capillary fibrosis with contracted kidney. The 
kidneys, however, may be little if at all affected, while the morbid change 
is far advanced in other organs. The blood condition which produces the 
high arterial pressure is the primary condition, and is not secondary to 
deficient renal excretion as heretofore held. The cardio-vascular changes, 
when found alone, may be taken as evidence of the existence of the dis- 
ease. The condition of high pressure is almost constantly present in old 
age, and in one form or another brings about a large proportion of the 
deaths of those over fifty years. The existence of high arterial tension in 
the pulse of young persons indicates a diathesis, and is of grave import- 
ance. The same condition being of frequent occurrence after the age of 
fifty is not of such great importance, unless present in an excessive degree. 
It then produces serious symptoms and calls for active treatment. 

Treatment. — Whether inherited or acquired, the fibroid diathesis is most 
intimately associated with lithaemia, and all treatment is primarily directed 
to this condition. Evidences in early life of faulty metabolism, of defect- 
ive oxidation or deficient elimination of waste products, should lead to the 
adoption of a carefully regulated diet and the persistent use of those drugs 
which stimulate these processes. When the condition is once developed 
and the evidences of high arterial tension are present, even greater care 
must be exercised in the diet. ■ From the earliest indications of disturb- 
ance in the nutritive processes, the persistent use of alkaline waters will be 
desirable. Mercury and Warburg's tincture are the most decided stimu- 
lants to the metabolic changes ; and later, when fibrous tissue is being 
formed, minute doses of bichloride of mercury may be given continuously. 

PHLEBITIS. 
Phlebitis may be acute or chronic. 

Morbid Anatomy. — In acute phlebitis the adventitia may be first involved 
and the inflammation extend inward, a clot forming in the calibre of the 
vein ; or the inflammation may commence within, in connection with sur- 
rounding inflammation, and extend outward. If there is extensive con- 
nective-tissue infiltration around the vein, adhesive obliteration of the vein 
results ; should the clot soften and disintegrate, pus formations result. The 
presence of a clot may be regarded as an essential accompaniment of all 
forms of phlebitis except the adhesive or chronic. 

In chronic phlebitis the external coats of the veins are very much thick- 
ened, while the intima may be normal. The connective-tissue around the 
vein is greatly increased, there is hypertrophy of its muscular tissue, and 
the vasa vasorum are very much dilated. In rare cases thickening, fatty 
degeneration, and calcification (" atheroma ") of the innermost venous coats 
are found. In these cases the outer layers will almost invariably exhibit 
"sclerotic" changes. This has been called "chronic endoiihlebitis.''' 

Etiology. — The commonest cause of phlebitis is the formation of a throm- 



VARIX. 



555 



bus. Periphlebitis may be induced by wounds, ulcers, abscesses, chronic 
visceral disease, phlegmonous erysipelas, separation of the placenta, osteo- 
myelitis, amputation, ligation of veins, pyaemia and septicaemia, cellulitis 
from any cause, and, according to some, by varicosity or permanent dila- 
tation. 

Symptoms. — If the vein is within reach of observation, it will be found 
hard, swollen, and tender ; prominences occur at the sites of the valves, 
pains dart along its course, and the limb may become stiff. When super- 
ficial, the veins can be felt, and the skin over them is livid red. When 
deep main trunks are involved, the limb is swollen and the skin pale, tense, 
and shining over it. 1 Abscesses in the course of the vessel, which may or 
may not communicate with its interior, are of common occurrence. Should 
the tissues become cedematous and should constitutional hectic or 
pyaemic symptoms supervene, suppurative phlebitis (peri-phlebitis) may 
be suspected. 

G-outy phlebitis occurs in those with hereditary gouty tendencies ; the 
skin over a vein becomes dusky or livid red, the vein is hard, and the limb 
is somewhat cedematous. All the symptoms may suddenly disappear, 
quickly to reappear in some distant part (metastatic phlebitis). Varicose 
veins in the gouty are especially liable to these manifestations, although 
loss of tone and local erythema are more to be blamed than gout for these 
venous inflammations. 

Differential Diagnosis. — Phlebitis is distinguished from lymphangitis by 
the fact that in the latter the glands are tender and enlarged from the out- 
set ; and bright red streaks are very numerous. 

In erysipelas, redness is in the form of a general blush ; — in phlebitis 
there is only a dusky red localized streak. 

Prognosis. — This is bad only in the suppurative variety. 

Treatment. — Absolute rest, splints to confine and render the affected 
limb immovable, and hot fomentations over the parts are the first indica- 
tions. Abscesses should be opened early, and when oedema occurs the parts 
must be bandaged. 

TAEIX. 

Varix or dilatation of the veins occurs most in obstructive diseases of the 
right heart. In a few cases the veins become dilated and varicose without 
any obstruction, the cause of the dilatation under such circumstances being 
very obscure. 

Morbid Anatomy. — When veins dilate they elongate : the dilatation is 
most marked immediately above the valves and the affected vein assumes 
an irregular outline. The walls are thickened from hypertrophy of their 
middle coat at some points, and' dilated at others. Dilatation may take 
place in the largest, the smallest, or in the medium sized veins : calcareous 
plates not infrequently form in their walls, and phlebolites and venous 
calculi often develop in the pouch-like protrusions in the veins, where the 
circulation is slowed. Local or general obstruction and a varicose condi- 
tion of the veins serve primarily as important aids in diagnosis and rarely 
require medical treatment. They are mainly surgical disorders. 

1 See phlegmasia alba dolens in works on Obstetrics. 



556 



DISEASES OF THE BLOOD-VESSELS. 



THROMBOSIS. 



Thrombosis is coagulation of the blood in the heart, or blood-vessels, 
during life. The colt or coagulum is called a thrombus, and is most com- 
monly met with in the veins. Parietal thrombi are those clinging to the 
wall of a vessel and not completely obstructing the flow. Occluding 
thrombi are those absolutely obstructing the flow. 

Morbid Anatomy. — In rapidly formed thrombi a considerable number of 
red blood discs are entrapped and the color is first dark red ; in such clots 
the fibrin at once completely fills the vessel, and the thrombosis is uniform 

or non-laminated. These are the usual charac- 
teristics of obliterating thrombi. In slowly formed 
thrombi fewer red blood discs are entangled, 
hence the color is lighter, sometimes, indeed, 
the clot is absolutely colorless. The structure 
is laminated or stratified, and the mass adher- 
ing to the wall of the vessel does not wholly ob- 
struct the current, or at least in its early stages. 
These primitive thrombi usually extend along 
the vessel to a branch whose blood current is 
sufficiently strong to arrest their progress. The 
projecting conical end of the coagulum becom- 
ing softened, small pieces may be detached and 
thus enter the circulation. 

A thrombus may organize or undergo shrink- 
ing, softening, or suppuration. 

Organization occurs oftenest in uniform 
thrombi situated in arteries. The leucocytes in 
venous thrombus a; by the bibod the clot or those from the vasa vasorum develop 

current of a small venous branch, s 

aguium Detached ^ )0rtions °f c °- new connective-tissue, and vessels permeate the 
new structure in whose meshes lies the debris of 
the clot. Progressive dilatation of the new vessels ultimately renders the 
original channel pervious: — " canalization of the thrombus" 1 

Instead of organization a thrombus may soften. Stratified thrombi 
usually soften. Molecular disintegration commences at the centre of the 
clot, which will be found filled with a purulent-looking milky or pulpy 
material, containing albuminous granules, molecular fat, granular detritus, 
and changed red and white corpuscles. This is not suppuration of the 
thrombus, nor should it be called puriform softening. Large cardiac 
thrombi suifering these changes resemble cysts. Those thrombi that break 
down into granular matter containing bacteria and pus celts, are specific 
or infectious thrombi (vide Pyaemia). A non-infectious thrombus, after 
softening, maybe wholly absorbed ; or, as central softening occurs, fibrin is 
deposited upon the periphery. Pus may enter such a thrombus from without. 

Suppuration is occasionally seen in the thrombi of veins surrounded by, 
or leading from, inflamed parts ; a multiplication of leucocytes takes place 




Fig. 114. 

Diagram showing the manner of de- 
tachment of small portions of a 



1 Coinil and Ranvier assert that there is merely an outgrowth of vascular granulations from the tunica 
intima, that penetrate the thrombus ;— and that the latter gradually disappears without taking part in the 
formation of the reticulated tissue which occupies its place obliterating endarteritis , '). 



EMBOLISM. 



557 



m the thrombus either by proliferation or immigration, and the whole 
softens down into a purulent fluid. In these cases the wall of the vein itself 
is always inflamed. These softened and broken-down thrombi are a common 
cause of embolism. When the middle coat of the vein is involved and in- 
tensely inflamed, true suppuration of the coats may occur, and thus throm- 
bosis may be a cause of abscess of the external coats of a vein. It is impor- 
tant to distinguish between thrombi and post-mortem coagula : — the latter 
are soft, divisible into two layers — a colored and an uncolored — are never 
laminated, their texture is looser, they never entirely fill the vessel, and they 
do not adhere to its wall. Heart clots that form during the death agony 
are, in color and consistence, midway between the two just mentioned. 
They are entangled with the colurnnae carneae and chordae tendineae, but 
can be separated with a little care. 

Etiology. — Any abnormality of the vessels, but especially of the tunica 
intima, will induce the formation of a thrombus (atheroma, phlebitis, endar- 
teritis, etc., etc.). Any neoplasm in a vessel may cause it. Wounds, blows, 
ligation, dilatation of the vessels or of the heart, and anything that will 
diminish heart power, or induce slowing of the blood current, will induce 
thrombosis. Hence we find it occurring in phthisis, cancer, old age, etc., 
etc. The veins of the pelvis and lower limbs, and in children the cerebral 
sinuses are the favorite seats of these " marantic"* thrombi. 

Compression thrombosis results from slowing of the current from mechan- 
ical causes outside the wall. In the heart thrombosis may be caused by 
endocarditis. Lymphatic thrombosis has chiefly been observed in the puer- 
peral condition. In leucocythaemia the capillary circulation being inter- 
fered with from the vast number of white corpuscles, clots readily form in 
the veins. Finally, venous thrombi are especially liable to form in the pockets 
of the valves. 

Symptoms. — The symptoms depend upon the extent of the obstruction to 
the circulation and the size and situation of the vessel : — for instance, 
when the femoral vein is plugged, phlegmasia alba dolens results. Throm- 
bosis of the cerebral vessels gives rise to special cerebral manifestations. 1 
Thrombosis of the portal vein is followed by the grave symptoms of py- 
lephlebitis. Moist gangrene, ascites, hydrothorax, oedema and cyanosis of 
the face and neck, hemorrhage from stomach, intestine or kidney— each 
may be a consequence of the plugging of the main vein issuing from the 
part. The special danger of venous thrombosis is the possible detachment 
of a portion of the thrombus, its transportation by the circulation to the 
heart, and its arrest there or in one of the branches of the pulmonary ar- 
tery (embolism). The result of arterial thrombi is anaemia of the part sup- 
plied, necrosis, or hemorrhagic infarction. 

EMBOLISM. 

An embolus is any solid body other than the corpuscles floating in the 
blood current. Embolism is the occluding of a vessel by an embolus. 
Thus it is seen that arterioles and capillaries are the usual seats of embol- 
ism, since in these vessels the current is toward ever-diminis hing branches. 

1 See Brain : Art. Embolism. 



558 



DISEASES OF THE BLOOD-VESSELS. 



In general an embolus is part or all of a dislodged thrombus ; for example : 
a clot in the femoral vein (milk-leg) crumbles ; particles are swept into 
the ascending cava, then through the right heart into the pulmonary 
artery, and some of the latter's branches having a calibre smaller than the 
diameter of the particles they will be plugged. 
Morbid Anatomy. — When small arteries are plugged the anastomoses 
may prevent any visible lesion from occurring. 
When a vessel of any size is plugged, the first re. 
suit is anaemia of the district supplied by the 
branches of the blocked vessel. Then there is 
backward pressure and regurgitation of blood from 
the veins, through the capillaries into the arteri- 
oles, whose vitality is impaired because of this venous 
substitution. Exudation and ultimate necrosis of 
vascular walls are followed by hemorrhage, and the 
blood coagulates forming a hemorrhagic infarc- 
tion. When an embolus causes anaemia and ne- 
crosis without hemorrhage, it produces what is 
called a white or ancBmic infarction. The primary 
and essential change white infarction is coagu- 
lation-necrosis. The shape of an infarct is conical 
Diagram showing the establish- because of the tree-like branching of the arteries 

ment of circulation by anas- , ° 

tomotic vessels after an Em- and capillaries beyond the site oi the embolus; 

and it is usually situated with its base toward the 
surface and its apex toward the centre of the 
organ. 1 In non-infective infarctions the mass be- 
comes decolorized, changing from dark red to dirty 
yellow, and then to white. At the same time it shrinks and finally may 
leave a depressed fibrous patch or cicatrix. In larger masses molecular 
disintegration and softening first occur and a pulpy granular puriform 
fluid forms, which becomes enclosed in a fibrous capsule, and finally be- 
comes cheesy or calcareous. In both cases there is a circumscribing zone 
of congested vessels. 2 

When a vessel is plugged, wholly or partly, and the vessel is a terminal 
artery, hemorrhage does not necessarily occur, and there occurs a white or 
anaemic infarction, which is to be distinguished from a decolorized hemor- 
rhagic infarction by microscopical examination. Some emboli are always 
followed by necrosis, others by hemorrhage. In the brain anaemic softening 




Fig. 115. 



bolism. 

A, Embolus plugging small Ar- 
tery. 

£, Anastomotic branch supply- 
ing blood to the area C. 



1 Cohnheim states that in order to produce hemorrhagic infarction the artery, must be a terminal artery, 
t. e., giving off no anastomotic branches before its final capillary distribution, and the veins must 
not have valves, and that these conditions are met with in the spleen, kidney, brain, certain branches of 
the pulmonary artery, and the central artery of the retina. Litten has opposed these views, and states 
that in genuine terminal arteries hemorrhagic infarction does not occur, and that infarction may take 
place after ligature of the vein. Hence venous reflux cannot be its cause. From his experiments it 
would seem that congestion and infarction following embolism are due to afflux of arterial blood into 
the territory from collateral channels ; his views more nearly correspond to Virchow's original theory. 
— Zeifschriftfiir Klinische Medicin, vol. i. 

2 The changes that occur in infective or specific emboli are described under pyaemia. Cornil and Ran- 
vier regard the decolorization which marks the white infarct as the result of fatty degeneration of the pa- 
renchymatous cell elements of the organ involved. The connective-tissue about them is infiltrated with 
white blood discs. But Litten regards white infarctions as due to coagulation-necrosis of the proto- 
plasm of the cells, having a remarkable tendency to calcification. 



THORACIC ANEURISM. 



559 



without hemorrhage is common. Necrosis may rapidly ensue after embol- 
ism (gangrene), or it may come on slowly as a withering or softening. The 
vessel wall at the site of the embolus undergoes changes similar to those 
described, as resulting from thrombi. If an embolus does not completely 
nil a vessel a secondary thrombus forms, by deposition of fibrin, and this 
extends till a strong current of blood arrests its progress. Emboli coming 
from venous thrombi usually induce pulmonary infarction ; emboli from 
the left heart, arterial aneurisms, arterial neoplasms, etc., produce infarc- 
tions in spleen, kidneys and brain, as a rule. 

When emboli produce death of part of an organ without true gangrene, 
Virchow gives the name necrobiosis. An embolic abscess is the same as 
a pysemic abscess. The influence of embolism in the production of 
aneurism is to-day recognized, even when the particle that plugs the vessel 
is not a sharp calcareous or atheromatous mass. 

THOKACIC A^EUKISM. 

An aneurism is a more or less abrupt dilatation of the calibre of an ar- 
tery ; the tumor thus formed must communicate with the channel of the 
vessel. Thoracic aneurism includes all those tumors which arise from the 
aorta and its branches within the thorax, or from the pulmonary artery. 

Morbid Anatomy. — The convexity of the ascending portion of the arch 
of the aorta is the most frequent seat of the aneurismal development, next 
the transverse portion of the arch ; next the descending portion of the 
arch, and least frequent of all the descending aorta. Aneurisms of that 
portion of the aorta which is embraced by the pericardium are of small size 
and are apt to pass unrecognized. 1 The junction of the ascending and trans- 
verse portions of the arch at the sinus magnum is a favorite seat of aneu- 
rism, it being nearly at right angles to the blood-stream from the heart. 2 

The only logical clinical classification of aneurisms is based on their 
shape. 

The whole surface of the artery may be dilated, and the aneurismal tu- 
mor be cylindrical, fusiform or globular in shape. 

There maybe a lateral bulging or sacculation of a portion of the circum- 
ference of the artery : — a sacculated aneurism. In both of these classes the 
arterial coats may be all intact, or any one or two of them may be absent 
or diseased. 

When the walls of an aneurism are made up of the surrounding tissue, 
it is called a consecutive diffuse aneurism ; and when blood finds its way 
between the coats of an artery, it is called a dissecting aneurism. 

The post-mortem appearances of aneurism will vary with its location, 
size and variety. In some cases nothing abnormal will be found except an 
unruptured aneurismal tumor ; in others the tumor will be found ruptured, 
the pericardium filled with blood, or extravasated blood will be found either 
in the bronchi, trachea, stomach, or pleural cavity, or an external rupture 

1 Of 703 cases of Sibson's (Medical Anatomy), 87 were within the pericardium, i. e., about 12 per cent. 

2 Anatomically, aneurisms are divided into true and false. True aneurisms are those in which all the 
coats of the artery are found in the walls of the aneurismal sac. False aneurisms are those in which a ru;> 
ture of one or more coats of the artery has occurred. 



560 



DISEASES OF THE BLOOD-VESSELS. 



may have been the immediate cause of death. Aneurisms arising from one 
of the sinuses of Valsalva, within the range of the valves, rarely attain a size 
larger than that of a small billiard-ball. They are sacculated and not infre- 
quently pedunculated, communicating with the aorta by a small orifice. 
They further exhibit a remarkable tendency to descend in the progress of 
growth, involving in their course the heart or the root of the pulmonary 
artery. By their position they are sheltered from direct influx from the 
ventricle, whilst they are exposed to the maximum force of reflux from the 
aorta. When, however, the orifice is partially or entirely above the level 
of the valves, the main pressure sustained by the sac is that during influx 
from the ventricle; hence the direction of growth is upward. 

Aneurisms near the sinus magnum produce erosion of the ribs and their 
cartilages, the sternum and the right clavicle : — sections of the bones show 
the lesions of osteitis. The adjacent muscular and connective-tissue is ex- 
tensively infiltrated. The descending cava and the left innominate vein 
may be so compressed as to have their channel completely closed. The left 
recurrent laryngeal, the left sympathetic, or the trunk of the vagus may be 
compressed, atrophied, or entirely destroyed. The thoracic duct may be com- 
pressed and ruptured into. Should aneurisms about the arch enlarge back- 
ward, the trachea, oesophagus, and right lung will surfer from the pressure. 

In aneurism of the descending arch, or thoracic aorta, the spinal extrem- 
ity of the ribs and the bodies of the vertebrae in the dorsal region may be 
destroyed, and the left bronchus may be obliterated, causing consolidation 
of the entire lung. The dorsal spinal nerves and sympathetic trunk may 
be destroyed by pressure. All the secondary changes in thoracic aneurism 
are "pressure effects," and they are never alike in any two cases. 

The aneurismal sac also varies greatly in the appearance it presents at 
the autopsy. All the tunics of the artery may be preserved ; but in large 
aneurisms while the external and internal coats can be traced all over the 
tumor, the middle coat ceases abruptly where the sac opens into the artery. 

When an aneurism begins with rupture or dis- 
ease of the inner coat of the artery, a lining 
membrane of new formation meets and coalesces 
with the intima, so that the appearance is the 
same as if no rupture or change had occurred. 
The aneurismal walls may undergo fatty or cal- 
careous degeneration. The contents vary with 
the size and shape of the sac and with the rapid- 
ity with which it has formed. The sac may be 
nearly filled with concentric layers of firm lami- 
nated fibrin containing small calcareous plates ; 

with looser layers 
of fibrin inclosing recent coagula. Sometimes 
fresh coagula and fluid blood are alone found. 
Those laminae of fibrin nearest the aneurismal 
wall are the firmest. 

Etiology. — The chief predisposing cause of 
aneurism is disease of the arterial walls, the most common of which are 




Fig. 11(5. 

Diagram illustrating the anatomy 
of spontaneous Arterial Aneurism. 01' it may be partially tlllecl 

A. Internal coat of Arte? 
B. Middle coat of same ; C. 
ternal coat. 
J) and E. External and internal 
coats of the aneurismal tumor 
showing the absence of the middle 
arterial coat. 



ery ; 
Ex- 



THORACIC ANEURISM. 



561 



chronic endarteritis and atheroma. Age and occupation may also be re- 
garded as predisposing causes, the period between forty and fifty being 
the favorite period of its development. It is a question whether aneurisms 
occurring in middle life are the result of senile changes or violent physical 
exertion. Atheroma and calcareous degenerations are commonest after 
sixty; hence muscular effort probably has much to do in developing the 
more frequent aneurisms in those who are younger, although it is doubtless 
aided by commencing degeneration of the arterial wall. Mechanics, por- 
ters, soldiers, and those liable to suddeu and violent physical exertion are fre- 
quent subjects of aneurism ; the irregularity and violence of the action is to 
be considered, rather than its severity. Habits of life, intemperance in eating 
and drinking, chronic alcoholismus and tight fitting garments (uniforms) 
predispose to aneurismal developments. The majority of these who de- 
velop aneurism before forty-five will give a syphilitic history ; hence syph- 
ilis must be ranked as a predisposing cause. Chronic Bright's, rheuma- 
tism, gout, lead and mercurial poisoning are included in the predisposing 
causes to arterial diseases, and consequently to aneurism. In aortic insuf- 
ficiency the hypertrophied left ventricle throws a larger column of blood 
with abnormal force against aortic walls ; chronic aortitis results and an 
aneurism may follow. 

The exciting causes are blows, falls from heights, wounds, excess or pro- 
longed venereal excitement, and sudden violent strains, exerted on a de- 
generated artery. 

Symptoms. — The early rational symptoms of thoracic aneurism vary with 
the site of the tumor. If the aneurism is near the sinuses of Valsalva, it 
will give rise to no symptoms until rupture discloses its existence, If a 
second murmur is heard over the pulmonary artery it may be caused by dis- 
placement of the valve, or diminution in the calibre of the pulmonary 
artery from pressure of an aneurismal tumor, and if it is accompanied by 
venous stasis and congestion of the upper half of the body, an aneurism 
may be suspected. With all aneurisms within the pericardium there will be 
some hypertrophy of the left ventricle. The development of an aneurism 
near the sinus magnum is usually accompanied by very positive symptoms. 
The patient often states that after some violent effort, some blow, or during 
an excess of some kind, "he felt something suddenly give way," and then 
followed a "boring'* pain near the sternum with dyspnoea, palpitation, and 
perhaps haemoptysis. 

As a rule there are no subjective signs of thoracic aneurism until the 
tumor presses on the adjacent parts. By the direction of the pressure the 
seat of the tumor may be determined. Aneurism of the ascending arch 
usually presses forward, upward, and to the right ; — of the transverse 
arch, backward and upward ; and of the descending portion of the arch, 
backward and to the left. In whatever direction an aneurism presses, pain 
is its first symptom. The pressure may be exerted upon (1) the nerves ; 
(2) the Mood- vessels ; (3) the trachea, oesophagus, the large bronchi, the lung- 
tissue, the thoracic duct, and, indirectly on the heart. 

The pain when present is constant. It is increased by acceleration of the 
circulation, and is localized in the region of the tumor ; usually it is asso- 



562 



DISEASES OF THE BLOOD-VESSELS. 



ciated with a sense of constriction. The pressure pain may be neuralgic, 
paroxysmal and wandering. It radiates to the neck and shoulder and 
may shoot down either arm. If the intercostal nerves are pressed on, there 
will be attacks of excruciating intercostal neuralgia. If erosion of verte- 
brae, sternum, or ribs occurs, there is a peculiar, constant " boring " pain. 
When one or both vagi or recurrent laryngeal nerves are pressed on, spasms 
and partial or complete paralysis of the laryngeal muscles cause dyspnoea 
and voice-changes ; the voice becoming husky. Sometimes there is com- 
plete aphonia. Violent paroxysms of dyspnoea are liable to occur, attended 
by a congested, anxious countenance, and violent respiration followed by ex- 
haustion. Cases are recorded where vomiting and pyrosis resulted from 
pressure on the pneumogastric. Pressure on the pulmonary plexus gives 
rise to a harsh metallic " brassy " cough. Pressure on the vagus may be 
followed by congestion of the lungs, oedema and gangrene. An inequality 
of the pupils may come from irritation or pressure on the cervical sympa- 
thetic : irritation causes dilatation of the pupil ; and pressure (when annul- 
ling the function) causes its contraction on the affected side. Disordered 
vision may thus become a symptom of thoracic aneurism. 

When blood-vessels are compressed only the main trunks of one side are 
involved, hence a delayed, even a suppressed radial pulse will be found 
only on that side. In a few cases I have found no pulsation in either carotid 
or subclavian on the affected side. Then cerebral anaemia and signs of im- 
paired nutrition in the limb on that side were present. The effect of im- 
peded venous return may lead to a diagnosis of the seat of an aneurism. 
When an aneurism near the sinus magnum enlarges forward, the upper 
half of the body shows congestion and oedema ; there is headache, drowsi- 
ness and other cerebral symptoms, and the eyeballs protrude. Aneurism 
of the innominata or of the right common carotid in the thorax, presses 
on the external jugular, and hence the right side of the head and neck is 
turgid. Such a condition on the left means aneurism of the left common 
carotid. 

When tracheal symptoms are urgent, they point to aneurism of the 
transverse portion of the arch enlarging backward. The flattening of the 
trachea induces difficult breathing, then follows a stridulous cough (with 
no expectoration), having a metallic ring, like a " nervous cough." Such 
compression may result from an accumulation of mucus which cannot be 
expectorated ; hence, dyspnoea arises. The pressure may even produce 
gangrenous patches, which lead to rupture and fatal hemorrhage. It is 
readily seen w T hy congestion of the lungs and pneumonia sometimes fol- 
low compression of the trachea. The signs of pressure on a large bronchus 
are, principally, a metallic cough, with tenacious mucous sputa, at times 
blood-streaked, and, possibly, evidences of pneumonia and gangrene. 
Pleurisy may be excited by a tumor's pressure, and it is always an important 
sign taken in connection with signs of pressure upon the trachea and bron- 
chus. 

Dysphagia may be induced, but the oesophagus is rarely ruptured into 
by an aneurism. Dyspepsia, reflex in origin, may be a symptom of thoracic 



THOKACIC AXEURISM. 



503 



aneurism. The lower third of the oesophagus is said to be widely dilated in 
some cases of this kind. Enlargement of the lymphatics below the sac 
results from pressure of an aneurism on the thoracic duct. Symptoms of 
mal-assimilation, wasting and inanition would also be present in such cases. 

All these symptoms are never present together in any one case, bnt when 
three or four of the prominent ones exist, they are strong evidence of 
thoracic aneurism. 

Physical Signs. — Inspection. — If the aneurism press on the cava descen- 
dens, the face, neck and upper extremity will be swollen, livid, or oedem- 
atous, the veins being turgid and varicose. Sometimes there is a thick, 
fleshy collar around the lower part of the neck, due to capillary tumes- 
cence. Bulging is seen at some spot on the chest, probably along the 
course of the aorta, and this may be as large as a cocoanut, or, again, may 
be perceptible only after careful inspection. Non-existence of a tumor 
does not, however, disprove the existence of an aneurism ; anenrismal tu- 
mors deeply seated will not produce bulging. When the visible tumor is 
large it is generally conical. The skin over it is smooth, tense and shining. 
Inspection may reveal pulsation in it, which is synchronous with the car- 
diac systole, and when this bulging occurs on the anterior surface of the 
chest there seem to be two beats within the thorax at the same time. 
Pulsations are, at times, only detected by bringing the eye to a level with, 
and looking across the chest. Aneurisms of the ascending arch usually 
enlarge first to the right of the sternum near the second costal cartilage, 
but if it is very large it may extend into both the mammary and infra- 
clavicular region. Aneurisms of the transverse arch protrude above the 
sternum, those of the descending arch to its left. In the latter case a 
visible tumor is uncommon. Aneurisms of the descending aorta enlarge 
to the left, rarely to the right, of the spine. They may sometimes give 
rise to violent pulsations near the heart and simulate extensive cardiac hv- 
pertrophy. 

Palpation discovers more accurately the size and the condition of the 
walls of the aneurism. The pulsation imparted to the hand is like that 
of a blow from the centre outward in all directions, dilating or expansile; 
there may be a diastolic pulsation as well as systolic. The impulse is some- 
times perceptible only when one hand is pressed over the sternum and the 
other over the interscapular space. When the transverse arch is involved 
the aneurismal thrill may be communicated to the hand by pressing the 
fingers down behind the sternum. Palpation should be employed to de- 
tect lung changes, fremitus, expansion, etc., etc.; it is noteworthy that con- 
solidation of lung substance induced by thoracic aneurism is characterized 
by absence of vocal fremitus. 

Percussion elicits circumscribed dulness at some point along the line of 
the aorta, corresponding to the seat and size of the aneurism. A resistance, 
peculiar to aneurism, and increased by the force of the percussion blow, 
will be noticed over all large aneurisms. Consolidation of adjacent lung- 
tissue may increase the area of dulness. 

Auscultation. — The heart sounds accompanied by " murmurs" peculiar 



564 



DISEASES OF THE BLOOD-VESSELS. 



to aneurism may at times be audible over the seat of the tumor, or both heart 
sounds may be replaced by murmurs, the character of which varies. They 
may be sawing, rasping, or grating. A diastolic murmur is rarer than a 
systolic, and is usually softer. With aneurisms near the sinus, the murmur 
is booming or splashing, and is accompanied by a thrill not transmitted in 
any direction. When a large bronchus is compressed, the respiratory mur- 
mur is weak or suppressed on one side and exaggerated on the other. 
There is loss of vocal resonance over the aneurism and over the side on 
which the bronchus is compressed. 

Differential Diagnosis. — It is always of the first importance to determine 
at what point in the course of the aorta an aneurism is developed. 

An aneurism near the sinuses of Valsalva may be mistaken for aortic in- 
sufficiency. The latter is distinguished by the previous history, absence of 
arterial degeneration, transmission of the murmur to the xiphoid cartilage, 
absence of a murmur over the pulmonary artery, and the existence of left 
ventricular hypertrophy and dilatation. Should the sinus of the right 
auricle be pressed on, both cavse will be obstructed and the liver will show 
evidences of congestion. 

The diagnosis between aneurism of the arch of the aorta and of the in- 
nominate artery is difficult. In the latter the tumor appears earlier in the 
neck, and on the right side at the sternal end of the clavicle ; while aneu- 
risms of the arch are usually limited to the second right intercostal space, or 
appear at the manubrium sterni or in the episternal notch, frequently ex- 
tending to the left of the median line. Pressure on the right subclavian 
or common carotid does not lessen the pulsation in aneurism of the arch ; 
while if the innominate alone is involved, the impulse will be markedly 
diminished. Impaired venous return and neuralgic pains are confined to 
the right side in innominate aneurism, while the venous congestion is 
bilateral and pain is on both sides in aneurisms of the arch. The bruit of an 
innominate aneurism is less intense than that of an aortic. The radial 
pulse is seldom altered in aortic aneurism, while a suppressed radial pulse 
on the right side is a common and important sign of aneurism of the in- 
nominate. The larynx and trachea are often pushed to the left by an in- 
nominate aneurism ; rarely by an aortic. 

Cancer of the pleura, mediastinal tumors, bony exostoses, pulsating em- 
pyema, abscesses between oesophagus and trachea, laryngeal disease, in- 
tercostal neuralgia, angina pectoris, consolidation of the lung near the apex, 
and hydropericardium, — all may be mistaken for a thoracic aneurism. 

In cancer of the pleura the personal and hereditary history is impor- 
tant. The pain in cancer is constant ; in aneurism it is wandering, and 
shifts with change in direction of the tumor. Anything increasing 
heart action increases the pain of an aneurism ; this is not so in cancer. 
The pulsation is dilating in aneurism ; heaving and lifting in cancer. 
A harsh double bruit is present in aneurism ; while if one is present in 
cancer it is soft and blowing. In aneurism the centre of dulness and the 
point of maximum dulness coincide ; this is not the case in cancer. 
Enlarged veins and glands (axilla, neck, etc.) accompany cancer ; they are 



THOKACIC ANEUKISM. 



565 



not present in aneurism. In aneurism there is a subjective sense of 
throbbing, never present in cancer. Infiltrated cancer of the lung induces 
retraction of the chest- walls, and is not likely to be confounded with tho- 
racic aneurism. 

Localized empyema which pulsates must occupy the cardiac area and push 
the heart to the right, and it has no murmur. Besides, the peculiar 
wandering pain of aneurism is absent in empyema, and in this condition 
the pulse is not altered. Irregular diurnal fever, chills, and sweatings 
occur in empyema, never in aneurism. The exploring needle will settle 
the question. 

An abscess between the trachea and oesophagus is attended by no 'bruit, 
no pulsation of an expansile character, no shifting pain, no pulse-difference. 
Deep-seated fluctuation, chills, fever, and sweats accompany it, however. 

An exostosis below the sternoclavicular articulation may pulsate, but 
the pulsation is lifting, not expansile, and there is no bruit. 

Laryngeal disease may be recognized by the vocal changes. A physical 
examination of the chest, and the laryngoscope will enable one to make a 
correct diagnosis. 

In intercostal neuralgia, the three diagnostic points of tenderness, i. e., 
at the exit of the nerve from the spine, midway between this and the 
sternum, and at the edge of the sternum where the terminal branches be- 
come superficial, will decide between it and aneurism. 

Angina pectoris may occur with thoracic aneurism. But in all such cases 
valvular disease or degeneration of the heart-walls will be found to co-exist. 
Hence the diagnosis rests on the signs of a tumor in the one case, and the 
symptoms of structural heart-disease in the other. 

Pulmonary consolidation at one apex, with a murmur m the subclavian 
or pulmonary artery, will be attended by the signs of phthisis and not by 
those of a tumor. Fluid in the pericardium gives a triangular outline of 
dulness never met with in aneurism. 

Prognosis. — Although cases of thoracic aneurism have apparently recov- 
ered, the rule is that they terminate fatally. The average duration is about 
two and one-half years : — some terminate in a few months, others live five 
or six years. There is always a liability to sudden death. The better the 
general health and the smaller the swelling, the better the prognosis. The 
prognosis in aneurism of the ascending arch is better than in any other 
form of thoracic aneurism. Death may occur from pressure on important 
organs, or from rupture of the sac. 

The sac may open into one of the serous cavities from sloughing, erosion 
or laceration of its wall ; or it may open externally, or into a mucous canal. 1 
When the sac bursts into the pericardium or pleura, it ruptures at the 
thinnest part ; if into the oesophagus, trachea, or a bronchus, it breaks at 
some point of adhesion between the two, which has subsequently become 
thinned. External openings are produced by gradual atrophy from press- 
ure, or by sloughing of the skin over the tumor. Pneumonia, pleurisy, 



1 In twenty-six ruptures, ten were into the pericardium, five into the left lung or pleura, four into the tra- 
chea, three into the right lung or pleura, three into the left bronchus or oesophagus, one externally. 



566 



DISEASES OF THE BLOOD-VESSELS. 



bronchitis and gangrene may occur as complications to cause death. Press- 
ure on nerves, lymphatics or ducts may induce death from exhaustion. 
Emboli may arise and become a cause of death. 

Treatment. — The treatment of thoracic aneurism is divided into those 
measures which come strictly within the province of the physician, and the 
more recent surgical procedures. In both, absolute rest is one of the essen- 
tials. Anything that accelerates or increases the force of the heart's action 
will do harm, in accordance with the simple physical law that every abnor- 
mal dilating force applied to the walls of an aneurismal sac must favor its 
growth and hasten the fatal issue. Blood rich in nutritive elements more 
readily deposits its fibrin, thus favoring that formation of laminated layers 
of fibrin within the aneurismal sac which is the first step in the curative 
process. Fluids must be taken in minimum quantities. Mr. Tufnell re- 
stricts the food taken to two ounces of bread and butter, and two ounces of 
milk for breakfast ; two or three ounces of bread with two or three ounces 
of meat for dinner, with two to four ounces of milk or claret wine ; and 
two ounces of bread and butter and milk for supper. Mr. Tufnell says that 
this dietetic treatment, combined with absolute rest in a recumbent posi- 
tion for two or three months, resulted in cure in a large percentage of cases. 

Various internal remedies have been used to favor the formation of a 
coagnlum within the aneurismal sac, either by increasing the coagulating 
power of the blood, or by acting in some specific manner upon the walls of 
the aneurism itself or upon the adjacent arterial walls. The principal 
drugs used for this purpose are ergot, iodide of potassium, acetate of lead, 
and the vegetable astringents. Iodide of potassium and ergot are the only 
ones that have stood the test of experience. Both are used at the present 
time, and seem to have power in staying the growth of aneurisms and re- 
lieving painful phenomena. A combination of the dietetic, rest, and 
iodide treatments has arrested the progress of aneurisms in a number of 
cases under my observation, and I have the records of ten cases of thoracic 
aneurism where cures were effected and have persisted for over two years. 
In using the iodide of potash, the patient should be placed in bed and all 
medication withheld for three or four days until his pulse rate is established. 
* The iodide is then to be given in increasing doses and finally maintained 
at the highest point possible without increasing this previously established 
pulse rate. 

The only remedy to be relied on for relief of the excruciating pain attend- 
ing aneurismal development is the hypodermic use of morphine. It not 
only relieves pain, but by its quieting and regulating influence on the heart 
it delays the growth of the aneurism. It also diminishes restlessness and 
impatience, and enables persons who are naturally irritable to obtain the 
necessary rest which is so important a factor in any plan of treatment. The 
external application of belladonna to the aneurismal tumor will often afford 
temporary relief to the local pain. The continued application of an ice- 
bag to an external aneurismal tumor will often afford temporary relief of 
the pain and reduce the tegumentary inflammation ; its use should not be 
continued too long. When a patient with aneurism has an undue fulness 



ABDOMINAL ANEURISM. 



567 



of the vessels, free purgation with salines will be attended by marked relief 
for a time. 

Surgical Treatment of Thoracic Aneurism. — Thoracic aneurism seldom 
presents features which justify surgical measures. The methods employed 
are ligation of one or more of the great vessels in the neck, galvano- 
puncture, the injection of coagulating substances into the sac, and the in- 
troduction of solid bodies with the object of starting consolidation. The 
two latter methods have only been employed in a few desperate cases, and 
death has always followed so rapidly that no deductions can be made. On 
theoretical grounds it is improbable that either method could do good, 
except in cases of pouched aneurism. Experience shows injection of coag- 
ulating fluids to be very dangerous, usually inducing suppuration of the 
sac. The permanent introduction of wire, horse-hair, and catgut has never 
been followed by good results ; but in at least one case of (ileo-femoral) 
aneurism no harm resulted. The temporary introduction of several acu- 
puncture needles and their retention from one to two days has been tried 
with good results in a few cases ; it is less dangerous than the other methods 
mentioned. G-alvano-puncture has been employed by Oiniselli in twenty- 
three cases, with five cures. The same method has been tried by other 
surgeons, but the clot is liable to break down and cause inflammation of the 
sac. This plan has been adopted when rupture of the sac was impending, 
to delay for a time the fatal result. In some cases of supposed innominate 
aneurism, which proved to be aortic, ligation of the carotid, or of the 
subclavian, has been followed by marked relief. In two cases of aneurism 
involving the transverse arch, the left carotid has been tied and the disease 
cured or arrested for a very long time. It would seem best to perform this 
when the sac involves only the arch. Tracheotomy may be performed only 
to insure a ^uiet death. 

ABDOMINAL ANEURISM. 

An aneurism of the abdominal aorta, or of any of its branches situated 
within the abdominal cavity, is called an abdominal aneurism. The cceliao 
axis, the mesenteries, the renal, and the common iliacs are the branches 
usually involved. The morbid changes are similar to those of thoracic 
aneurisms, except that the pressure effects are different. The splanchnic 
nerves, semilunar ganglia, and the solar plexus may be involved. The bile- 
duct or the renal vessels, the stomach and the duodenum may be pressed 
on and narrowed. The bodies of the vertebrae may be eroded. Abdominal 
aneurisms are not so often caused by " atheromatous " changes in the walls 
of the artery as are thoracic aneurisms. 

Etiology. — Its development is always preceded by some form of arterial 
degeneration. It is rare before thirty-five, and is met with in men oftener 
than in women. 

Symptoms. — Intermittent, paroxysmal pain is its prominent symptom. 
Agonizing pain in the back darts along the branches of the lumbar plexus. 
This pain is apt to be continuous, and indicates erosion of the spinal column. 



568 



DISEASES OE THE BLOOD- VESSELS. 



Nausea and vomiting may result from pressure on the stomach ; dyspha- 
gia from pressure on the oesophagus ; jaundice from pressure on the bile- 
duct ; changes in the urine from pressure on the renal vessels ; and anasarca 
of the lower limbs from pressure on the inferior cava, or in one limb from 
pressure on one of the iliac veins. Aneurisms here may burst into the 
peritoneal cavity, the retroperitoneal tissue, the spinal canal, or into the 
substance of the mesentery, meso-colon, or great omentum, and in the 
last-named instances there will be more or less obstruction about the region 
of the pylorus. They may also open into the intestinal canal, the lung, 
the pleura, the inferior cava, the pelvis of the kidney, the ureter, bile- 
passages, or the oesophagus. Barely are the liver and heart displaced. 

Physical Signs. — Palpation discovers in some instances a smooth, elastic 
tumor to the left of the median line. It has an expansive, dilating impulse 
(rarely double), and synchronous with the radial pulse. 

There is dulness over the tumor. 

On auscultation a single prolonged post-systolic murmur may be heard. 1 
A double murmur over the aneurism in front is rare. Seldom can any 
murmur be heard when the patient is in any other than a recumbent pos- 
ture. 

Differential Diagnosis. — If an abdominal aneurism is of considerable size, 
the constant pain in the back and the presence of a dilating tumor will 
establish a diagnosis ; forcible pulsation of the aorta may simulate an 
aneurism, but the throbbing is felt along the entire course of the aorta 
and its branches, and is not localized as in aneurism ; then the absence of 
pain and of the "expansive " impulse and murmur will establish the diag- 
nosis. A cancerous or other solid tumor may have a pulsation communi- 
cated to it by the underlying aorta ; but the knee-chest position will re- 
move doubts. In thin subjects especially, by grasping the solid, uneven 
mass, it is easy to decide for or against an aneurism. 

Prognosis. — Hayden gives fifteen days to eleven years as the extremes ; a 
year or eighteen months is the average duration. After rupture the pa- 
tients have lived for some time ; but death is certain sooner or later. 

Treatment. — Posture, rest, a restricted diet, and mild laxatives are advo- 
cated in the treatment of abdominal aneurism by Bellingham. Tufnell's 
plan may also be followed. Iodide of potassium and ergot reduce vascu- 
lar tension and are highly recommended. Aconite is highly recommended 
by English surgeons. Pressure, ligation, tourniquets, etc., etc., are meas- 
ures resorted to by surgeons. 

MEDIASTINAL TUMOES. 

Cancer and sarcoma are, independent of aneurism, the most frequent 
mediastinal tumors. In rare instances lymphadenomata, lipomata, cysts, 
enlarged lymphatics, fibromata and osteomata may develop in the medias- 
tinum. The lymphatic glands in the anterior mediastinum are most fre- 



1 If the patient be placed in the knee-elbow position, and a murmur still persists, then the tumor is in 
all probability an abdominal aneurism, not a tumor to which aortic pulsations have been transmitted. 



THE URIKE. 



569 



quently the seat of these developments, although they may originate in any 
mediastinal tissue. In exceptional cases the thymus gland is the original 
seat of the new growths. The primary cause of their development is un- 
known : they occur at any age, but are most frequently met with between 
twenty and forty. 

The symptoms of mediastinal tumors are those of pressure, e.g., aphonia, 
dysphagia, cyanosis, pain, and a sense of constriction about the chest. 
Displacement of the heart without any other recognizable cause is an almost 
diagnostic symptom. 

The physical signs vary with the size and site of the tumor, which may 
pulsate and have a distinct bruit. Mediastinal tumors, mediastinal ab- 
scesses, aneurism, pericardial or pleuritic effusions and chronic pneumonia 
all produce symptoms which are strikingly similar ; and the diagnosis of a 
mediastinal tumor is arrived at mainly by exclusion. The exploring trocar 
is often the only means by which a diagnosis can be reached. 

Prognosis. — Mediastinal tumors sooner or later terminate fatally. Lebert 
states that their average duration is thirteen months. In a case of Jac- 
coud's, death occurred on the eighth day. 

The treatment is palliative. 

DISEASES OF THE KIDNEYS. 

THE URINE. 

The urine in health is a clear, amber colored liquid of acid reaction, 
saline taste, and having a peculiar aromatic odor. The amount voided in 
twenty-four hours ranges between forty and fifty ounces. Its specific 
gravity varies from 1.012 to 1.030 ; the average being about 1.020. After 
exposure to the air the acidity of the urine, which is due mainly to the 
presence of the acid phosphates, continues for a few days, and then an acid 
or alkaline fermentation takes place. The former is caused by the growth 
of a round cell vegetable ferment, and is accompanied by the crystallization 
of uric acid and the precipitation of the acid urate of soda. The alkaline 
change is the result of the growth of the micrococcus urea, and is marked 
by decomposition of the urea and the formation of carbonate of ammonia 
and the triple phosphates. 

Normal Constituents of the Urine. — Generally speaking, these may be 
regarded as the products of the metamorphosis of the tissues of the body ; 
the most important organic constituents are urea, uric acid, hippuric acid, 
oxalic acid, kreatinin, xanthin, and the coloring and extractive materials. 

Urea. — This substance represents the result of the retrograde metamor- 
phosis of the nitrogenous body tissues and the excess of the nitrogenous ele- 
ments of the food. It is formed in the tissues, taken up by the blood and 
lymph, filtered by the kidneys, and appears in the urine to the amount of 
five to six hundred grains daily. Urea is abnormally increased in amount 
in all febrile and nervous affections, in pyaemia and diabetes ; it is abnor- 
mally diminished in nephritis, anaemia, cholera, and starvation, and mar 



570 



DISEASES OF THE KIDNEYS. 




be entirely absent in acute yellow atrophy of the liver. Urea is a feeble 
base, extremely soluble, and cannot be detected except by chemical exami- 
nation. 

Uric acid is generally found in the urine combined with some base, 
especially lime or soda. Its origin is similar to that of urea. In health 
six to nine grains are passed every twenty-four hours ; this amount is in- 
creased by a highly albuminoid diet and in certain febrile conditions. It 
is diminished by out-door exercise. Uric acid appears in the urine as a 
crystalline deposit, which will be described hereafter. Besides the above 
constituents, the urine normally contains small quanti- 
ties of kreatinin, hippuric acid and xanthin, which may 
be said to represent the less completely oxidized products 
of tissue change. 

Coloring and extractive materials. — The normal color of 
the urine is due to the presence of a pigment, called urohae- 
matin ; a substance closely allied to the coloring matter 
of the bile, and derived from the blood by the action of 
fig. 117. the liver and spleen. Another normal pigment of the 
Hippuric Acid, x 2o0. ur j ne j g j n( ji caT1) a peculiar substance which under certain 
conditions gives rise to indigo-blue. The extractives are certain volatile 
organic acids which give to the urine its peculiar aromatic odor. 

The inorganic constituents of the urine are chlorine, sulphuric acid, 
phosphoric acid, potassium, sodium, calcium, magnesium, oxygen, hydro- 
gen and nitrogen. 

Chlorine. — The average amount of chlorine passed daily is about one 
hundred grains ; an increase in this amount has no special significance, but 
a diminution or absence has been noticed in all acute febrile diseases with 
the one exception of intermittent fever. 

Sulphuric Acid. — The amount daily passed averages about thirty 
grains. Sulphuric acid in the urine arises from the animal and vegetable 
food taken into the system, and from changes in those tissues which con- 
tain sulphur and sulphates. 

Phosphoric Acid. — About fifty grains of this acid are eliminated in 
the twenty-four hours. It is abnormally increased in all inflammatory 
diseases of the nervous system, in severe nerve lesions and in rickets. It 
is abnormally diminished in most febrile and inflammatory diseases, es- 
pecially in pneumonia and Bright's disease. The rest of the inorganic con- 
stituents of the urine, which amount to about one hundred grains daily, 
will be considered under the head of urinary sediment, as they generally 
appear in that form. 

Albumen. — When albumen appears in the urine it may have its origin 
in the kidneys or depend upon the presence of pus or free blood ; this 
question can only be settled satisfactorily by the microscope. Albuminous 
urine is generally of low specific gravity. In diseases of the kidney the 
serum-albumen which is found in the urine has its origin in the blood, 
and either by the increase or diminution of the blood pressure within the 
glomerules., the albumen is transuded within the capsule of Bowman, and 



THE UKI^E. 



571 



then is washed along the uriniferous tubules with the urine. When albu- 
men appears in the urine in acute and chronic Bright's disease some 
structural change in the kidney is indicated ; but it may appear independ- 
ent of any structural lesions under the following conditions, viz. : febrile 
and inflammatory diseases, impediments to the circulation of the blood, 
pregnancy and the puerperal state, saturnine intoxication, hydremia and 
atony of the tissues, after the use of certain drugs, and in some people after 
taking certain articles of food. 

Urinary Sugar. — When the urine contains much sugar it is of a pale, 
yellow color, sweetish taste, and increased in amount. Its specific gravity 
is always high, generally between 1.030 and 1.040, although cases are occa- 
sionally met in which it is as low as 1.008. Sugar, except in a very small 
quantity, is not found in normal urine, so when it is constantly present 
in large amounts a grave pathological lesion is indicated. Diabetes niel- 
li tus is the only disease in which sugar is found in the urine in large quan- 
tities, but traces of it appear after disturbances of the abdominal circula- 
tion, after injuries to certain portions of the nervous system, after inter- 
ference with respiration, in the urine of women just after weaning a child, 
and sometimes it is temporarily present without any assignable cause. 

Bile, — Urine containing bile varies in color from a deep reddish brown 
to a dark green, and generally has an acid reaction and high specific gravity. 
The coloring matter of the bile, such as bilirubin, biliverdin, and bili- 
prasin, is the portion -which usually appears in the urine in disease. It is 
especially noticed in those who are jaundiced. The bile salts are some- 
times present. 

Lactic acid has been found in the urine in diabetes, acute yellow atrophy 
of the liver, trichinosis .and osteomalacia. 

Fat.— Fat is not very often found in the urine, but when it is present it 
gives to that fluid a milky appearance, for it is held in the form of an 
emulsion by the albumen present. The 
urine shows a tendency to spontaneous 
coagulation, and in a short time a white 
layer rises to the top which disappears 
on the addition of ether. Under the 
raicroscope minute globules of fat, some- 
times with blood and lymph corpuscles, 
are seen. 

Leucin and Ty rosin. — The urine 
often contains large quantities of these 
substances, which arise from the prolonged action of 
the pancreatic ferment upon the nitrogenous elements 
of the food. 

Leucin appears either in the form of white crystal- 
line scales freely soluble in water, or as small, round, yellow bodies looking 
something like spherical fat cells. 

Ty rosin is in the form of white masses consisting of long shiny needles 
arranged in star-shaped groups. Leucin and tyrosin appear in those 



o 



•<?oo.o 

Fig. 118. 

Fat globules from 
chylous urine, 
x 250. 




Fig. 119. 
Leucin ar.d Tvrosin. 



Globules of Leucin. 
Tyrosin. ; x 250. 



572 



DISEASES OF THE KIDNEYS. 



diseases in which oxidation is very greatly impaired, such as acute yellow 
atrophy of the liver, typhoid fever, small-pox, and in hepatic diseases 
generally . 

URINARY SEDIMENTS. 



A 



Hoc 





Many deposits, in crystallizd and non-crystallized forms, appear in the 
urine, some of which are passed with it, and others are separated from 
it after its passage. The following are the most important : 

Uric Acid.— The strong acids which appear in the urine during the 
stage of acid fermentation quickly decompose the urates, and set the uric 
acid free. This is deposited in the form of yellowish-red colored crystals 

which assume a multitude of forms. The 
most common are lozenge-shaped and rhom- 
boidal crystals, having angles more or less round- 
ed ; they also appear, especially when abun- 
dant, as aggregated or flat stellate crystals. 
Should any doubt arise as to the character of 
the crystals, dissolve the sediment in a drop of 
potassic hydrate, then add a little hydrochloric 
acid, and the uric acid, if present, will recrystal- 
lize into one of its numerous forms. The clinical 
importance of uric acid crystals has already 
been referred to. 

Urates. — When the urine contains abundant 
amorphous urates it is generally turbid, but 
becomes clear on heating. On careful obser- 
vation a fine powdery sediment will be seen, 
which clings to the glass and varies in color 
from a light fawn to a pink. The urates are in a 
state of solution in normal urine, but when 
that fluid becomes concentrated 
or has lost the temperature of & 
the body, the urate of soda will ^ ^ 
become deposited in an amor- 
phous condition, appearing under 
the microscope as mossy granu- 
les. Urate of ammonia appears ^ 
only after the urine becomes j£& 
alkaline, occurring as brown- " 
ish spherical bodies, with or with- Fig. 122. 
out fine projecting spiculae. The Urate of Ammonia. 

1 0 , ., , £ , A. Cluster of Brown 

urates may be deposited after spherules. 
slight indigestion, great mental \uSh%SiZ'- 
and physical exertion, and in ^suaS^Tmf 
acute febrile and inflammatory 
diseases ; they are often the forerunner of urinary calculi, and of derange- 
ments of the liver and of the other chylopoetic viscera. 



Fig. 120. 

Uric Acid. 

A. The most common form. 

B. Disintegr ted crystals. 

C. Formation of rounded masses 

x 250. 



A 






Fig. 121. 

Urate of Soda. 

Amorphous granules in clusters 
resembling moss. 
Granules 'in strings sometimes 
mistaken for granular casts. 
x 250. 



UKIN-ABY SEDIMENTS. 



573 



a 

o o 
O ° 



Oxalate of Calcium. — Calcium oxalate is often held in solution in the 
urine, but when it is precipitated it takes one of two 
forms, either as small, colorless, sharp -edged, octa 
hedral crystals resembling envelopes, or as dumb- 
bell shaped crystals, entangled with mucus. The 
presence of the oxalate of lime crystals is due 
to the -reduction of the compounds of oxalic and 
carbonic acids which are normal to the urine, or to the 
ingestion of certain articles of food. When oxalate of 
calcium occurs constantly in the urine it produces the 
so-called oxaluria or oxalic acid diathesis, and is apt to 
lead to the formation of the mulberry calculi, and in 
time exert its poisonous effects on the brain and spinal 
cord. The crystals of calcium oxalate are found in the urine in 
of disturbed respiration, emphysema of the lungs, rachitis, and 
epileptic convulsions. 

Earthy Phosphates. — The earthy phosphates are the most common 



❖ S3 °Q 

Fig. 123. 

Oxalate of Calcium. 
The octahedra, most fre- 
quently present, are 
seen on the left. The 
comparatively rare 
form of dumb-hells is 



also shown. 



c 250. 

cases 
after 

sedi- 




Fio. 124. 



ment met with in the urine, in fact, when the urine is alkaline they are 
never absent ; they present themselves as the am- 
monio-magnesian or triple phosphates, or as the 
phosphate of calcium. During the stage of alkaline 
fermentation, the ammonia produced combines 
with the phosphate of magnesium present, and the 
result is that the crystals of the triple phosphates, 
being insoluble in an alkaline fluid, are thrown 
down in large quantities, as also are the crystals of 
the phosphate of lime, the separation of the latter de- 
r pending upon the presence of one of the fixed alka- 
JA/ lies, as the carbonate of sodium. The crystals of the 
f^s^^&s£%^ triple phosphates vary according as they are the re- 
sult of rapid or slow crystallization : in the former 
case they assume a feathery form, looking some- 
thing like two ferns crossing at an acute angle ; in 
the latter case they appear as triangular prisms with 
bevelled edges. The phosphate of lime forms an 
amorphous transparent sediment like the urates, 
but is distinguished, from them by the action of heat, which causes an 
increased precipitation, and by that of nitric acid, a few 
drops of which clear up the urine. A sediment of the 
earthy phosphates does not of necessity indicate that there 
is an abnormal amount in the urine, but it does show the 
alkaline state of the urine and the possible results of such 
a condition, and it points out the danger of the formation 
of phosphatic calculi. An increase of the earthy phos- 
phates has been noted in certain diseases of the bones, such 
as rachitis. 

Cystine, which is a crystalline body derived from the 



Triple 



Amraonio-Masnesian, or 
Phosphate. 

A. Large colorless prisms. 

B. Forms rapidly deposited 

x 250. 




Fig. 125. 
Phosphate of Lime, 
x 350. 



574 



DISEASES OF THE KIDKEYS. 




Fig. 126. 
Cystine, x 250. 



liver, is not often found in the urine, but when it is it presents itself in 
the form of flat hexagonal plates, which are of neutral reaction and can be 
dissolved by the caustic mineral alkalies. When this 
substance occurs in the urine it is apt to give rise to cal- 
culi. Cystinuria seems to run in families. 

Organized Sediments. — Mucus and Epithelium. All 
urine contains a varying amount of mucus, derived from 
the urinary passages and from the bladder, which sepa- 
rates in the urine as a light, flaky cloud. Under the 
microscope mucus presents itself in one of two forms, 
either as mucous corpuscles in the form of small, round 
granular cells containing one or more nuclei, or as trans- 
parent masses of mucous coagula, which look very much like granular 
casts and for this reason have been called mucoid casts. An abnormal 
amount of mucus in the urine shows that there is irritation at some point 
along the urinary tract ; this may be the re- 
sult either of a local inflammation or of a 
general constitutional disease, such as pneu- 
monia or typhoid fever ; when there is a mu- 
cous sediment in the urine, there is always 
found entrapped in it a large number of 
epithelial cells of different varieties, which 
for convenience of description m^y be di- 
vided into three classes. First, round, 
spherical cells having distinct nuclei de- 
rived from the tubules of the kidney, or from 
the deep layers of the mucous membrane lin- 
ing the pelvis or from the male urethra. 
Second, columnar and ciliated cells derived 
from the cervix of the uterus. Third, flat 
cells with large distinct nuclei which have 
their origin in the bladder or vagina ; in the 
former case they are much larger and granu- 
lar. The situation of an inflammation con- 
fined to some portion of the urinary tract 
may sometimes be determined by noting the 
character of the epithelial cells passed in the 
urine whenever it can be determined whether 
the cells came from the tubules or pelvis of 
the kidney, or from the bladder or lower part of the urinary passage. 

Blood may appear in the urine in varying amounts, and may come from 
any portion of the tract ; when the urine contains blood it will have a 
reddish or smoky appearance, and deposit, on standing, a coffee-ground like 
sediment, and will show by chemical analysis the presence of both albumen 
and fibrin. The appearance of the urine, the amount of blood, and the 
cause of its presence will vary greatly according to the portion of the 
urinary passages from which it comes '.—first, when the quantity of blood 




Fig. 127. 

Epithelium from Urinary Deposits. 

B. Large , flat bladder cells. 

B 2 . From bladder— deeper layers. 

V- Cells from vagina. 

U. Ciliated cells from cervix of uterus. 

C. From mucosa of uterus. 

P. Cells from pelvis of kidney. 
T. From collecting tubules. 
G. From prostatic portion of urethra. 
x 250. 



URINARY SEDIMENTS. 



575 



is small, and it is equally diffused throughout the urine, in all probability, 
it is deriyed from the parenchyma of the kidneys, and especially from the 
Malpighian tufts ; this condition is met with as the result of Bright's dis- 
ease, congestion of the kidney, injury, the use of certain drugs, such as 
eantharides, the formation of abscesses secondary to renal infarctions, and 
from the presence of adventitious growths. Second, when 
the urine contains much blood and distinct clots are visi- O ~q 

ble, it is safe to infer that the blood is derived from q ^ 

the pelvis of the kidney, from the ureters, or from the O 
bladder ; in the former case it is generally the result of 
pyelitis, renal calculi, parasites, or morbid growths ; in the 
latter case it is present as the result of vesical calculi, or 
erosions and ulcerations of the mucous membrane. Blood 
may appear in the urine as the result of disease of the ^ooT" 
urethra, but then the cause of its presence can easily be a. Suoiiea red cor- 
determined. Certain constitutional causes may give rise to V nrfnto- se 




bloody urine, for it appears in the following diseases: _ jific gravity. 



urine of low spe- 
cific gravity. 
Crenaied corpus- 

fevers, scurvy, purpura, cholera, myelitis, and in the des . from dense 

'J > urine, x 250. 

hemorrhagic diathesis. 

Pus, when present in the urine, gives to it a milky appearance, and, on 
standing, a yellowish-green sediment is precipitated which, as long as the 
urine is acid, can easily be mixed with it, but when the urine becomes 
alkaline, the sediment will have a gelatinous, ropy appearance and soon 
undergo ammoniacal decomposition. Albumen is always found in urine con- 
taining pus, and varies in quantity with the amount of pus present. The 
microscopical appearance of pus is sufficient to determine its presence ; for 
the shape, size and granular appearance of the pus corpuscles, with their 
granular nuclei rendered more distinct by the addition of acetic acid, cannot 
4& H be mistaken for anything else. Pus appears in the 

L ® @ * urine either as the result of some suppurative inflam- 
H mation along the genito-urinary tract or from the rup- 
A ®^ ^ ure °^ some ne ig n Dorin g abscess, but it must be re- 
® membered that in women it may be derived from the 

genital organs. The significance of pus in the urine 
(B\B (f"> depends upon its source, which may be determined by 

C$ © © remembering the following points : — if the urine is 
acid, when voided, the pus probably has its origin in 
the kidneys ; if it is alkaline, its origin is in the blad- 
der ; if its presence is accompanied by slight colicky 
a. Pus corpuscles as ordi- pains over the course of the ureters, probably suppli- 
es. The m fa^n7jr^alld e with ration is going on in them. In inflammations of the 
acetic acid, x 300. ure thra pus can be pressed out of the meatus. 
Casts are peculiar cylindrical bodies consisting of exudative material or 
coagulated matter formed in the urinary tubules of the kidney as the 
result of disease, and then washed out by the urine secreted behind them. 
They vary in size and number according to the nature of the disease which 
gives rise to them, but it may be rightly stated that the more numerous the 



Fig. 129. 
Pus. 



576 



DISEASES OF THE KIDNEYS. 




t;i . " 
*. 'I 

V 



Fig. 130. 
EpitheJial Casts, 
x 250. 




casts and the longer time they are present, the more extensive will be the 
structural lesions in the kidney. The following are the principal varieties 
of casts met with in the urine : 

Epithelial casts consist of tubular masses of renal epithelium, especially 
from the tubules of Bellini in the medullary por- 
tion of the kidneys ; they are also, at times, de- 
rived from the epithelial lining of the pelvis 
and calices of the kidney. Occasionally the 
epithelial cells present a norma! condition, but 
generally they show granular degeneration. This 
variety of casts indicates desquamative nephritis. 
When they are found mingled with pus cor- 
puscles a serious inflammatory condition is in- 
dicated. 

Hyaline casts are structureless, transparent cyl- 
inders, having a tendency to fracture transversely, 
and are derived from the fibrinous exuduation 
which has passed through the degenerated walls 
of the renal vessels and coagulated in the tubules 
of the kidney. Large hyaline casts are met with 
in the atrophied stage of all forms of Bright's 
disease. Small hyaline casts are found in the 
acute stage, and sometimes 
when no lesion can be appreci- 
ated. 

These casts are solid, fibrinous cyl- 
inders, which have a finely granular appearance caused 
by the presence of the debris of the degenerated renal 
epithelium. Blood and pus corpuscles and granular cells 
are often found embedded in this granular matter. These 
casts are most often found in the advanced stages of 
Bright's disease, and indicate the large white or granular 
kidney, or that extensive destruction of the paren- 
chyma of the kidney is taking place. 

Fatty casts are made up of a material supposed 
be mixture of olein with cholesterin, and some 
buminous matter ; fat globules, varying greatly 
size, and also some epithelial 
cells and granular material 
may be found in them. These 
casts show that the degenera- 
tive changes in the kidney are 
fatty, and they indicate the 
same conditions as granular 
casts. 

Blood casts consist of coagu- 
lated fibrin and red blood corpuscles. By some they are thought to indi- 



Fig. 181. 
. Hyaline Casts. 

Delicate hyaline casts. 
Dense, so-called waxy casts. 

Granular Oasts. — 





Fig. 132. 
Granular Casts. 

A. Large granular casts. 

B. Small fin ely granular 

casts, x 250. 



to 
al- 
in 




Fig. 134. 
Blood Casts, 
Collecting-tube blood casts. 
Mucous casts. 



UE^MIA. 



577 




Fig. 135. 
Spermatozoa, 
x 500. 



cate the disease of the renal blood-vessels, especially amyloid or fatty de- 
generation of the Malpighian tuft. 

Spermatozoa are occasionally met with in the 
urine, and give to it, when present in abundance, a 
milky white appearance. If a drop of the urine 
be placed under the microscope the characteristic 
tadpole appearance of the spermatozoa can easily 
be recognized. Spermatozoa appear in the urine 
after coitus, involuntary nocturnal emissions, 
and occasionally after defecation. They have 
also been found in the urine of typhoid fever 
patients. 

Animal and Vegetable Organisms. — Fully 
developed hydatids and echinococci, or only 
portions of these, may appear in the urine, 
having been developed at some portion of the 
genito-urinary tract or poured into it by the 
rupture of some hydatid cyst. A small uni- 
sexual parasite, the Bilharzia haematobia, has 
been found in. the urine, especially during the 
epidemics of haematuria occurring in North- 
ern Africa. Bacteria, or fermentation spores, 
form in urine which is undergoing decom- 
position. Sarcinse have been observed in al- 
kaline urine. Penicilium glaucum has been 
found in acid albuminous urine. Torula cerevisiae often forms in diabetic 
urine. 




Fig. 1 



A. Torula cerevisice.—B. Penicilium glau 
cum. — C. Sarcince Vent, x 300. 



UREMIA. 



Decrease in the elimination of the solid constituents of the urine is fol- 
lowed by two well marked combinations of symptoms, — one in which nau- 
sea, vomiting, and convulsions are indicative of cerebral irritation ; and a 
second in which headache, drowsiness, and coma depend upon decrease and 
abolition of nervous function. These conditions, with associated symp- 
toms, are called uraemia. 

The primary cause of both these conditions is to be found in a failure of 
the kidneys to perform their normal function of elimination, and the con- 
sequent accumulation in the circulation of some or all of the poisonous ele- 
ments of the urine. This condition may occur in the course of any disease 
in which suppression of the renal secretion takes place ; such arrest of the 
function of the kidneys most frequently occurs in the different forms and 
stages of Bright's disease, in the puerperal state, in connection with the 
surgery of the urethra, cystic, tubercular, and cancerous disease of the kid- 
ney, and in suppurative nephritis ; by far the largest number occur in acute 
Bright's disease. 

37 



578 



DISEASES OF THE KIDNEYS. 



A number of theories have been advanced in regard to the exact element 
which acts as the poisonous agent in uraemia. The earliest accepted view 
is that which attributes the symptoms of uraemia to retained urea. Fre- 
nch's theory was that urea, as urea, was innocuous, and that the poisonous 
agent was carbonate of ammonia resulting from decomposition, in the blood, 
of urea into carbonate of ammonia and water, which decomposition was 
ascribed to the action of a ferment in the blood ; this theory has been dis- 
proved. Another hypothesis which has attracted much attention is that 
the phenomena of uraemia are due to cerebral anaemia and the attending 
cerebral oedema. This is the mechanical theory. Still more recent experi- 
menters have claimed that urea is formed in the kidneys from nitrogenous 
matter in the blood, and that uraemic manifestations mainly depend upon 
the accumulation, in the blood, of kreatin and kreatinin. Again, others 
have claimed that the phenomena of uraemia are due to the retention, in 
the circulation, of the products of nerve waste. It has also been claimed 
that some forms of uraemia may be associated with structural changes in 
the brain, similar to those which occur in the retina in cases of neuro- 
retinitis. 

Mahomed (Brit. Med. Jour., 1877, ii. 10-42) calls attention to the cere- 
bral lesion which, he says, accounts for the epileptiform convulsions of 
uraemia, viz., numerous punctiform hemorrhages in the gray matter of the 
cerebral convolutions. They are true hemorrhages. He ascribes other 
cerebral symptoms to oedema of the brain following increased tension. 
Similar to oedema is the "hyaline exudation into nervous tissue " found 
by Gull and Sutton. Similarly, headache results from increased tension 
without exudation. Gubler (Paris, 1878) describes the "diminished num- 
ber and impaired respiratory capacity of the red blood corpuscles '' in 
uraemia, due (G. states) to kreatinin and ammonium carbonate. Hence 
there is more or less " asphyxiation of the nerve centres." He also believes 
arterial spasm to result in sudden retention of effete products. He regards 
the dyspnoea as at times due to kreatinin, at times to ammonium carbo- 
nate ; in one the breathing is hurried, in the other it is the " Cheyne- 
Stokes respiration. " 

The experiments and facts upon which these theories are based lead to 
the following conclusions : that uraemic toxaemia depends upon the pres- 
ence in excess, in the blood, of poisons normally eliminated by the kidney. 
This excess may be due to failure in kidney function or abnormal forma- 
tion of the poisonous elements. Four classes of poisons are now recog- 
nized : 

(1.) Products of tissue disintegration. 

(2.) Aliments; prominently the potash salts. 

(3.) Absorbable products of intestinal decomposition. 

(4.) Various secretions ; as, the bile and saliva. 

The uraemic poison is complex in character, and may vary not only in 
the proportion of its component elements, but in the elements themselves. 
The potash salts are regarded by many authorities as the most poisonous 
elements of the urinary secretion. 



URAEMIA. 



579 



Symptoms.— An acute uraemic attack is usually preceded by certain pre- 
monitory signs, such as oedema in various parts of the body, restlessness 
or an almost irresistible desire to sleep, vertigo, headache, delirium, nau- 
sea, vomiting, diarrhoea, and impaired vision. The countenance has a pale, 
waxy or dingy appearance, and the urine is scanty, high-colored, bloody, 
albuminous, and contains casts ; the body and extremities may become 
violently convulsed, or the patient may pass rapidly into a state of coma. 

The convulsions may consist of a single paroxysm, or a succession of 
paroxysms may follow one another at intervals of a few minutes or several 
hours, the patient during the interval lying in a state of more or less pro- 
found insensibility. They may almost exactly simulate epilepsy, or they 
may be unattended by loss of consciousness. During the convulsions 
the face becomes livid, the eyes are glassy, and the pupils are contracted 
or dilated ; at the commencement of the convulsive attack, they are gener- 
ally contracted. Frothy mucus, which is sometimes bloody, collects around 
the mouth, and there is a strong urinous odor emanating from the per- 
spiration. The pulse is accelerated, and the temperature is raised in some 
instances as high as 107° F. A low temperature may be present in the 
aged. Sudden coma may occur with convulsions. Eestless delirium is the 
chief symptom in many cases. Intense dyspnoea, and articular symptoms 
are very rare. 

Urcemic coma may come on gradually, twenty-four or forty- eight hours 
elapsing before the stupor is complete, or the patient may fall suddenly 
into a state of profound coma, its advent resembling an attack of cerebral 
apoplexy. Headache, giddiness, disorders of vision, vomiting, or delirious 
excitement may precede the coma. There are periods when the coma is so 
profound that nothing arouses the patient ; at other times he is easily 
aroused, or arouses himself and attempts to speak and sit up, swallowing 
fluids with difficulty. If the system has become accustomed to the pres- 
ence of the urinary poisons, a considerable excess of urea and effete uri- 
nary products may exist in the blood for a long period without giving rise 
to any but the premonitory symptoms of acute uraemia. When once this 
balance is destroyed and a certain excess of urea and its allies in the blood 
is reached, the kidneys become embarrassed by the excessive demand made 
on their excreting power, and rapid and intense renal congestion follows, but 
either convulsions, coma, or both, result in this way ; acute uraemia may 
be developed in the chronic as well as the acute stage of renal disease. 
Uraemic coma is always accompanied by stertor. The stertor is peculiar : 
it is not the " snoring" of apoplexy, but a sharp, hissing sound produced 
by the rush of expired air against the teeth or hard palate. At first the 
respirations are accelerated, but they soon become slow and labored ; the 
pupils are dilated, but they are not irregular ; they may be normal ; they 
react slowly to light. The pulse is increased in frequency and lacks firm- 
ness ; at first the temperature is raised, but after a time it falls below the 
normal standard ; the face is pale. 

Differential Diagnosis. — Acute uraemia simulates in some of its phenom- 
ena those diseases in which convulsions and coma are prominent symptoms. 



580 



DISEASES OF THE KIDNEYS. 



The phenomena of an epileptic seizure are almost identical with those 
of an uraemic convulsion, and it is exceedingly difficult to distinguish one 
from the other. If the previous history is known, the chronic character 
of the epilepsy will in some instances distinguish it from acute uraemia, 
and an examination of the urine will generally determine the uraemic char- 
acter of the convulsions ; in epilepsy one side is convulsed more violently 
than the other ; while in uraemia both sides of the body are equally con- 
vulsed. In epilepsy the temperature is not elevated, and although there 
is a loss of consciousness, reflex sensibility continues from the beginning 
to the end of the paroxysm, which is not the case in uraemia. Immedi- 
ately following uraemic convulsions there is deep coma ; following an 
epileptic seizure there is merely a deep sleep, from which the patient may 
be aroused. The initial cry and corpse-like pallor of the face in epilepsy 
are wanting in uraemia. 

In cerebral apoplexy coma always precedes convulsions, and with the con- 
vulsions there is facial paralysis and hemiplegia ; there is also clonic 
spasm of the paralyzed parts. The urinary symptoms of uraemia are ab- 
sent and the stertor is less sharp and hissing. 

In hysterical convulsions the patient falls with a scream into a convul- 
sive, tetanic or cataleptic condition. Close inspection shows that the 
patient is not unconscious, and the pupils are normal, as are the pulse and 
temperature. The limbs are jerked irregularly, the breathing is spasmodic 
and .is attended by a choking sensation ; opisthotonos is very common. 
There is no lividity of the face, nor distention of cervical blood-vessels, 
and the close of the paroxysm is usually accompanied by the discharge of 
a large quantity of pale urine, — non-albuminous and free from casts. 

Cholcemic convulsions very closely resemble uraemia, but may be dis- 
tinguished from them by the jaundice which precedes or accompanies their 
development, and by the antecedent history of hepatic disease. Convul- 
sions originating in meningitis and other cerebral affections are distin- 
guished by the accompanying characteristic symptoms of these affections. 

The points in the differential diagnosis of urcBtnic coma are similar to 
those of uraemic convulsions. It may be distinguished from the coma of 
apoplexy by the absence of paralysis. 

From opium poisoning it may be distinguished by the rise in temperature. 
The temperature in opium poisoning is often below the normal. In opium 
coma the respiration is slow and peculiar, and the pupils are uniformly con- 
tracted. Uraemic coma is distinguished from epileptic coma by the ante- 
cedent history of the patient, the presence of bloody froth about the mouth, 
and the indentations on the side of the tongue ; from alcoholic coma, by the 
temperature, and the character of the breathing, which is "puffy" in alco- 
holic coma, and a hissing stertor in uraemia. In all cases of coma, an ex- 
amination of the urine is important before reaching a diagnosis. 

Prognosis. — From experiments as well as from the clinical history of acute 
uraemia, it is evident that the primary cause of death is a poison, the exact 
nature of which is obscure, but which resembles in its action narcotic 
poisons. This poison acts primarily on the nerve centres, and produce^ 



URJEMIA. 



581 



changes in the blood which interfere with or arrest oxygenation. This 
action is followed by certain structural changes in the different tissues of 
the body. When these poisons are introduced into the circulation in small 
quantities, so that its elimination can be effected in a short time, it only 
temporarily disturbs the functions of organic life ; but when it is intro- 
duced in large quantities, oxygenation of the blood is arrested, and it under- 
goes certain changes which render it incapable of supporting life. The 
prognosis, then, in each case will depend upon the amount of the poison, 
and the length of time the system is under its influence. 

If the symptoms of excessive uraemic toxaemia are present, and there are 
evidences that the poisoning has been going on for a considerable time, the 
prognosis is much more unfavorable than when the acute uraemic symptoms 
are mild and of recent date. 

Treatment. — It is claimed that the most important thing to be accom- 
plished in the treatment of acute uraemia, is to secure as rapidly as possible 
a free eliminative action of the skin, bowels, and kidneys. The favorite 
method of elimination is by diaphoresis, accomplished by the hot-air baths. 
Pilocarpi n has recently been used to accomplish the same results. In con- 
nection with diaphoresis, a vicarious action of the bowels is induced by the 
administration of drastic purgatives, such as elaterium, pulvis purgans and 
scammony. The testimony in regard to the use of diuretics is conflicting. 
Many object to their use, on the ground that inflamed organs should not 
be stimulated. 

Digitalis acts efficiently — is diuretic without stimulating the kidneys. 
It increases the power of the heart's action and increases the tension in the 
Malpighian tufts. The diminished secretion of urine is due to obstruction 
in the capillary circulation of the kidneys. Digitalis, by increasing the 
heart power, overcomes such obstruction. To obtain its effects in such con- 
ditions, larger doses are required than are usually administered. My rule 
of practice in these cases is to give half an ounce of the infusion every three 
hours for twenty-four hours, or at least until its specific effect is produced. 
In the majority of severe cases of acute uraemia, when the patient is in 
convulsions or coma, the excretory functions of the skin, bowels and kid- 
neys are completely arrested, so that diaphoresis cannot be induced, or, if 
induced, it is not eliminative, and the bowels do not respond to purgatives 
although the patient may swallow them in large doses, and digitalis in 
large doses fails to restore the urinary secretion. At one time under such 
circumstances free general blood-letting was used extensively, but the result 
was unsatisfactory. 

If there is acute uraemia, the avenues of elimination are shut off, and the 
question arises: — what means have we to counteract this uraemic poison, and 
open again the avenue of its elimination, or, at least, to hold the patient until 
the normal eliminating process shall be re-established ? The first indication 
is to diminish reflex sensibility, and subdue spasmodic muscular paroxysms, 
for these, if continued, will either directly terminate life, or end in equally 
fatal insensibility. The remedy which for some years has been employed 
for the accomplishment of these results is chloroform. It has been exten- 



582 



DISEASES OF THE KIDNEYS. 



sively used, and, I believe, is regarded as the safest and most reliable means 
for controlling uraemic convulsions. Hydrate of chloral and bromide of 
potash are also more recently recommended, but their action is not swift or 
powerful enough. Although many authorities recommend the use of chlo- 
roform in uraemic eclampsia, few make mention of its employment in acute 
uraemia independent of the puerperal state. Its only known clinical effect 
is to control muscular spasm, and in a large proportion of cases it fails to 
give more than temporary relief to those patients who pass from successive 
convulsions into a state of complete coma, and die without any apparent 
neutralizing effect from the chloroform. In the few cases in which I have 
administered chloroform in non-puerperal uraemic convulsions, it has 
seemed to me to have no other effect than to arrest convulsive movements 
by rapidly hastening the patient into a state of insensibility. In no in- 
stance have I known its administration to be immediately followed by di- 
aphoresis or a return of the urinary secretion. It has seemed to be more 
difficult to establish diaphoresis or diuresis by diaphoretics and diuretics in 
patients with uraemia to whom chloroform had been administered, than in 
those who had not taken it. 

Therefore, I believe that while chloroform temporarily controls muscular 
spasm, it prejudices the chances of ultimate recovery by the changes its in- 
halation produces in the blood, which changes increase rather than retard 
the development of the uraemic toxaemia. With these impressions one nat- 
urally seeks an agent which not only has the power to control muscular 
spasm, but shall also at the same time tend by its action to reopen the ave- 
nues of elimination, either by counteracting the effects of the uraemic poi- 
son on the nerve centres, and thus facilitating the action of diuretics and 
diaphoretics, or by acting itself directly as an eliminative. 

I believe morphine administered hypodermically to be such an agent. 

There are two questions that very naturally present themselves in con- 
nection with the use of morphine in acute uraemia. 

First. Can morphine in full doses be administered without danger to 
patients with acute uraemia ? 

Secondly. What are the effects of such administrations ? 

If one turns to recognized authorities for an answer to the first of these 
inquiries, he will find that nearly all make mention of the use of opium in 
uraemic toxaemia only to warn against the danger attending its administra- 
tion. During the first years of my professional life, I regarded opium as 
one of the most dangerous remedial agents that could be administered to 
uraemic patients, rarely daring to give more than five grains of Dover's 
powder to a patient with albuminous urine, and if fatal coma followed 
such administration, more than once do I remember to have felt that a Do- 
ver's powder which I had administered might have been the cause of the 
fatal coma. In 1868 I administered my first hypodermic injection of 
morphine to a patient with acute uraemia. 'The effects which followed its 
administration in this case taught me that in some cases with marked urae- 
mic symptoms morphine could be administered hypodermically not only 
safely, but with apparent advantage. Since that time I have used mor- 



RE^AL HYPEREMIA. 



583 



phine hypodermically in the treatment of these patients, not only during 
the premonitory stage, but also during the active manifestations of uraemic 
intoxication, and its administration has been uniformly followed by good 
results. In no instance have I caused a fatal narcotism. 

From the histories of quite a large number of puerperal and non-puerpe- 
ral cases of acute uraemia, in which morphine was successfully used, I have 
reached the following conclusions : 1 — -first, that morphine can be adminis- 
tered hypodermically to some if not to all patients with acute uraemia with- 
out endangering life. Secondly, that the almost uniform effect of morphine 
so administered, is, first, to arrest muscular spasms ; secondly, to establish 
profuse diaphoresis ; thirdly, to facilitate the action of cathartics and 
diuretics, especially the diuretic action of digitalis. Thus, morphine 
administered hypodermically becomes a powerful eliminating agent. The 
rule is to give small doses at first, not to exceed one-sixth of a grain. If 
convulsions threaten, and a small dose does not arrest the muscular spasm, 
it may be increased to one-quarter or one-half of a grain, and the hypo- 
dermics may be repeated as often as every two hours. It must be given 
in sufficient quantities to control convulsions ; neither the contraction of 
the pupils nor the number of the respirations is a reliable guide in its 
administration. 

I would not discard all (perhaps none) of those means which have been 
relied on for the relief of patients in acute uraemia, but would urge that 
hypodermic injections of morphine not only control muscular spasms, but 
aid in establishing the eliminating processes, and thus become another 
means of saving life in these often fatal cases. Dry and wet cupping, leech- 
ing and poulticing over the loins may be employed to aid in this re-estab- 
iishment of the suppressed renal function. 

DISEASES OF THE KIDNEYS 
will be considered in the following order : 

I. Renal Hyperemia. VII. Renal Calculi. 

II. Renal Hemorrhage. (Embo- VIII. New Growths. (Cancer, etc.) 
lism and Infarction.) IX. Parasites. (Hydatids.) 

III. Nephritis. (Bright's Disease.) X. Perinephritic Abscess. 

IV. Pyelitis. XI. Hematuria. 
V. Hydronephrosis. XII. Chyluria. 

VI. Cystic Kidney. XIII. Cystitis. 

RENAL HYPEREMIA. 

{Congestion.) 

Renal hyperaemia may be active or passive. Passive renal hyperaemia, or 
congestion, is almost always due to a mechanical obstruction of the venous 
circulation, and is sometimes called "chronic renal congestion." 

Morbid Anatomy. — Active renal hyperemia has its seat mainly in the 

1 New York Med. Eec, Aug. 1, 1873. 



584 DISEASES OF THE KIDNEYS. 

renal arteries and in the Malpighian tufts. The kidneys are much increased 
in size ; the hyperemia may involve the cortical or medullary portion, and 
may be more intense in one portion than another ; it is usually most marked 
at the base of the pyramids. The kidneys are of an unnaturally dark color, 
their capsule is non-adherent, their surface is smooth, and they are softer 
and moister than normal. 

On section, dark spots are noticed scattered over the cut surface which 
correspond to the Malpighian tufts, and the vessels of the cones are filled 
with blood. A dark fluid follows the section, which is partly serum and 
partly blood. The stars of Verheyen are prominent. A microscopical ex- 
amination shows that these changes are due to an engorgement of the blood- 
vessels, and a more or less abundant infiltration of serum into the inter- 
tubular structure of the kidneys. 

Passive hyperemia, or "chronic renal congestion/' has its seat in the 
veins, which are overfilled with venous blood, while the amount of blood 
contained in the arteries may be even less than normal. The kidneys are 
but slightly, if at all, increased in size, are firmer than normal, their cap- 
sule is non-adherent, and their surface is smooth and of a uniform red color. 

The tubular epithelium is gran- 
ular, opaque and flattened from 
coagulated fibrin which may 
partially fill the lumen of the 
tubes. The convoluted tubules 
may be filled with blood. The 
stroma is unaltered. Hyperemia 
of, and hemorrhages into the 
mucous membrane of the pelvis 
and ureters may occur in very 
severe cases. 

Upon section, it will be noticed 
that the medullary portion is of 
a darker color than the cortical, 
that the cortical portion has 
streaks of red rather than an 
uniform redness. The Malpig- 
hian tufts are not prominent. 
The veins are dilated, tortuous, 
and varicose, the abnormal hard- 
ness of the kidney being due to 
the constant distended condi- 
tion of the efferent capillary 
vessels. The epithelium of the 
convoluted tubes may have a 
peculiar stiff appearance, not 
the result of an inflammatory 
process. Coagula of yellowish hyaline material are sometimes found in the 
glomeruli, arranged in concentric layers. 



In chronic cases the surface is uneven. 




Fig. 137. 
Eenal Hyperemia. 
Vertical section of part or" a Malpiqhian Pyramid in Pass- 
ive Hypercemia. 

A , A. Collecting tubes. 

B, B. Dilated, tortuous vessels. 

C) 0. Collecting tubules containing blood, x 300. 



EENAL HYPEKiEMIA. 585 

Both these varieties of hyperemia may lead to, or be accompanied by 
inflammatory processes in the tubular and intertubular structures of the 
kidneys. Active hyperemia may be the stepping-stone to acute parenchy- 
matous nephritis. It is only a step from congestion to some of the more 
chronic inflammatory forms of kidney disease. When to passive hypere- 
mia there is added inflammatory swelling of the epithelium of the tubules, 
the kidneys will.be enlarged, and the epithelium of the convoluted tubules 
will be swollen, granular, fatty, and disintegrated. When the inflamma- 
tion extends to the stroma the kidneys will be diminished or enlarged, but 
retain the stony hardness of non-inflammatory congestion. The capsule 
will be adherent, and on section the cortical portion will be slightly dimin- 
ished, and there will be patches of new connective-tissue throughout its sub- 
stance,— the process not being unlike the " cirrhotic " form of Bright's. 
If the passive hyperemia is due to heart disease, the kidneys will be in- 
creased in size, the capsule will be non-adherent and the surface smooth. 
The cortical substance will be -pale instead of red, and the medullary portion 
of a darker color than normal, the gross appearance very closely resembling 
that of the "large white kidney." There will be well-marked changes 
in the epithelium of the tubules, in the stroma, and in the walls of 
the arteries. These are the large stony kidneys of chronic heart dis- 
ease. Chronic passive hyperemia is sometimes called cyanotic indura- 
tion." 

Etiology. — Active renal hyperemia, or fluxion, may be produced by ex- 
posing the body to sudden changes of temperature, by any of the blood 
poisons which give rise to the acute infectious diseases, by malaria (and it 
is sometimes a prominent feature of a violent malarial paroxysm), by the 
prolonged and excessive use of certain drugs which give rise to irritation of 
the urinary passages, as cantharides, copaiba, turpentine, cubebs, nitrate of 
potash, carbolic acid, etc., and by the irritating condition of the urine in 
diabetes, cholemia, etc. It sometimes accompanies Basedow's disease. 
The early stage of acute inflammations of the kidneys is attended by active 
renal hyperemia. Paralysis of the vaso-motor nerves of the kidneys (sup- 
posed to occur in hysteria and allied states, polyuria, etc. ) is said to be a 
cause of active renal hyperemia. 

Passive renal hyperemia, or renal congestion, has its most frequent 
cause in organic disease of the heart. All valvular lesions of the heart, or 
structural diseases of the cardiac valves which interfere with venous return, 
come under this head, as well as all those forms of pulmonary disease 
which interfere with the pulmonary circulation, and are followed by dilata- 
tion of the right heart, e. g., emphysema and fibroid phthisis. Congestion 
may also be produced by pressure on the emulgent renal veins or inferior 
vena cava in pregnancy and by other abdominal tumors. The formation 
of a thrombus is also followed by it. Some of the cases of so-called albu= 
minuria in pregnancy are examples of passive hyperemia from the pressure 
of the pregnant uterus. 

Symptoms. — The symptoms of both varieties of renal hyperemia are for 
the most part confined to changes in the urine. In active hyperemia the 



586 



DISEASES OF THE KIDNEYS. 



urine is scanty, high colored, of high specific gravity, containing a large per- 
centage of albumen, with few blood casts and hyaline tube casts. 

In passive hyperemia, without any structural changes in the kidneys, the 
quantity of the urine is not much diminished, its specific gravity remains 
about normal, the amount of albumen is small, and only small hyaline 
casts are present. It is often of an acid reaction, and deposits urates. The 
amount of urea is a little below normal. The simultaneous appearance of 
blood and albumen in the urine is so common in renal congestion that the 
presence of albumen alone, without blood globules, almost excludes it. Be- 
sides the changes in the urine in active hyperemia, there is usually slight 
oedema of the face and lower extremities, with nausea and a persistent 
headache. 

Passive hyperaemia is often produced by chronic cardiac or pulmonary 
disease, attended by a cough with a watery blood-stained expectoration, and 
by dyspnoea that often becomes so severe as to prevent the patient from 
lying down. The cough and dyspnoea depend in part upon the accompany- 
ing heart or pulmonary disease, but there is also a nervous element in it 
which is characteristic of the renal complication. There is loss of appe- 
tite, nausea and occasional vomiting ; there is a continuous headache, rest- 
lessness and insomnia, which, added to the dyspnoea, make the patient's 
condition distressing. There is loss of flesh and strength, and steadily in- 
creasing anaemia. These symptoms gradually become worse, and general 
dropsy develops, and the patient may die from the general anasarca, or from 
convulsions and coma. 

The history of these cases varies greatly : some get progressively worse, 
others pass from an apparently hopeless condition to one of comparative 
comfort, and these attacks are repeated at intervals for a long period. 
However desperate the condition may appear, a return of a comparatively 
comfortable condition is always possible. That form of renal congestion 
which is so often met with in pregnancy is usually accompanied by the 
presence of albumen and casts in the urine before any other symptoms are 
developed; afterward the patients become anaemic, and suffer from per- 
sistent headache, vomiting, and oedema of the face, feet and legs ; they 
become " water-logged." In a few cases the first symptom may be a con- 
vulsion. In all cases the thing to be dreaded is the onset of convulsions, 
which rapidly follow each other until coma is reached. 

Differential Diagnosis. — Renal congestion is distinguished from Brighfs 
disease by the general condition of the patient, the presence or absence of 
cardiac or pulmonary disease, or venous obstruction. The urine, though 
scanty, is above normal in specific gravity, and always deposits blood, 
renal epithelium, or tube casts. 

Prognosis. — The prognosis in active renal hyperaemia, when the cause is of 
a transient character, is good. Renal congestion which occurs in the ad- 
vanced stage of cardiac disease and pulmonary emphysema has much to do 
with causing a fatal termination, and after it is once developed it is never 
recovered from. That form of active hyperaemia which occurs in congestive 
malarial fevers is sometimes so intense as to entirely arrest the function of 



RENAL HYPEREMIA. 



587 



the kidneys, and then ifc becomes a direct cause of death. The renal con- 
gestion of pregnancy is usually relieved by the removal of its cause, which 
should never be delayed if the symptoms become urgent. 

Treatment. — The most important thing to be accomplished in the treat- 
ment of active renal hyperemia is to find out, and as quickly as possible 
remove its cause. The treatment is to be addressed to the kidneys. Place 
the patient in bed in a room with a temperature of 80° F., and apply a dozen 
wet cups over the lumbar region. Administer a powerful drastic purge, 
induce free diaphoresis, and let the patient drink freely of diluted muci- 
laginous drinks. The hot-air or warm vapor-bath, and even blood-letting 
in intense fluxion, are to be employed. Camphor is advocated in some 
cases of active hyperemia. In passive renai hyperemia the main thing to 
be accomplished is to relieve the venous congestion ; it is to remembered 
that there is too much blood in the veins and too little in the arteries. 

There are three ways of restoring the natural state of the circula- 
tion : — 

1st. By general bleeding. 

2d. By increasing the force of the heart's action. 

3d. By causing the dilatation of the capillary arterioles. 

A free bleeding from one of the large veins will temporarily relieve the 
venous congestion and cause a better filling of the arteries, but it exhausts 
the patient, and is only admissible in the renal congestion of pregnancy 
when the symptoms are urgent. By increasing the propelling power of the 
heart, the amount of blood in the arteries is increased and that in the veins 
diminished. This is the usual mode of procedure in the passive renal 
hyperemia which depends upon chronic heart and lung disease. Digitalis 
is the drug which has been most extensively employed to accomplish this. 
It must be given in full doses and continued until the desired effect is in- 
duced. The best mode of its administration is in the infusion ; a tablespoon- 
ful of the infusion of the leaves may be given every three or four hours until 
its specific effect is produced or the quantity of urine is greatly increased. 
Recently the fluid extract of convallaria in half-drachm doses has been 
recommended as a substitute for digitalis. My experience with it has been 
very unsatisfactory ; its action is not only temporary, but far less certain 
than digitalis. 

The drugs that seem to have some power in dilating the capillaries and 
arterioles are nitrite of amyl and nitro-glycerine. The nitrite of amyl may be 
given by inhalation in doses of from three to five drops every four hours. 
The nitro-glycerine may be given ri a one per cent, alcoholic solution, one 
drop every three or four hours. Under its use albumen has disappeared 
from the urine in quite a number of instances, and remained absent so 
long as the patient continued the drug. 

If counter-irritation is employed it must be mild in character — a few dry 
cups over the lumbar region, or some mild embrocation is all that is neces- 
sary. The intestines should be occasionally unloaded by a full dose of 
calomel combined with rhubarb. When the venous obstruction is directly 
mechanical, as in pregnancy and fluid accumulation in the abdominal 



588 



DISEASES OF THE KIDNEYS. 



cavity, something may be accomplished by so changing the position of the 
patient as to relieve the pressure on the renal veins. 

If passive renal hyperemia, especially in heart disease, is attended by 
great restlessness and dyspnoea, morphine may be given hypodermically in 
sufficient quantities to give relief and make the patient comfortable, even 
though but a small quantity of urine is being passed. 



RENAL HEMORRHAGE. 



(Embolism and Infarction.) 
Eenal congestion and renal hemorrhage are very often associated, for 
renal hemorrhage often occurs as a result of renal congestion. 

Morbid Anatomy. — The anatomical changes in a kidney which is the seat 
of renal hemorrhage do not differ essentially from those already described 
as present in a renal hyperemia, unless there are hemorrhagic infarctions 
or renal calculi. Blood may be effused into the uriniferous tubules or the 
interstitial tissue, giving rise to ecchymotic spots varying in size, from 
which, on section, blood flows freely. The vessels will be found ruptured, 
and the epithelia and stroma of the kidney are stained with blood pigment. 
The epithelia soon become opaque, granular, and infiltrated with fat, and 
finally disintegrate. Incident to the great increase in the blood pressure, 
diapedesis of the red corpuscles may occur ; this is true renal hemorrhage, 
having its origin in the Malpighian tufts. The blood escapes between the 
vascular tuft and its capsule, which is slightly dis- 
tended. 1 

The most frequent form of renal hemorrhage is that 
which occurs in connection with renal embolism and in- 
farction. Its occurrence is marked by the development 
of hard uniform masses in the cortical portion of the 
kidney ; these masses are usually wedge-shaped, and 
have their sharp edges toward the hilus of the kidney 
and their base toward its surface. 2 They vary in size 
according to the size of the vessel obstructed ; they may 
be capillary, and then are of very small size. These in- 
farctions when first formed are of a dark red color, and 
are as firm as normal kidney-tissue ; very soon they be- 
gin to change in color, losing their dark red hue and 
becoming lighter, and their centres present a yellowish 
appearance ; sometimes they undergo cheesy change, 
which always commences at their centres. Around 
these infarctions a zone of redness is formed ; this zone 
is in the normal kidney-tissue, beyond the infarction. 
A congestion takes place in the vessels, due to changes 
in the uriniferous tubes adjacent to the capillaries in 
that portion of the kidney which surrounds the infarc- 
tion ; there is also a more or less rapid production of 
cells in this surrounding zone. If the infarction does 




Pig. 138. 
Renal Hemorrhage. 
Diagram showing Hem- 
orrhage from the vas- 
cular tufts of the glo- 
meruli. 

A, B. Afferent and effer- 
ent vessels ; C. Capsule; 
D. Tuft; E. Epithe- 
lium covering tuft and 
lining capsule ; F. Ori- 
gin of convoluted tubule. 

At G, the blood is seen es- 
caping from the tuft 
and entering the tubule. 



1 Cornil and Ranvier. 



8 Raver's so-called " Rheumatic Nephritis. 



REGNAL HEMORRHAGE. 



589 




not disappear by absorption, this zone-change continues until there 
is more or less cicatricial tissue developed about the infarction, which 
shrinks in consequence of the contraction of the tissue, gradually 
diminishes in size, and after a 
time disappears altogether, leav- 
ing only cicatricial tissue to mark 
its former site. The surface of the 
kidney may be depressed over an 
atrophied infarction. 

On the other hand, the produc- 
tion of cells may be so rapid and 
abundant that the entire mass 
undergoes purulent transforma- 
tion, producing abscesses which 
will occupy the seat of the infarc- 
tion. This is one of the ways in 
which abscesses are formed in the 
kidneys. In these cases there is 
always a certain degree of sup- 
puration occurring at the margin 
of the affected area. Again, these 
infarctions may undergo a still 
more rapid degeneration, increas- 
ing in size and becoming necrotic, 
so that at the autopsy a gangre- 
nous mass is found as the result of 
the necrotic change which has 
taken place in the infarction. More or less suppuration also attends it. 
Again, there may be little masses found scattered throughout the substance 
of the kidney, especially in the cortical portion, looking very much like 
ecchymotic spots, which are simply capillary thrombi : these are usually 
due to some slowing of the circulation in the capillary vessels. These 
capillary thrombi may be very numerous, and they may undergo changes 
similar to those which take place in the larger infarctions. 

At the autopsy the kidneys may be found studded with minute abscesses ; 
unquestionably these little collections of pus are nothing more than minute 
capillary infarctions or thrombi which have undergone purulent transforma- 
tion. Thus a single abscess or many abscesses of the kidney may form as 
the result of infarctions. This form of renal hemorrhage is especially liable 
to occur in passive renal hyperemia. 

Etiology. — Intense hyperemia of the kidney is a cause of renal hemor- 
rhage, especially in the first stage of acute nephritis. It may also result 
from injuries, and in connection with the development and passage of renal 
calculi. It may also occur in connection with the development of morbid 
growths in the kidney, especially cancer. Blood changes, such as occur in 
purpura, scurvy, etc., may cause it. Passive obstructive hyperaemia from 



Fig. 139. 
Renal Hemorrhage. 
Diagram illustrating Renal Infarction. 

A. Embolus in an interlobular artery. 

B. Cheesy centre of the infarct. 

C. C. Zone of redness. 



590 



DISEASES OF THE KIDNEYS. 



cardiac disease may become so intense as to give rise to it, with or without 
the occurrence of infarctions. 

Symptoms. — It is attended by no constant or distinctive subjective symp- 
toms. Our knowledge of its occurrence, during life, rests almost exclu- 
sively upon the results of an examination of the urine. Its existence can- 
not be recognized, unless the blood is effused into the uriniferous tubules 
or into the hilus of the kidney and discharged in the urine. At autopsies, 
large infarctions of the kidney are often found which, during life, have given 
no indication of their existence, because there was no extravasation of blood 
into the uriniferous tubules, and consequently no blood appeared in the urine. 

The course of a renal hemorrhage depends to a great extent upon the 
cause which produces it. When dependent upon the presence of a renal 
calculus, the hemorrhage occurs after every violent exertion. When it 
arises from cancer or other tumors, it is generally profuse and persistent. 
The bleeding which accompanies inflammation of the kidneys in the infec- 
tious diseases is never severe ; it may be so slight as only to be recognized 
by a microscopical examination of the urine. That form of renal hemor- 
rhage which occurs in malarial districts in hot climates is usually profuse . 
and occurs periodically. When it is caused by an infarction, the patient is 
usually seized with a chill at the time the infarction occurs, followed by 
pain in the back, and more or less nausea and vomiting. If, therefore, 
these symptoms are developed in connection with cardiac disease or pyae- 
mia, it is evidence that renal infarctions have occurred. 

When valvular disease of the heart exists with ulcerative endocarditis or 
extensive calcareous degeneration of the arteries, embolic infarction may be 
suspected, when in addition to the sudden appearance of blood and albu- 
men in the urine there is fever and vague pains in the lumbar regions. 
Small abscesses, the sequelae of infarcts and circumscribed spots of gangrene, 
cannot be diagnosticated. 

Prognosis. — The prognosis depends upon the conditions and circum- 
stances under which the hemorrhage occurs. If it occurs in connection 
with renal calculi or cancerous disease of the kidney, the prognosis is bad ; 
life is endangered under these circumstances by the exhaustion produced 
by the continued loss of blood. Occurring in connection with infectious dis- 
eases, it has no particular significance ; it merely is an indication of intense 
renal hyperaemia. When there is reason to believe that a hemorrhagic infarc- 
tion has occurred in the kidney, the event must always be regarded as at- 
tended with danger to life ; not that it is necessarily fatal, or that the prog- 
nosis is necessarily unfavorable, but the fact that infarctions exist will cause 
anxiety as to the development of the other degenerative changes in the kid- 
neys, and as to the lodging of emboli in other parts, particularly the brain. 

Treatment. — The first thing to be accomplished in its treatment is to find 
out and, if possible, remove its cause. In many cases where the main causa- 
tive disease is amenable to treatment, the hemorrhage does not require any 
special attention. During the occurrence of the hemorrhage, the patient 
should be kept absolutely at rest. If there is danger of exhaustion from 
repeated and profuse hemorrhages, ice-bags may be applied to the lumbar 
region, and styptics administered internally. 



NEPHRITIS. 



591 



The remedial agent which seems to have the greatest control over these 
hemorrhages is tannic acid, it being expelled from the system through the 
kidneys in the form of gallic acid ; a powerful astringent is thus brought 
directly in contact with the uriniferous tubes and urinary passages. Ergot, 
muriate of iron, alum, the acetate of lead, and turpentine are sometimes of 
service. Ergotin given hypodermically in connection with morphia is in- 
dicated if hemorrhages are profuse. If the hemorrhage is of malarial ori- 
gin, large doses of quinine and arsenic are indicated. The danger from 
acute renal inflammation must always be borne in mind when renal hem- 
orrhage occurs in connection with the infectious diseases ; the proper meas- 
ures for the subduing or arresting of such inflammations must be promptly 
resorted to. 

NEPHRITIS. 

{Bright' s Diseases.) 

A great variety of inflammatory changes in the kidney have been gen- 
erally classed under the comprehensive name of Bright's Diseases. Dr. 
Bright first called the attention of the profession to this class of diseases 
in the year 1827, at which time he described, and represented by colored 
drawings, various morbid appearances of the kidneys, which he showed 
were of every-day occurrence and were frequently associated with general 
dropsy. Dr. Bright regarded granular degenerations as the principal, if 
not the only pathological lesion present in this class of diseases ; he accord- 
ingly designated it as a granular nephritis. 

Eecent and more extended investigations have shown that there are 
several morbid processes in the kidneys of those who are the subjects of 
this class of diseases, and that the kidneys in the course of these morbid 
processes present a great variety of appearances. 

A great number of terms claiming to be expressive of these different 
morbid appearances have been employed, such as the large white kidney, 
the large granular kidney, the small fatty granular kidney, the large and 
small red granular kidney, the waxy kidney, and the cirrhotic kidney. 

In studying the morbid changes which occur in this group of diseases 
it is important to remember that there are three distinct anatomical 
elements in the kidney which are primarily or secondarily involved in 
these changes ; namely, the uriniferous tubules, the blood-vessels, and the 
intertubular tissue (or stroma). 

I shall describe nephritis under the following heads : 
I. Acute Nephritis ; which may be — 

(a) Parenchymatous ; also designated glomerular, catarrhal, croup- 

ous, desquamative, etc. 

(b) Interstitial ; also designated diffuse interstitial nephritis, and 

surgical kidney. 
II. Chronic Nephritis ; which may be — 

(a) Parenchymatous ; known as large white kidney, large and small 

granulo-fatty kidney. 

(b) Interstitial ; known as cirrhotic, gin-drinker's, or hobnail kidney. 

(c) Amyloid ; known as waxy or lardaceous kidney. 



592 



DISEASES OF THE KIDNEYS, 



ACUTE NEPHRITIS. 
(Acute Bright' s Disease.) 

Acute nephritis may be wholly recovered from, prove fatal, or lead to 
chronic nephritis. 

Morbid Anatomy. — The gross and microscopical appearances of the 
kidneys in acute nephritis will vary according to the intensity and 
character of the processes which attend its development. The kidneys 
are usually increased in size, their capsule non-adherent, their surface 
smooth and mottled, presenting an irregular combination of red vascular 
engorgement and unnatural pallor ; sometimes they are of a dark purplish 
color, dotted here and there with spots of ecchymosis. The stars of 
Verheyen are more or less prominent, and the kidneys are softer than 
normal. 

On section, the cortical portion is relatively increased in thickness, and 
is dotted over its entire cut surface with dark or bright red points, which 
correspond to the situation of the Malpighian tufts, which in some instan- 
ces stand out prominently upon its cut surface. The cortical substance 
between the MaljDighian tufts may be of a paler color than natural. Some 
distinguish between a "red" and a "pale" kidney in acute nephritis. The 
engorgement will usually be most marked at the base of the pyramids, at 
the junction of the cortical and medullary substance — in the arterial arcade. 
The medullary portion will be of a darker color than normal, darker even 
than the cortical portion ; sometimes it will present a striated appearance 
(red and white lines alternating), the lighter lines corresponding to the 
changed uriniferous tubes, the red lines to the congested intertubular 
vessels. 

The lining membrane of the pelvis of the kidney is usually congested. 
The inflammation of the mucous membrane of the pelvis and calices is 
attended by exudation of a turbid fluid containing cells. 

When such a kidney is examined microscopically, it may be found to 
present quite a variety of appearances. First, The epithelium of the con- 
voluted tubes and of the Malpighian tufts may become swollen, increasedly 
granular, and their nuclei more or less obscured ; as a result, the lumen of 
the tubes becomes obliterated and filled with swollen cells — the changes 
corresponding to those which occur in catarrhal inflammations of the 
mucous surfaces. The cells of the convoluted tubes of the cortex will 
have undergone cloudy swelling. These changes are common in the acute 
nephritis of fevers. There will be no cell infiltration around the tubules in 
the intertubular tissue. 3 Some cases are very mild. Even though albumen 



1 Cell accumulations about the glomeruli and tubuli contorti are said by Traube to be primary, and the 
epithelial changes to be secondary. 



ACUTE NEPHRITIS. 



593 




and casts were found during life, no marked structural changes are 
found in the kidney. In all probability, in these cases, changes have 
taken place in the capillaries of 
the Malpighian tuft which allow 
of the escape of albuminous ma- 
terial from the blood. 

In another class of cases the epi- 
thelial cells, especially of the con- 
voluted tubes, become filled with 
albuminous and fatty granules, 
desquamation follows, and the 
tubes become filled with broken- 
down epithelium and fatty mat- 
ter. Colloid material is often seen 
in the tubes. The epithelia, in a 
few cases, undergo simple atrophy. 
In some cases of acute nephritis 
all these processes may be pres- 
ent at the same time in the same 
kidney. The centre of the urin- 




Fig. 140. 
Acute Nephritis. 



iferOUS tubes will often Contain Se °ti m °f the cortex of a Kidney showing " cloudy swell- 

A . Part of a capsule of a Malpighian body. 
i?, B. Convoluted lubes shotting the cloudy, swollen epithe- 
lium. The nuclei are obscured. 
C. Ascending limb of HenWs loop. 
D. Slight round-cell infiltration in interlobular tissue. 
x 350. 



a hyaline material which resem- 
bles coagulated fibrin ; this hya- 
line material may have mingled 
with it, or may be surrounded by 
disintegrated epithelium and blood globules ; it resembles fibrinous in- 
flammatory exudation. In addition to these tubular changes, more or 
less cell development takes place in the intertubular structure, especially 
around the Malpighian tufts and the small veins. 

Again, in another class of cases, a 
typical example of which is furnished by 
the kidney of scarlet fever, the changes 
seem to be confined principally to the 
glomeruli. The epithelia covering the 
capillary tuft, and those lining the cap- 
sule of Bowman, proliferate, and the 
capsular space becomes filled with des- 
quamated epithelium, often to such an 
extent that the capillary vessels of the 
tuft are compressed, and the circulation 
through them impeded. In the vessels 
of the Malpighian body, and in the 
capillaries between the tubes, are found 
an abnormal number of white corpuscles 
and some detached endothelial cells. 
The epithelia of the convoluted tubes 
are often swollen and filled with fat 




Fig. 141. 

Glomerulo-nephritis, case scarlet- fever. 

a, Compressed vascular tuft. 
5, Increased glomerular nuclei, 
c, Proliferated lining cells of glomerulus filling 
lar 



594 



DISEASES OF THE KIDNEYS. 



granules. Some make this a distinct form of Bright's disease and call it 
glomerulo-nephritis. Minor changes in and about the glomeruli are found 
in the majority of kidneys of acute nephritis. In most cases these pro- 
cesses quickly terminate either in recovery or death ; in a few they become 
chronic. When blood extravasations are abundant, the name "hemorrhagic 
nephritis" has been given to it. 

Etiology. — Its most common cause in the adult is exposure of the surface 
to sudden changes of temperature, as is indicated by the class of subjects 
in which it is most liable to occur — bakers, firemen, moulders, and those 
whose occupation subjects them to sudden, repeated changes of temper- 
ature. Again, it occurs among those who are addicted to the use of alco- 
hol ; they may not be habitual drinkers or greatly intemperate, but they 
occasionally "go on a spree," and while in a state of intoxication expose 
their surface to sudden changes of temperature or to prolonged cold after 
violent exercise. Under these circumstances it is not the alcohol that 
develops the tubular inflammation, but the sudden changes of temperature 
to which these persons subject themselves in consequence of such indul- 
gence. The daily use of alcohol may be indulged in for years without leading 
to acute nephritis, provided the individual exercises care in regard to expos- 
ure, and therefore it should not be included in the list of its direct causes. 

Occasionally it happens that a very 
trifling exposure to sudden changes 
in temperature is sufficient to develop 
it, such as sitting in a draught of air 
and exposing the lightly covered 
loins to a current of cold air while 
the individual is in a heated condi- 
tion. In this climate the failure to 
wear flannel next the body through- 
out the year involves the risk of 
developing at some time an inflam- 
matory process in the uriniferous tu- 
bules. It is not clear how such ex- 
posure excites tubular inflammation. 
Euneberg states that congestion (e.g., 
passive hyperemia) and the conse- 
quent slowed circulation and dimin- 
ished pressure in the glomeruli, is 




a 

Fig. 142. 

Acute Nephritis. 

Section of the cortical portion of a Kidney, show- 
ing advanced degenerative changes in the 
parenchyma. 

A, A. Convoluted tubules f iled with broken-down 
epithelium and granulofatty matter. 

B. Swollen epithelium of one of HenWs tubes. 

C. A collecting tubule. Epithelium nearly nor- 

mal, x 350. 



the cause of the albuminuria or tubu- 
lar inflammation. The theory that 
the nephritic inflammation is due to the reflex influence of the nervous 
system — there being a connection between the sympathetic nervous system 
and the surface of the body — rests on the same basis which is employed to 
explain the occurrence of pneumonia and bronchitis after exposure to 
cold. 

Another very common cause of acute nephritis is the circulation of 
morbid elements in the blood ; such elements are very numerous, em- 



ACUTE NEPHRITIS. 



595 



bracing all those poisons which give rise to specific forms of infectious dis- 
eases. The infection of scarlet fever is one of its most frequent causes, 
especially in childhood. Every epidemic, however, is not attended by 
renal complications, for there are some seasons when a type of scarlatina 
prevails, in which scarcely a case will have renal complications ; while dur- 
ing other seasons almost every case will be attended by them. Such vari- 
ations can only be accounted for by regarding the occurrence of nephritic 
complications as dependent upon a difference in the scarlatinal infection. 

Another class of causes is included under the head of renal irritants 
which may be introduced into the stomach : among these are the balsam 
of copaiba, spirits of turpentine, cantharides, phosphorus, arsenic, and 
lead. The prolonged use of these remedies, or their administration in over- 
doses, not infrequently gives rise to tubular nephritis. Another cause is 
acute internal inflammations, especially inflammation of the lungs : one 
should always be on the watch for its occurrence during a pneumonia. 

Another frequent cause is pregnancy. It was formerly supposed that 
pregnancy produced Bright's disease by interference with the renal circu- 
lation from pressure on the renal veins ; but probably this is rarely its 
cause. During pregnancy there is an abnormal quantity of excrementi- 
tious material to be carried out of the system by the kidneys, which not 
only calls upon these organs for increased labor, but the material elimi- 
nated acts as an irritant on the uriniferous tubes, and tubular inflammation 
is the result. It may occur at any period of pregnancy, but it is rare be- 
fore the third month, and is of more frequent occurrence during the later 
months. In connection with pregnancy, this form of kidney disease rarely 
terminates in chronic nephritis. It often disappears rapidly and never 
recurs, or it may appear in successive pregnancies, and finally lead to the 
development of chronic Bright's disease. Again, passive renal hyperemia 
dependent upon obstruction to the return circulation from cardiac or pul- 
monary lesions may cause acute Bright's disease. 

There is a degeneration of the epithelium of the uriniferous tubes which 
occurs under certain circumstances independent of inflammation. It is 
not amyloid ; it is not, strictly speaking, a fatty change ; but it occurs 
during the degenerative processes of old age, and is a result of senile 
change. In this sense, extreme old age may be regarded as a cause of 
tubular epithelial degeneration in the kidneys. 

Symptoms. — The presence of urea and its allies, kreatin, kreatinin, etc., 
in the blood, in abnormal quantities, gives rise to the phenomena which 
attend the development of acute nephritis. The symptom which usu- 
ally first attracts the attention of a patient is oedema of the face. There 
may have been signs of gastric disturbance prior to its occurrence, but they 
nave not been distinctive in character. After exposure to sudden varia- 
tions in temperature, or after an attack of some form of acute infec- 
tious disease, or without any known cause, there is noticed a slight pufli- 
ness about the eyes in the morning ; if the patient is anaemic, the oedema 
may appear in the feet and ankles at the same time This oedema usually 



596 



DISEASES OF THE KIDNEYS. 



increases very rapidly. With the occurrence of the oedema there is great 
restlessness. Toward evening there is a little quickening of the pulse and 
a slight rise in temperature — never typical ; the patient complains of head- 
ache, which increases in severity from hour to hour ; at times he is very 
drowsy. Complete, sudden, but temporary blindness may occur at its very 
onset, the ophthalmoscope showing no morbid appearances. 

If the patient is closely questioned, he will state that die has recently 
noticed some change in his urine, that it has been scanty and high colored, 
and he has had a frequent desire to pass it. Perhaps he has had some pain 
in the back and loins ; he may complain of nausea and perhaps of vomit- 
ing ; the latter is sometimes so troublesome that the physician may direct 
his attention to the stomach as the seat of the disease, and treat the pa- 
tient for some form of gastric lesion. There is more or less acceleration 
of the pulse, which is irritable in character. The skin is usually unnatu- 
rally dry ; occasionally it is moist, but when it is so the perspiration has a 
peculiar urinous odor. These, in brief, are the symptoms which attend 
the development of a mild form of acute Bright's disease. 

In a favorable case, after the patient has reached the condition described, 
he begins to improve ; the urine is increased in quantity, the oedema grad- 
ually disappears, the headache moderates, the gastric disturbances disap- 
pear, and in the course of two or three weeks he has entirely recovered. 

In a certain proportion of cases, instead of improving, the patient steadily 
grows worse ; the oedema steadily increases until the cellular tissues of the 
entire body become oedematous. As a result of the pulmonary oedema there 
is dyspnoea. Dyspnoea in this connection is not always dependent upon an 
oedematous condition of the lung, for urgemic dyspnoea may occur inde- 
pendent of any change in the lung-tissue. When there is general ana- 
sarca the dyspnoea is usually due to pulmonary oedema ; it may be accom- 
panied by more or less pulmonary congestion, giving rise to a watery expec- 
toration, which may be streaked with blood. If the disease progresses, the 
anasarca will gradually increase until the patient becomes " water-logged." 
With the general anasarca the surface of the body assumes a peculiar, pale, 
waxy appearance ; there is oedema of the scrotum and penis, or labia, and 
more or less effusion into the peritoneal, pleural, and pericardiac cavities. 
Hydrothorax may so impede respiration as to cause death. 

As the uraemia becomes more profound, a series of nervous phenomena 
are developed : the patient becomes exceedingly restless, muscular twitch- 
ings occur, and these may soon be followed by convulsions, coma, and 
death. If this class of patients do not die from the direct toxic effect of 
the urea, they may have complications, such as meningitis, pericarditis, en- 
docarditis, pneumonia, etc., which may rapidly lead to a fatal issue. This 
is the most unfavorable of all the types of acute parenchymatous nephritis. 
Such cases sometimes follow scarlet fever. The same type of cases is also 
met with in connection with other infectious diseases. 

There is still another type of acute nephritis which is occasionally met 
with, called by some acute diffuse nephritis. It is ushered in by violent 
symptoms : the patient is seized with a chill, intense pain in the back and 



ACUTE NEPHRITIS. 



597 



along the ureter, with retraction of both testicles ; there is delirium, great 
nervous disturbance, urgent cerebral symptoms, and the patient may pass 
quickly into a state of coma and die within two or three days. The chill 
in these cases is followed by high temperature ranging from 104° F. to 
106 F. ; there is often almost complete suppression of urine, perhaps not 
more than two ounces being secreted in twenty-four hours. The delirium 
which is present so closely resembles that of meningitis that it is often 
difficult to differentiate between the two conditions. In these cases there 
is intense, active renal hyperemia, and the tubules are extensively filled 
with an inflammatory exudation. Very soon after the accession of the 
ushering-in symptoms, oedema of the face will be developed, and soon 
after its occurrence the patient will pass into a state of coma, which is 
usually followed by death. If these patients recover from the acute stage, 
the kidneys will be permanently damaged. 

Connected with the history of acute nephritis, there are symptoms which 
are of special importance, and which I shall consider more in detail ; these 
are the changes in the urine, the dropsy, and the nervous phenomena. 
These are present to a greater or less degree in all cases, and their exist- 
ence is necessary for its diagnosis. 

The urine in all varieties is diminished in quantity, high colored, and 
sometimes smoky in appearance ; it is of high specific gravity, perhaps as 
high as 1.030. A sediment, in which there are red and white blood-corpus- 
cles, forms soon after the urine is voided. The amount of urea eliminated 
in the twenty-four hours is diminished to one-half or one-quarter the nor- 
mal amount. When tested for albumen, from one-third to one-half of the 
entire bulk of the urine will coagulate. In testing for albumen it is well 
to employ both heat and nitric acid. Albuminous urine is usually coagu- 
lated by heat below the boiling point, and by nitric acid. If both of these 
tests are carefully used, one will rarely be led into error ; but mistakes are 
often made when only one of these agents is employed, for the reason that 
heat alone will not coagulate albumen in urine which is neutral or alkaline ; 
in such cases the addition of nitric acid coagulates and precipitates the al- 
bumen. In true albuminuria, where serum-albumen appears in the urine, 
there is some kidney change. In false albuminuria, where albumen, not 
serum -album en, appears in the urine, the kidneys maybe healthy. 1 Re- 
cently, opinions have changed in regard to albuminuria. 2 If a portion of 
the urinary sediment be microscopically examined, casts will be found which 

1 See text books on "Urinary Analysis'' for modes of determining the different albumens ; also Appen- 
dix to Foster's "Physiology." 

2 Albuminuria itself is, according to Gull's statements, as common in young men and boys as spermator- 
rhoea ; Moxon confirms this. Young girls from fourteen to seventeen have it. Depressing mental emo- 
tions cause a lowered pressure in the vessels, and this, according to Runeberg's ingenious theory, is the 
one cause of albuminuria. Leube and Furbruger incline to the opinion of an individual permeability of 
membrane. Temporary nervous innervation may in some instances induce transient albuminuria, with or 
without healthy kidneys. Drs. Brunton and Power (St. Barthol. Hosp. Rep., 1877) take issue with Bartel's 
statement that albuminuria is always of renal origin. There are different albumens, some derived from 
the blood, others from the digestive organs. Diminution and increase of blood-pressure in the glom. 
eruli have both been advanced as prime causes of the albuminuria. Probably blood-pressure plays but an 
unimportant part. Cohnheim regards changes in the epithelium covering the glomeruli as an important 
factor. These changes are, no doubt, in part produced by the stagnant inflammatory current. The vessels 
of the glomeruli unquestionably allow most of the albumen (in acute albuminuria) to exude. 



598 



DISEASES OF THE KIDKEYS. 



correspond to the contents of the uriniferous tubes already described ; these 
casts consequently vary in appearance and composition. Those which are 
most characteristic are the epithelial casts, which may contain blood -glob- 
ules ; in yery active forms of the disease, the casts may be entirely composed 
of coagulated blood, called blood casts ; casts of this form and composition 
are found in no other form of nephritis, unless it is complicated by acute 
tubular inflammation. In addition to epithelial and blood casts, small and 
large hyaline casts may be found. The small hyaline casts are formed in tubes 
the epithelium of which has not been removed. In addition to the casts, free 
epithelial cells and blood-globules may be seen. Hyaline and epithelial 
casts are sometimes found independent of Bright's disease, and saccharine 
urine may "be loaded with them. 1 Distinctly formed cell elements in a cast 
point to an origin in the straight or collecting tubes. 

Dropsy occurs early ; there have been several theories advanced as to its 
cause, but none are perfectly satisfactory. One theory is, that it is due to 
the sudden removal from the body of a large amount of albumen ; whereas 
in the most rapidly developed dropsies no albumen is carried out of the 
body, for the reason that the patient passes little or no urine. 2 Another 
cause assigned for the dropsy is, that the kidneys fail to eliminate the 
watery portion of the blood in the form of urine, and that the dropsy occurs 
as the result of the retention of the watery elements ; yet very extensive 
dropsies occur while the patient is passing more than the normal quantity 
of urine. 3 Again, it is said that dropsy occurs in consequence of the 
anaemic condition of the patient. The anaemic condition undoubtedly con- 
tributes to the ease with which the transudation of fluid through the walls 
of the vessels takes place ; but a patient may be exceedingly anaemic and 
yet no dropsy be present, and dropsy very often occurs before the patient 
shows any evidence that he is in an anaemic condition. 

I regard dropsy as a necessary symptom of acute nephritis, but the exact 
cause of its occurrence in many cases cannot be satisfactorily determined. 

Nervous symptoms are of great importance and prominence. Undoubt- 
edly these are due to the presence of some irritating poison in the circula- 
tion, which acts directly upon the nerve centres. 4 Usually the nervous 
symptoms first manifest themselves by headache ; therefore headache is a 
symptom which must not be lightly regarded, for it is often the precursor 
of more dangerous symptoms. If persistent and severe, and permitted to 
pass unrelieved, it may be followed by convulsions. The larger proportion 



1 Sou they regards it as an error to suppose that the larger casts are derived from the larger tortuous 
tubes. Nothing but cellular elements can pass through Henle's loops (diameter 1-1200 to 1-1000 in.); " when," 
he says, " a cast is assumed to come from the profounder renal tissue and to be of grave significance, an 
error is committed, based on ignorance of anatomy. 11 Hyaline casts probably form in Henle's loops. 

2 Cohnheim, in his work on pathology, regards inflammatory changes in the walls of the cutaneous and 
subcutaneous vessels— whose causes are the same as those of acute Bright's— to be the reason of anasarca 
in many instances,— the vessels being rendered more permeable. 

3 Cohnheim (Virchoiv's ArcJiiv. 1877, 96, p. 106), after most elaborate experimentation, regards oedema as 
the result, net of dilution of the blood or of increase in the relative amount of water, but of hydrcemid 
plethora, i. e., increase in the absolute amount of water. This fact, with changes in the walls of the ves- 
sels, is accepted by most authorities as the most plausible and probable cause of oedema in acute 
Bright's. 

4 The different theories in regard to the causation I have considered under the head of acute urcemia. 



ACUTE NEPHRITIS. 



599 



of cases of acute nephritis will suffer from more or less severe headache, 
without any subsequent convulsions ; but the fact that convulsions do fol- 
low it is sufficient to cause one to watch for the indications of their occur- 
rence. If the poisoning goes on gradually, the patient will first become 
drowsy, the drowsiness passing into stupor, and frequently into coma. A 
large number of patients with acute nephritis unquestionably die from the 
direct effect of urea and its allies upon the nervous centres ; but a still 
larger number die from complications. 

Differential Diagnosis. — If a patient has headache, some fever, more or 
less oedema, nausea, and perhaps vomiting, with scanty, high-colored 
urine of high specific gravity, containing epithelial, small hyaline, or blood 
casts, it is certain that acute renal disease exists. There may be other 
pathological conditions existing in the kidneys at the same time, but this 
train of phenomena gives unmistakable evidence that some of the urinifer- 
ous tubes are the seat of acute inflammation ; the acute may be engrafted 
upon the chronic. In every case which presents this train of symptoms, 
frequent examinations of the urine should be made. The general symp- 
toms and the changes in the urine in acute nephritis are so obvious that it 
can scarcely be overlooked or mistaken for any other disease. The only 
circumstances under which it is possible for this affection to pass unrecog- 
nized are those in which dropsy is not a prominent symptom, and when 
a careful examination of the urine has not been made. 

It is not always easy to determine whether acute nephritis is primary or 
secondary — that is, whether it has occurred in kidneys that were healthy 
previous to its occurrence, or in those that were already the seat of chronic 
disease. The previous history of the patient, and the presence or absence 
of cardiac hypertrophy, are the only means to guide one under such cir- 
cumstances. 

The points of differential diagnosis between congestion of the kidneys 
and acute Bright's disease have already been given. 

Acute nephritis is distinguished from paroxysmal hcematuria and albu- 
minuria by the abrupt commencement and brief duration of these affec- 
tions, by the marked nervous and gastric symptoms, the slight jaundice, 
and the absence of dropsy. Granular pigment in hematuria, and a very 
great quantity of albumen and tube casts in paroxysmal albuminuria, are 
characteristic urinary symptoms. Haematuria with a tendency to suppres- 
sion has few tube casts. 

Prognosis. — The tendency of acute nephritis is to recovery, but the chances 
of recovery are much better in the young than in those past middle life/ 
In those cases which terminate in recovery the characteristic symptoms of 
the disease disappear within two or three months from the commencement 
of the attack. So long as albumen continues in the urine, however small 
in quantity, recovery cannot be regarded as complete. The indications of 
a fatal termination are very scanty urine, frequent and distressing vomit- 
ing, extensive anasarca, severe and persistent headache, convulsions, coma, 
typhoid symptoms, and the occurrence of complications. 



600 



DISEASES OF THE KIDNEYS. 



The pulmonary complications which render the prognosis unfavorable 
are oedema, pneumonia, and capillary bronchitis. The great danger in 
pneumonia which complicates acute Bright's disease is the sudden develop- 
ment of pulmonary oedema in portions of the lung not involved by the 
pneumonia. Another dangerous complication is inflammation of the se- 
rous surfaces, especially endocarditis and pericarditis. Acute meningitis 
is a rare but always a fatal complication. There may be complete loss of 
sight ; this form of amaurosis is usually temporary, and is unattended by 
any change in the retina recognizable by the ophthalmoscope ; it is proba- 
bly due to the direct effect of the urea upon the retina. Subacute gastri- 
tis, functional hepatic derangement, and oedema glottidis are also compli- 
cating conditions which render the prognosis unfavorable. 

In a small portion of cases patients pass rapidly from acute into chronic 
nephritis. The passage from acute into chronic is indicated by a copious 
secretion of paler urine containing few casts. The individual may be able 
to resume his ordinary avocations, but the oedema of the feet and ankles 
does not entirely disappear, and the urine remains albuminous. 

Treatment. — Formerly, general and local blood-letting was practised in 
the treatment of all acnte renal diseases. At the present time general 
blood-letting is never resorted to, unless in the very acute form which is 
attended by violent cerebral symptoms. 

This was followed by the diaphoretic and cathartic plan of treatment in 
which it was proposed to supplant the function of the kidney by increasing 
the functions of the skin and bowels, and thus afford the kidney com- 
parative rest. Under this plan of treatment the patient is given two or 
three hot-air baths each clay, and hydragogue cathartics to produce three 
or four watery discharges from the bowels in twenty-four hours. Such 
treatment will decrease the dropsy, and for a time this class of patients will 
appear very much relieved ; but after a few active purgations, and a few 
hot-air baths, they will begin to complain of extreme weakness, and very 
soon reach a point at which the combined action of these agents fails 
even to relieve the distressing symptoms, and their condition is then worse 
than before their administration was commenced. 

Several years ago I became convinced that this depurative plan of treat- 
ment was wrong, because it rapidly depleted patients who could not bear 
depletion. Exhaustion can as certainly be produced by diaphoresis and 
hydragogue cathartics as by repeated general bleedings. Besides, the 
repeated use of hydragogue cathartics interferes with the processes of 
digestion and assimilation. 

In the treatment of acute nephritis, there are three important things 
to be accomplished. First : the elimination of urea and its allies. Sec- 
ond : the removal, as rapidly as possible, of the inflammatory products 
which obstruct the uriniferous tubules. Third : to counteract the effect 
of urea and waste products upon the nervous system. Although no organ 
can assume the renal function, and any attempt to secure such vicarious 
action of the skin and bowels as will fully relieve the kidney, has been 



ACUTE NEPHRITIS. 



601 



proven dangerous to the patient, nevertheless, something may be done 
to render the solid elements of the urinary secretion less irritating to the 
organ. The hepatic function is most closely connected with that of the 
kidney, and stimulation of the liver will be found to afford most decided 
relief to the kidneys. For this purpose some preparation of mercury is 
to be preferred. It should not be given in such doses as to induce pro- 
fuse catharsis, but in small amounts frequently repeated, and sufficient to 
maintain a free action of the bowels. While I do not accept the extreme 
views of those who believa uraemia to be an intestinal absorptive disease, 
I am convinced that cliolagogue cathartics used in moderation are of de- 
cided value in renal disease, but such catharsis must be carefully dis- 
tinguished, both as to its objects and results, from the use of hydra- 
gogae cathartics, which are intended simply to reduce dropsy and remove 
such poisonous elements as may be held in solution by the dropsical 
fluids. 

Mercury thus employed is also a direct stimulant to the parenchymatous 
action of the kidney necessary for the removal of the urinary poisons, and 
at the same time becomes a factor in accomplishing the second indication, 
the removal of the inflammatory products in the uriniferous tubes. These 
products not only interfere with the elimination of the urinary solids, but 
if they remain in the tubes they induce degenerative processes. 

In connection with the increase of parenchymatous function, an aug- 
mentation of the watery elements in the renal secretion tends to accom- 
plish the desired result. Digitalis is the most valuable drug for this pur- 
pose. Its action must be watched, however, and if the amount of urine 
is not increased its use is to be discontinued. In most cases it increases 
the urinary secretion without stimulating the kidneys ; it overcomes the 
obstruction in the renal circulation, and thus causes an increased flow of 
the watery portion of the urine through the Malpighian tufts into the 
upper portion of the uriniferous tubules. Thus the obstruction in the tubes 
is washed out, and at the same time the eliminative function of the kid- 
neys is increased, so that the urea is carried out of the system much 
more rapidly and completely than it can be by the skin or bowels. If 
diluent drinks are given, water is the lest. Spirits of nitrous ether, acetate 
of potash, tincture of the perchloride of iron, or squills, may often be 
advantageously combined with digitalis. 

In connection with the administration of digitalis I would recommend 
the application of dry cups over the region of the kidneys. In order that 
the dry cupping may be more effective, each cup should be removed as 
soon as the vessels beneath are well filled. The object is to draw the blood 
from the arteries into the capillaries, but not with sufficient force to cause 
extravasation. After dry cupping, warm poultices over the kidneys may 
be applied with benefit ; digitalis leaves may be used for a poultice, and 
thus applied thev will increase the diuretic effect of the drug administered 
internally. After the free administration of digitalis and the application 
of dry cups, if the uraemic symptoms are still urgent, hot-air baths and 



602 



DISEASES OF THE KIDNEYS. 



hydragogue cathartics may temporarily be resorted to, to aid in carrying 
the patient over the period of greatest danger ; but their use should not 
be continued after free diuresis is established. 

The next object to be accomplished is to relieve the nervous symptoms : 
the means to be employed to accomplish this are the same as in the treat- 
ment of acute uraemia. For the successful management of acute Bright's 
disease, whatever may have been its exciting cause, the patient must be 
kept in bed, in a large, well-ventilated apartment with a temperature of 
75° F. Milk should be the only article of diet. Skimmed milk is advo- 
cated highly ; besides being nourishing, it is a good diuretic. If this plan 
is systematically carried out from the very commencement, the urine soon 
becomes copious, the albumen gradually diminishes, and the dropsy passes 
away. As soon as the flow of urine commences, the administration of 
digitalis must be discontinued, and diluent drinks are to be given. If the 
renal secretion be not re-established in twenty-four hours, hot-air baths, 
hydragogue cathartics, or pilocarpin hypodermically in one-eighth or one- 
tenth grain doses, are to be used. 

The usual method of producing profuse diaphoresis is to place the patient 
in bed and cover him with flannel blankets, and then by means of the hot- 
air apparatus introduce a constant current of hot air beneath the bed- 
clothes, until profuse perspiration is induced and the excretory power of 
the skin is taxed to its utmost. The bath should be continued from half 
an hour to an hour ; then the patient should be allowed to gradually be- 
come cool, and, when so, to resume his clothing and walk about the room 
or ward, the temperature of which should be above 70° F. These baths 
may be repeated once or twice each day, or every other day, as the condi- 
tion of the patient may demand. The effect usually produced by these 
baths is a rapid subsidence of the oedema. It may not require more than 
half a dozen baths to entirely remove the dropsy from a " water-logged " 
patient, and, as far as that one symptom is concerned, to give complete 
relief ; but the relief is only temporary. 



ACUTE SUPPURATIVE INTERSTITIAL NEPHRITIS. 

{Surgical Kidney.) 

Morbid Anatomy. — The kidney is intensely hyperaemic, softer than nor- 
mal, and the fat about it is oedematous. When the thickened and opaque 
capsule is stripped off, pus often flows from beneath it. The surface shows 
arborescent injection. 

On section several purulent foci are seen in the cortex and pyramids, 
about the size of a pea ; these, coalescing, may form a large abscess. 
When pyaemia is its cause, the abscesses are wedge-shaped, and colonies 
of bacteria are found surrounding the shreddy necrotic tissue, and in the 
centre of the suppurating mass the epithelium is cloudy and desquamated. 



ACUTE SUPPURATIVE INTERSTITIAL NEPHRITIS. 



603 



Cell-infiltration takes place in the adjacent connective-tissue, and second- 
ary thrombi are found in the small veins. Micrococci are found in the 
arterioles. 1 When the abscesses are wedge-shaped they are called "meta- 
static; but when circular they are merely spots of "suppuration in foci." 

In chronic suppurative nephritis, decomposing pus, calcareous salts, and 
a serous, fntid fluid are contained in a sac whose wall is connective-tissue. 
With these (so-called) chronic abscesses, cysts and renal atrophy are 
present. In large pyaemic or non-pyaemic abscess, ulceration may take 
place at the tips of the pyramids, and the abscess may open into the pel- 
vis, the intestine, externally, or into the peritoneum. The liver has been 
involved from the breaking of a renal abscess into its softened parenchyma. 
(Rayer. ) 

Diffuse purulent infiltration 2 is of rare occurrence ; then the whole kid- 
ney seems to be a mass of pus ; the surface and cut section are homogene- 
ous-looking. Pus is readily scraped off, and ecchymoses are seen studding 
its surface. 3 

Etiology. — Any of the causes of pyelitis may be, secondarily, causes of 
surgical kidney. Pyaemia, ulcerative endocarditis, typhoid fever, and 
puerperal fever may be complicated by it. Wounds, blows, and severe 
contusions cause it. Reflex irritation and some as yet unknown nervous 
conditions are supposed by many to be the cause. Certain spinal diseases 
are attended by it, perhaps from disturbance of " trophic influences/' 

Symptoms. — There is lumbar pain, tenderness on pressure over the kid- 
ney, recurring chills, fever, languor, anorexia, emaciation, perhaps diar- 
rhoea, nausea, and vomiting ; the mouth and skin become clammy, sordes 
may collect on the teeth, the breath becomes offensive, and there is drowsi- 
ness which rarely passes into coma. These symptoms (especially the chills 
and febrile movement) are often severe, and then the disease is of short 
duration. The patient passes rapidly into a state of stupor without con- 
vulsions and with a subnormal temperature. The urine may be in excess 
of the normal quantity or be scanty ; albumen is present in varying quan- 
tities ; hyaline and pus casts and renal epithelia are also present in varying 
amounts. Blood is always found in the acute cases. The specific gravity 
is never very high. The . urine is in many cases ammoniacal. Should a 
tumor be felt, it will fluctuate ; but rarely is there a distinct tumor. 

Differential Diagnosis. — From pyoemia it is distinguished by the absence 
of recurring chills and siveats ; by its lower temperature ; by absence of 
joint and lung symptoms, and by the purulent bloody urine. It is often 
difficult to distinguish it from septicaemia. 

A perinephritic abscess is distinguished from suppurative nephritis by 

1 This is Kleb's parasitic nephritis ; the infecting particle? or spores ascend (presumably from the blad- 
der) to the pelvis; thence up the tubules. Hyaline casts in " parasitic nephritis " have spores and alga? on 
their periphery. Cornil and Ranvier think they may be formed in the kidney during life. 

2 Full descriptions are given in Erichsen's Surgery, P- 712 et seq.. vol. ii. 

3 Marcus Beck (in " Quahrs Diet, of Med.," pp. 1562-5) describes acute interstitial nephritis without 
suppuration as one variety of the surgical kidney : infiltration of small round cells in the intertubular 
structure and about the Malpighian tufts being the chief pathological event. An acute or sub-acute 
interstitial (non-suppurative) nephritis I have already described. 



604. 



DISEASES OF THE KIDNEYS. 



its tumor, and by the fact that in uncomplicated perinephritis urinary 
symptoms are absent. 

Pyelitis has the characteristic angular "tailed" cells from the mucous 
membrane of the pelvis in the urine, and the constitutional symptoms are 
insignificant compared with those of suppurative nephritis. 

Prognosis. — The prognosis is always grave. The free discharge of a 
large abscess may prolong life, and, if unilateral, be followed by recovery. 
Death from complications is its frequent termination. In the aged it is 
almost necessarily fatal. Asthenia, uraemia, and complications cause 
death. 

Treatment. — The treatment is for the most part surgical. Tonics, 
stimulants, and condensed nutriment are indicated from its onset. A 
pure milk diet is advantageous. Dry cupping, fomentations, and poultices 
or leeching over the loins are of service. The bladder is to be washed out 
with any of the antiseptic fluids usually employed for that purpose, two or 
three times a day. Benzoic acid or benzoate of ammonia may be given to 
relieve the offensiveness of the urine. 

CHRONIC PARENCHYMATOUS NEPHRITIS. 

As already stated, chronic parenchymatous nephritis may be a sequela 
of the acute form, but it is oftener a chronic process from its onset. 
Under this head may be included large granular fatty kidney, the large 
white kidney and the small granular fatty kidney. 

Morbid Anatomy. — Chronic parenchymatous nephritis may develop with 
any form of renal lesion in which there is a protracted interference with 
the normal nutrition of the tubes. In the large granular fatty kidney, but 
few of the epithelial cells of the uriniferous tubes at first undergo change ; 
but, as the transformation becomes general, the affected tubes become 
loaded with exfoliated epithelium in all stages of the process, from the 
earlier condition of cloudy swelling, to the final development of granulo- 
fatty metamorphosis. The mucous membrane of the pelvis and calices is 
thickened, opaque, and anaemic, or it presents a varicose dilatation of its 
veins. The kidneys are enlarged, their capsules are non-adherent, and 
their surface smooth ; their color is paler than normal, presenting a more 
or less yellow appearance ; sometimes they are mottled with red and white. 

On section, the enlargement of the organ will be found to be due chiefly 
to an increase in the size of its cortical substance, which is of a pale yel- 
lowish color. There is but little change in the medullary portion. . The 
Malpighian tufts do not stand out prominently, for there is more or less 
fatty material in the dilated portion of the uriniferous tubes around the 
Malpighian tufts, which gives them a somewhat pale appearance. The vas- 
cularity of the whole kidney seems to be very much diminished ; but here 
and there spots of hemorrhage or congestion are seen. The principal 
changes take place in the convoluted tubes of the cortical portion, espe- 
cially in those which surround the Malpighian tufts. 



CHRONIC PARENCHYMATOUS NEPHRITIS. 



605 



These sections 
are very opaque ; 



of the cortical substance 
under a 



in 



this form of degeneration 




low power they show little 
more than uriniferous tu- 
bules irregularly distended 
■with fatty granules , and va- 
ricose. To the unaided eye 
the tubules look like streaks 
of sebaceous matter. At 
some points they are greatly 
increased in size, at others 
they are of normal calibre. 
In the Malpighian bodies are 
found oil granules in vary- 
ing quantities, but the capil- 
laries of the tuft are un- 
changed. Under a high 
power, fine fat granules are 
seen about the nuclei in 
the protoplasm of the epi- 
thelial cells, and also in 
the cells of the external coat 
of the small vessels. Gran- 
ulo-fatty material covers a 
homogeneous vitreous sub- 
stance in Henle's tubules. 
The lacunas and cells of the 
intertubular connective-tissue are also filled with fine fat granules. 

Large Wliite Kidney. — In this variety of parenchymatous nephritis, 
the kidneys may be twice their normal size, of an ' ' ivory-white " color, 
their surface smooth, and their capsule non-adherent. 

On section, the enlargement is found to be due to an increase in the 
volume of the cortical substance. The medullary portion shows no appre- 
ciable alteration. The microscope will show that the morbid changes are 
confined almost exclusively to the epithelium of the convoluted tubules and 
that lining the Malpighian bodies. The epithelium is granular, and so 
much swollen that the lumen of the tubes is obstructed and may be dis- 
tended with a hyaline material. There is a dilated and varicose condi- 
tion of the tubes, with some thickening of their walls. In some cases 
Henle's loops present alterations similar to those that occur in the convo- 
luted tubes. 

Small Granular Fatty Kidney. — The atrophic alterations in the kidney 
in this variety (or stage) of parenchymatous nephritis are entirely different 
from those of atrophy produced by interstitial nephritis. The epithelium 
which may have been the seat of fatty or granular change, disintegrates, 
liquefies, and is absorbed or passes off in the urine. The tubes, deprived of 



Fig. 143. 

Chronic Parenchymatous Nephritis. 

Section, from the Cortex of a Kidney. 

Slightly thickened capsule of the glomerulus. 

Vascular tuft, nearly normal. A small amount of gran- 
ular matter is seen beneath the capsule. 

C, C. Convoluted tubules — epithelium nearly destroyed. Some 
of the tubes are entirely filled with fatty granules. The 
nuclei of the epithelia are yet plainly seen. 

Longitudinal section of Henle's looped tube — ascending por- 
tion. 

A small artery. x 350. 



606 



DISEASES OF THE KIDNEYS. 



their epithelium, collapse. Some claim that renal atrophy and granular 
degeneration of the kidney are the same. That these processes are asso- 
ciated is yery evident. During the process of atrophy, developments occur 
in the walls of the tubes and in the intertubular tissue, which lead to, 
or are followed by, thickening of the tubules and blood-vessels. The 
processes of inflammatory atrophy are always slowly progressive. An 
atrophied white kidney is markedly diminished in size, its surface is 
uneven and more or less nodular; its capsule is adherent and slightly 
thickened, and when removed portions of kidney tissue may be removed 
with it ; the denuded surface is more or less granular, its color varies, 
it may be white, have a stellate vascularity, or present a mottled appear- 
ance. 

On section, it will be found that the diminution in the size of the kid- 
ney is mainly due to atrophy of its cortical substance ; the medullary por- 
tion retains very nearly its normal dimensions ; the cortical substance be- 
tween the pyramids will be somewhat atrophied. The kidney is firm and 
tough. The granulations on its surface and in its substance are the pyra- 
mids of Eerrein. Under low power a section of the cortical substance will 
show an increase in the stroma of the organ, the walls of the vessels will be 
thickened and the Malpighian tufts will have lost their distinctness. The 
uriniferous tubules will be denuded of their epithelium, in some places filled 
with granular or fatty material, and distended ; in others they will be en- 
tirely obliterated, atrophied, and more or less shrivelled. This form of 
kidney degeneration may be distinguished from the contracted kidney of 
interstitial nephritis by the larger size of the organ, its less firm consis- 
tency, its more uneven surface, its pale yellow and large granulations not 
only on its surface but throughout its substance, evidently formed by the 
accumulation of fat in the tubules, and by the absence of cysts either on its 
surface or in its substance. It is not necessary that the small atrophic 
Kidney of chronic parenchymatous nephritis should have been preceded by 
an enlarged fatty or granular kidney. 

Etiology. — Chronic parenchymatous nephritis may be the sequela of 
acute. It is more common in males than in females, it occurs in early 
adult life rather than past middle life. Exposure, moderate alcoholism, 
bad hygiene, phthisis, diabetes, arthritis deformans, emphysema, and 
chronic cardiac diseases predispose to its development. The cause is 
sometimes undiscoverable. 

Symptoms. — This form of chronic Bright's disease may be ushered in by 
acute symptoms or come on insidiously ; in either case, when once fully 
developed, the symptoms are identical. There are two symptoms which 
are always present, viz. : albuminuria and dropsy. If its advent is marked 
by acute symptoms, its development is attended by the phenomena of acute 
Bright's ; the patient rapidly reaches a condition bf general anasarca ; his 
countenance assumes a pallid appearance ; the pallor is not like the clear 
pallor of phthisis, nor the dingy pallor of cancer, but is peculiar to the dis- 
ease. When he has reached an apparently hopeless condition his urine 



CHRONIC PARENCHYMATOUS NEPHRITIS. 



007 



becomes gradually increased in quantity. His appetite returns, nausea 
disappears, he suffers less from restlessness, the anasarca gradually dimin- 
ishes, the sleep becomes refreshing — in short, there is a gradual improve- 
ment in all his symptoms. The improvement may be continued or 
relapses may occur, but after a few weeks or perhaps months he may reach 
a condition of comparative health ; this class of patients never so far 
recover that no traces of the disease remain. There will always be some 
oedema along the line of the tibia and over the internal. malleolus, and the 
albumen will never entirely disappear from the urine. Patients in such a 
condition are always inspired with the hope that they will reach com- 
plete recovery ; but they are liable at any time to a sudden return of 
their dropsy. 

When the disease comes on gradually without any acute symptoms one 
of its earliest indications is increased frequency of micturition ; the oedema 
may not be very extensive, but it is always present ; perhaps there is at no 
time pain in the back or loins ; but there is a time, early in the history of 
the disease, when the urine is scanty and high colored ; afterward it be- 
comes copious, of a pale color and low specific gravity. The gastric and 
nervous symptoms, so prominent in acute Bright's, are never severe ; there 
is gradual loss of energy with progressive emaciation ; the skin becomes 
dry and harsh, the surface assumes a peculiar pale, sallow appearance, there 
is often great thirst, very troublesome dyspeptic symptoms, and often marked 
signs of anaemia. The pulse becomes feeble and irregular in force, and the 
patient grows old rapidly. 

The urine after a time becomes more abundant than normal, of low spe- 
cific gravity, sometimes as low as 1.010, and the quantity of albumen is in- 
creased. Fatty and hyaline casts are present ; when the stage of atrophy 
is reached the urine sometimes becomes very abundant, and, although the 
albumen at times may be small in quantity, it never entirely disappears, 
and large hyaline and fine granular casts are always present. As the elim- 
ination of urea is steadily diminished, it is important to subject the urine 
to frequent quantitative analyses. Cardiac hypertrophy develops, and 
albuminous retinitis is of frequent occurrence. Degeneration of the 
cardiac walls and dilatation of its cavities develop secondarily to, or coinci- 
dently with, the hypertrophy. 

It is to be remembered that the symptoms and course of this form of 
Bright's disease are not continuous ; there will be remissions, periods when 
these patients seem to be recovering, and suddenly the urgent symptoms 
of chronic anaemia will develop, and the patient passes into a state of list- 
lessness, stupor, or coma, and death rapidly ensues. 

Differential Diagnosis. — When the urine is abundant, of a pale color, low 
specific gravity, highly albuminous, and contains fatty, granular and hyaline 
casts, accompanied by oedema of the lower extremities, one readily makes a 
diagnosis of chronic parenchymatous nephritis, especially if a careful analy- 
sis of the history of the patient corresponds to the usual course of its de- 
velopments. A state of uraemic stupor, with a dry tongue and sordes on 
the teeth, may be mistaken for typhoid fever, yet the history of the case 5 
and a careful examination of the urine will soon remove all doubts. 



608 



DISEASES OF THE KIDNEYS. 



If the urine is carefully examined it is hardly possible for one to con- 
found the ancemia and cachexia which sometimes attend the stage of 
atrophy of chronic parenchymatous nephritis with the cachexia of other 
chronic diseases. The mistakes that are made in diagnosis, or rather the 
failures to recognize its existence, are usually due to the fact that a careful 
examination of the urine has not been made. In every case of persistent 
dyspepsia careful examination of the urine should be made. 

Prognosis. — One of the most constant attendants of the advanced stage of 
this form of Bright's disease is the development of cardiac hypertrophy. 
It is probably due to interference with the systemic capillary circulation, 
and it is an evidence that the renal disease has existed for a long time ; it 
suggests the possible occurrence of cerebral hemorrhage, and therefore 
renders the prognosis unfavorable ; visceral inflammations, especially pneu- 
monia and bronchitis, are liable to occur, and often are the direct causes of 
death. 

The most frequent serous inflammations in this connection are pleurisy, 
pericarditis, and meningitis. They are usually insidious in their develop- 
ment, and always render the prognosis unfavorable. Another complication 
which may render the prognosis unfavorable is subacute inflammation of 
the mucous membrane of the stomach. Patients never entirely recover 
from the structural changes which occur under such circumstances. 
Amaurosis is first indicated by the patient's inability to see distinctly; sub- 
sequently he has more or less difficulty in reading print which formerly he 
had read with ease ; lenses do not improve his vision ; after a time the 
sight may be entirely lost. This amaurosis is due to a neuro-retinitis ; it 
is present to a greater or less degree in a large number of these patients. 
The structural changes in the kidneys in the advanced stage of this form 
of Bright's disease are such that they do not admit of repair. All portions 
of the kidney, however, are not equally involved ; consequently the de- 
purative function of the organ is not suspended, but only imperfectly 
carried on. So long as the degenerative process is not progressive this class 
of patients may get on quite comfortably, but its tendency is to progress 
until it reaches a point beyond which life cannot be sustained. In a large 
number of cases, long before this limit is reached, some one of the com- 
plications to which reference has been made will cause death. 

In the advanced stage, the most trustworthy prognostic indications are 
to be obtained by comparing the evidences furnished by examinations of 
the urine with the general symptoms ; one must always be cautious in giving 
a prognosis, for the ursemic symptoms may suddenly be greatly aggravated 
by exposure to cold or errors in diet, and the patient quickly passes from 
a condition of comparative good health into ursemic coma. Although in 
all advanced cases the prognosis is unfavorable, still there is reason to 
hope that by judicious management, even in the most unpromising, relief 
may be obtained from many of the more distressing symptoms, and life be 
prolonged. 



CHRONIC PARENCHYMATOUS NEPHRITIS. 



609 



Treatment. — At one time mercurials were extensively employed in the 
treatment of this form of Bright 's disease, with the idea of keeping up 
their constitutional effects for months. This plan is now abandoned. It 
is important that the diuretic plan of treatment should be continued when 
a patient passes from acute into chronic parenchymatous nephritis. Digi- 
talis in moderate doses, or at intervals, is always indicated ; it is important 
that the accumulations in the nriniferous tubules should be removed the 
same as in the acute stage. When the eliminating function of the kidney 
is decreased, as indicated by low specific gravity with abundant flow, or when 
digitalis alone fails to increase the quantity when the urine is scanty, then 
calomel and squills should be combined with digitalis. 

There is another element which enters into the treatment. The most 
important thing to be accomplished in the treatment of this form of Bright's 
is the establishment of healthy nutrition ; the nutrition of the kidneys is 
always imperfectly performed, and these patients are always more or less 
anaemic. For this reason it is important that the nutritive processes be 
carried to their highest point ; that after the degenerated material is re- 
moved from the uriniferous tubes, the degenerative inflammatory processes 
may be arrested and the epithelial lining of the tubes restored. Digitalis 
combined with iron should be given in sufficient quantity to produce mod- 
erate diuresis. In most instances milk is the best article of diet. Adults 
will often take two or three quarts in twenty-four hours ; when taken 
freely it supplies an abundance of liquid, which acts to some extent as a 
diuretic. In most cases a moderate amount of stimulants will be of ser- 
vice. Wines are to be preferred, and they should be taken with the food. 

The patient must be placed under the best hygienic conditions, in a uni- 
form temperature, and the surface of the body must be covered with flan- 
nel ; over-indulgence of every kind, and exposure of the surface to cold must 
be carefully avoided ; a residence in a uniformly dry climate is of the utmost 
importance. The urinary secretion must be carefully watched both as to 
its quantity and quality. In the stage of atrophy there will be no necessity 
for the administration of diuretics, for the urinary secretion is abundant. 
The disease is attended by great feebleness, and on account of their feeble 
dige cf :ve power this class of patients will be compelled to take food in small 
quantities and at short intervals ; they will generally be greatly benefited 
by cod-liver oil, combined with iron. Wines are always indicated in 
moderation. Whenever the urine becomes scanty, two or three full 
doses of digitalis should be administered and dry cups applied over the 
kidneys. 

The urgent symptoms, such as dropsy, etc., must be relieved by an oc- 
casional hot-air bath, hydragogue cathartics or stimulating diuretics, and 
at the same time great care must be exercised lest the depletion be carried 
too far. Jaborandi or the hydrochlorate of pilocarpin may be cautiously 
used in very urgent cases ; they are prompt and efficacious, but sometimes 
dangerous. Iron and cod-liver oil are the two great remedial agents in this 
disease, and should be daily administered, unless the condition of the stom- 
39 



610 



DISEASES OF THE KIDNEYS. 



ach of the patient shall contra-indicate their use. Milk should be the prin- 
cipal article of diet. By living in a warm climate, by constant watchfulness, 
and by following the rules given in acute Bright's disease, a fatal termina- 
tion may be long delayed, although complete recovery cannot be hoped for. 

Let me impress this fact : that no depleting remedies should be em- 
ployed, except in times of emergency, when, from some sudden renal con- 
gestion, the function of that portion of the kidney structure which is still 
performing the work of elimination becomes suddenly arrested or impaired, 
and acute ursemic symptoms are developed. 

CHRONIC INTERSTITIAL NEPHRITIS. 
(Cirrhotic Kidney.) 

In this form of nephritis the morbid processes do not pass through dis- 
tinct stages. The changes consist essentially in an increase of the inter- 
tubular structure, and a consequent atrophy of all the other structures. 
As has been stated, it has been called the gouty, hob-nailed, or small red 
kidney. 

Morbid Anatomy. — Kidneys that are the seat of interstitial nephritis are 
at no time very much increased in size. The changes are characterized by 
a gradual increase in the connective-tissue of the kidneys and by atrophy of 
the tubules. In its early stage the capsule is somewhat adherent, the sur- 
face uneven, and the stroma of the cortical substance somewhat increased. 

In the advanced stage of the process the kidneys are diminished in size, 
sometimes to one-fourth their normal bulk ; their capsule becomes thick- 
ened and very adherent ; the thickening of the capsule is quite character- 
istic, and ' there is more or less prolongation of the connective- tissue from 
the capsule into the cortical substance, in consequence of which a portion 
of the kidney structure will be removed when the capsule is torn oh*, leav- 
ing the surface of the organ uneven and ragged, having sometimes a finely 
granular appearance and of a reddish color. Such kidneys have a dense 
fibrous feel, and dilated veins are sometimes seen upon their surface. 

On section it is found that the diminution in the size is due to decrease 
in the cortical substance. It is more markedly diminished in this than in 
any other form of Bright's disease ; it will also be noticed that the blood- 
vessels are more distinctly visible than in the normal kidney. The Mal- 
pighian tufts, however, are not as prominent ; the medullary portion retains 
very nearly its normal appearance and is not markedly diminished in 
size. 

The principal change, so far as retraction is concerned, takes place in 
the cortical portion. This portion may be reduced to one-sixth its normal 
thickness. The shrinking is not only apparent in the cortical substance 
beyond the bases of the pyramids, but also in the tissue between the 
pyramids. Cysts are usually found m the cortical portion, especially near 
its surface. These cysts are of varying size, and may be the result of a 
variety of changes. 



CHRONIC INTERSTITIAL NEPHRITIS. 



611 



The changes which occur are usually as follows : — 

First, there is cellular infiltration of the intertubular connective-tissue 
of the cortical substance, most abundant around the capsule of the Mal- 
pighian tufts ; this gradually develops into a fibrillated structure ; in this 
stage of the process the tubes and their epithelium are but slightly, if at 
all, implicated. The Malpighian tufts 
are diminished in size, their capsule 
thickened, and around the tufts are 
laminated, concentric zones of connec- 
tive-tissue, between whose lamellae are 
flat, stellate, or small round cells. The 
intertubular growth, by its pressure 
and contraction, causes atrophy of the 
tubes, which in some places are obliter- 
ated, in others irregularly distended, 
and they contain degenerated epithelial 
products ; as the atrophy proceeds the 
intertubular tissue becomes filled with 
granular and fatty debris. The walls 
of the small arteries 1 become thickened 
by hypertrophy of all their coats, espe- 
cially the middle, but they have an ir- 
regular outline. The firm, dense mass 
of connective-tissue between the Mal- 
pighian tufts completely obliterates the 
expanded uriniferous tubules, bringing 
the tufts much nearer to each other 
than in the normal kidney, but it does 
not as a rule obliterate them. The 
shrinking and even total disappearance 
of the convoluted tubes near the tufts, cause the tufts to almost touch 
one another. The Malpighian tufts are sometimes obliterated, but their 
• obliteration is usually due to the development of cysts. The cysts are often 
" colloid cysts." 2 

Sometimes connective-tissue formations extend into the medullary por- 
tion, and more or less shrinking of the pyramids occurs as a result. It is 
usually, however, confined to the cortical portion. Those tubes that retain 
their normal diameter are filled with fatty, granular, or colloid cells ; 
and their lumen contains hyaline or colloid casts. Blood pigment often 



1 Johnson regards induration of the arterial walls as due to an hypertrophy of the muscular coat : Gull 
and Sutton regard it as a deposit of a hyalin-fibroid, or hyaline-granular mass infiltrating the walls of the 
arterioles and capillaries. Cornil and Ranvier say it is neither : it is but a chronic arteritis to them, both 
inthna and adventitia being involved, i. e., endarteritis and periarteritis. 

2 Concerning colloid casts, Cornil and Ranvier state that 11 after inflammatory destruction of the nor- 
mal cells of the convoluted tnbules there are developed cells— not having the character of secreting cells— 
but assuming the cubical or flat form ; these cells undergo colloid transformation and fuse into a colloid 
mass, which is increased by the deposit of successive layers, while at the same time new cells at the periph- 
ery become colloid.'" 




Fig. 144. 

Chronic Interstitial Nephritis. Early. 

Section from the Cortex of a Kidney in Cir- 
rhosis. 

A. Capsule of a Malpighian body thickened with 

concentric layers of connective-tissue, con- 
taining flat and round cells. 

B. Vascular tvft of the glomerulus diminished in 

size. 

C. Afferent and efferent vessels of tvft. 

D and E. Convohded tubes in transverse and 
longitudinal section— Epithelium, nearly 
normal. 

F. Small artery in longitudinal section, x 350. 



612 



DISEASES OF THE KIDNEYS. 



stains the cells of the tubules. The tubules in an uncomplicated cirrhotic 
kidney contain coagulated fibrin, which will be indicated by the presence 
of hyaline casts in the urine : all the tubular changes are secondary. 

The pelyis and calices are congested ; the submucous tissue is dense and 
thickened ; sometimes the pelvis and calices are dilated. In the advanced 
stage of this form of kidney degeneration the organs are very greatly dimin- 
ished in size — their capsules exceedingly thickened, their surface finely 
granular, and the vessels on the surface varicosed and much enlarged. The 




Fig. 145. 

Section from the Cortex of a Kidney in advanced Cirrhosis. 

A, A, A. Malpighian bodies with shrunken tufts and thickened capsules which fuse 

with, the intertubular connective-tissue. 

B, B. Nearly obliterated convoluted tubes. 

C. Small Arteries with thickened walls. 

D. Convoluted lubes containing colloid material, x 60. 

cortical substance is tough and fibrous ; the kidneys are of a red or buff color, 
and usually a number of small cysts are scattered through their substance. 

Etiology. — The two most common causes of this form of kidney degenera- 
tion are gout and rheumatism. One of these causes is so frequently associ- 
ated with its development that it has given the name of "gouty kidney " 
to it. The constant and continued use of alcohol may be regarded as 
another cause of cirrhotic kidney, for we not infrequently find this condi- 
tion of the kidney associated with cirrhosis of the liver ; and the same steady 
and prolonged indulgence in the use of alcoholic drinks which produces 



CHROMIC INTERSTITIAL NEPHRITIS. 



613 



cirrhosis of the liver, may produce cirrhotic kidney. These are its three 
principal causes. 

It is occasionally met with in connection with lead poisoning. It has been 
claimed that the passive hyperemia of the kidneys which occurs in con- 
nection with some forms of heart disease leads to the development of cir- 
rhotic kidney. Cold, especially in a variable climate, exposure, poverty, and 
bad hygiene are strong predisposing causes. It is met with most often in 
and after middle life. Active brain workers are more liable to it than 
those who are indolent and phlegmatic. 

Symptoms. — The early symptoms of the cirrhotic form of Bright's disease 
are always obscure. It is so insidious in its development that its commence- 
ment can rarely be determined. One of its earliest and most constant signs 
is a frequent desire to pass urine, which may contain neither albumen nor 
casts. Dropsy may be absent, and there may be none of the symptoms 
which usually mark the presence of kidney disease. There may be only 
ill-defined nervous symptoms during life, and yet at the autopsy extensive 
cirrhotic degeneration of the kidneys may be found. 

Usually the disease is developed in the following manner : an individual 
notices that he is growing feeble without any apparent cause ; he is suffering 
from dyspeptic symptoms ; he notices that he is passing a larger quantity 
of urine than normal, and perhaps at the same time there will be a slight 
swelling of the lower extremities after prolonged exertion, such as stand- 
ing or walking. This oedema comes and goes, is more marked at night on 
retiring, and disappears in the morning on rising. The complexion assumes 
a dingy hue. His disposition changes, he is morose, fretful, and his mem- 
ory is treacherous. Insomnia and headache are tormenting, and there 
may be sudden loss of sight. The appetite is lost or is capricious. It is 
for the relief of their dyspeptic symptoms that this class of patients usu- 
ally consult a physician, and a plan of treatment is adopted for their 
relief, with the assurance that they will be better as soon as they can leave 
off work and take rest. A single or repeated examinations of the urine 
may fail to detect either albumen or casts, and the promises of speedy re- 
covery become more positive. The case goes on ; the patient becomes 
more and more feeble, he has a careworn look, the complexion is altered, 
the eye has a peculiar expression on account of the oedema of the conjunc- 
tiva, nervousness and restlessness increase, and insomnia becomes con- 
stant ; suddenly under great excitement convulsions occur and the indi- 
vidual passes into coma, remains insensible for twenty four hours and dies. 
Perhaps the urine was examined the day before the convulsion and no al- 
bumen was found ; but if it is examined at the time of the seizure both 
albumen and casts are present. 

The three prominent symptoms of this form of Bright's disease are 
changes in the urine, the dropsy and the nervous phenomena. 

The urine is increased in quantity and of low specific gravity. It is 
characteristic of the urine in this form of nephritis that albumen is 
sometimes present and sometimes absent. In the other forms, albumen is 



614 



DISEASES OF THE KIDNEYS. 



always found in greater or less quantities. It may be necessary to examine 
several specimens before casts will be found, but when found, they usu- 
ally are of the large hyaline variety ; granular casts are infrequent ; often 
several examinations of the urine are necessary before any satisfactory evi- 
dence of the disease can be obtained. 

Dropsy is never very marked. Slight oedema of the feet and ankles after 
exertion is present in most cases. When oedema of the feet and ankles is 
constant, and is associated with the general symptoms and conditions of the 
urine which have been described, the diagnosis is readily made. When as- 
cites is present, it is due to changes which have taken place in the livei 
rather than to those in the kidney. 

Its most prominent symptoms are associated with its nervous phenomena : 
they come and go in a manner not well understood. The earliest and 
most constant is headache, which is often violent ; occurring as it very 
commonly does with gout and rheumatism, it is very apt to be regarded as 
gouty or rheumatic in character. With these headaches there is more or 
less disturbance of nerve function, such as vertigo, temporary inability to 
speak, loss of sight and hearing, diplopia, myopia, presbyopia — numbness, 
neuralgic pains, muscular cramps, chorea, temporary and partial paraly- 
sis in one arm or leg, hemiplegia or paraplegia. Nervous dyspnoea is not 
uncommon, and it may be accompanied by " Cheyne-Stokes' respira- 
tion." There may be confusion of thought or impairment of memory; con- 
firmed mania may be developed. Uraemic vomiting inducing great prostra- 
tion, and anaemia — unaccompanied by dropsy — are alarming symptoms. 
There may be excessive itching of the surface. These patients are al- 
ways liable to convulsions after severe mental or physical exertion ; from 
the convulsions they may pass directly into coma, or become delirious, 
with a brown, dry tongue, dilated pupils, and thus gradually become 
comatose. 

It is always important to remember the dangers to which these patients 
are constantly exposed. Cardiac hypertrophy is present in a greater or less 
degree in the advanced stage. The hypertrophy is usully confined to the 
left ventricle. The presence of left ventricular hypertrophy without val- 
vular insufficiency is sufficient to direct attention to the kidneys. If, in 
connection with the cardiac hypertrophy the urine is abundant and of 
low specific gravity, containing only a trace of albumen, the evidences of 
contracted kidney are almost positive. Many theories have been advanced 
to explain the connection between cardiac hypertrophy and the cirrhotic 
kidney ; some regard it as purely mechanical, produced by "the obstruc- 
tion to the renal circulation and the consequent increased pressure in the 
aorta ; " but there is no condition of renal obstruction that will explain 
the hypertrophy. Others claim that the walls of the renal and of all 
the other arteries progressively hypertrophy from the altered condition of 
the blood and the retained urinary excretion, until the heart becomes 
hypertrophied as "a result of the antagonism of forces." The order of 
its occurrence seems to be, first, capillary resistance ; second, high arterial 



CHROXIC INTERSTITIAL NEPHRITIS. 



615 



tension ; third, cardiac and arteriole hypertrophy ; 1 fourth, fibroid degen- 
eration of the cardiac walls and secondary dilatation. 

Amaurosis is a frequent attendant of cirrhotic kidney ; the loss of sight 
comes on gradually ; one eye only may be affected, but usually both eves 
are equally involved ; the cause of the loss of sight is a true neuro-retini- 
tis, which can readily be recognized by an ophthalmoscopic examination. 
The optic papilla is cloudy and swollen ; the retinal veins are distended 
and tortuous, and there are white patches on the retina. White dots and 
streaks in the perimeter of the macula lutea, are thought to be character- 
istic. 

Differential Diagnosis. — This variety of Bright's disease may be mistaken 
for diabetes. The thirst, the large quantity of urine passed, the dyspeptic 
symptoms, the progressive emaciation, the absence of casts and albumen 
lead toward diabetes ; but the low specific gravity of the urine and the 
absence of sugar soon settle the question. The presence of a gouty or 
rheumatic diathesis, the insidious development of the disease, the large 
quantity of urine, its low specific gravity, with little or no albumen and 
only occasional casts, are sufficient to distinguish this from the other forms 
of Bright's disease. 

Prognosis. — When the anatomical changes which characterize this form 
of renal disease are once established, their tendency is to progress; and 
although a long period may elapse between their commencement and the 
fatal termination, yet whenever there is reason to believe that the morbid 
processes are advanced the patient is constantly in danger from complica- 
tions. Serous inflammations are not as liable to occur as in other varie- 
ties of Bright's diseases, but mucous inflammations are more frequently 
met with, especially bronchitis, which assumes a chronic type. 

Its complications are pericarditis, pneumonia, acute and chronic bron- 
chitis, pleurisy, chronic gastric and intestinal catarrh, cirrhosis of the 
liver, atheroma and sclerosis of arteries, eczema, and psoriasis. In its 
advanced stage hemorrhages from mucous and serous surfaces, as well as 
into the substance of organs, are liable to occur. The most serious of 
these hemorrhages are the cerebral. It is more frequently associated with 
cerebral apoplexy than any other form of kidney disease. Hemorrhages 
in the retina are common. 2 It must be remembered that inflammation of 
the uriniferous tubes may be ingrafted upon cirrhotic kidney, and that 
the three forms of degeneration may be present in the same kidney. 

Treatment. — In this form of kidney disease no special plan of treatment 
can be adopted. It has been claimed that the long-continued administra- 
tion of mercury in small doses has the power to arrest or prevent connec- 
tive-tissue development. When cirrhotic kidney is developed in connection 

1 Dickenson regards the vascular lesions as partly hypertrophy, and partly fibroid. 

2 In 100 cases reported by Mahomed seventeen died of heart disease and fifteen of apoplexy, i. e., 
thirty-two per cent, of cardio-vascular changes. Of thirteen who died of surgical diseases, he^ays many 
died indirectly from failing heart. Eighteen died of lung diseases (eleven from severe bronchitis and 
emphysema, and seven from pleurisy and pneumonia). 



616 



DISEASES OF THE KIDNEYS. 



with a gouty or rheumatic diathesis, the prolonged use of mercurials is 
contra-indicated. When it is developed in connection with lead-poisoning, 
mercurials are most decidedly contra-indicated. Mercurials are of especial 
advantage in those cases in which cirrhotic kidney is developed in connec- - 
tion with a cirrhotic liver. The bichloride is the preparation usually 
employed in such conditions. If the disease develops in connection with 
gouty or rheumatic manifestations, the same means which are employed 
to relieve gouty or rheumatic articular manifestations will afford relief. 

Many of these patients will derive great benefit from residing for a time in 
those localities where they may constantly use water from alkaline springs. 
The Grermans and French recommend very extensively the use of alkaline 
waters in the treatment of this class of diseases. Milk, skimmed milk, and but- 
ter-milk have all been vaunted as possessing curative properties ; hence the 
once famous "milk cure." Although these patients appear anaemic, their 
nervous symptoms are aggravated rather than relieved by the use of iron. 
In a certain proportion of cases cod-liver oil will be found of service, espe- 
cially when combined with the hypophosphite of soda; diuretics are not 
indicated, but when a marked diminution in the urinary secretion occurs, 
their temporary employment may be of service. When the disease is devel- 
oped in connection with cirrhosis of the liver, an occasional hydragogue 
cathartic may be attended with benefit. It is of the utmost importance 
that this class of patients should make a permanent residence in a warm 
climate, and that all the exciting causes of cirrhotic development should 
be carefully avoided. Although a cure cannot be hoped for, the progress 
of its development may be delayed, and by carefully watching the condition 
of the nervous system, and by timely interference, the development of the 
graver forms of nervous disturbance may be delayed or prevented, and the 
life of the patient prolonged. For symptoms or complications that demand 
a narcotic or anodyne, opium is to be used in preference to all others. In 
its advanced stages, inhalation of oxygen has caused disappearance of albu- 
men. 1 

Whenever there is extensive general anasarca, and the respiration be- 
comes impeded by oedema of the chest-walls, or by an cedematous condition 
of the lungs, and all other means have failed to relieve the dropsy, prompt 
and sometimes permanent relief may be afforded by making free incisions 
through the skin into the areolar tissue above the ankles, or by pricking 
the parts with needles in many places. 2 Those dyspeptic and gastric symp- 
toms which are so obstinate and distressing can usually only be relieved by 
a carefully regulated diet. 



1 Dujardin-Beaumetz. 

2 See London Lancet, 1877, i. 649. Southey uses drainage tubes in anasarca. 



WAXY KIDNEY. 



617 



WAXY KIDXEY. 
("Amyloid Form " of Bright' s Disease.) 

Amyloid degeneration is always chronic ; it has no acute stage, and can- 
not, strictly speaking, be regarded as a nephritis aside from the associated 
changes. It usually invades several organs of the body simultaneously ; 
when the kidney is the seat of this degeneration its tissues become infil- 
trated with amyloid material. Cornil and Ranvier found that waxy de- 
generation in the kidneys was invariably associated with chronic paren- 
chymatous nephritis ; they are, moreover, convinced that the latter condi- 
tion always precedes amyloid degeneration. 

Morbid Anatomy. — The primary waxy changes take place in the walls 
of the minute arteries ; secondarily the secreting tubes and cells are in- 
volved. At first, when the walls of the vessels are principally involved, 
there is little change in the appearance of the kidneys. They may be 
slightly increased in size, firmer, and of a paler color than normal. 

On section the Malpighian tufts appear more prominent than normal, 
and present the appearance of gray translucent points, which reflect light 
better than the surrounding tissue. Usually both the cortical and medul- 
lary portions are simultaneously, but unequally, involved ; by the "iodine 
test" the amyloid change, however slight, will become very distinct, and a 
section under the microscope will show the change to be most marked in 
the vessels in the Malpighian 
tufts, the vasa recta and in the 
middle coats of the small arteries. 

In a more advanced stage of 
the process the kidneys will be 
increased in size, their capsules 
be non-adherent, their surfaces 
smooth and of a pale color with 
stellate vascularity. 

On section the increase in the 
size will be found to be due to an 
increase in the cortical substance, 
which is denser than normal. 
The medullary substance is but 
slightly increased. The normal 
anatomical outline of the cortical 
and medullary portion is lost, the 
Malpighian tufts are indistinct, 
looking like little grains of boiled 
sago, and the whole cortical sub- 
stance has a peculiar waxy ap- 
pearance. Under the microscope 
an entire section will present a 
shining yellow appearance, as if all the tissues of the organ were infiltrated 




Fig. 146. 



Waxy Kidney. 
Section from the Cortex of a Kidney in commencing Amy 
lend Degeneration. 
A. Malpighian body. The lower part of the vascular 
tuft is the seat of the amyloid change. 

B, B. Convoluted tubes ^containing hyaline and granulo* 

fatty matter. 

C, C Arteries, with coats showing ivaxy degeneration. 

D, D. Epithelium of convoluted 'tubes containing granu- 

lar and fatty matter . x 300 



518 



DISEASES OF THE KIDNEYS. 



The Malpighian tufts are large 
together ; the small arteries are 
vious. On examination 



with amyloid material. The glomeruli, most of the arterioles, the small 
veins and the basement membrane of the tubules will be infiltrated. 
The epithelial cells of the convoluted tubes are not infrequently flattened. 
The contents of the tubes may be made up of broken-down epithelium and 
fatty granules, mingled with a material which is fibrinous in its nature ; 
this material will not, however, give the characteristic reaction of amyloid 
matter. Fatty, granulo-fatty, and hyaline materials are found, in all 
cases in addition to the above. Usually the kidneys atrophy and become 
very much diminished m size, sometimes less than one-half their normal 
size ; their capsules are adherent, their surfaces uneven, granular, and of 
a pale color. 

On microscopical examination it will be seen that the diminution 
in size is due to decrease of both the medullary and cortical portions. 

and prominent, and are grouped 
enlarged and at points are imper- 
of sections from different portions of the kidney, 
the tubules will be found at all points 
more or less atrophied and their walls 
collapsed ; some are obliterated ; the 
blood-vessels will appear thickened, and 
their outline will be more or less irregu- 
lar. Iodine upon the degenerated Mal- 
pighian tufts will give the characteristic 
amyloid reaction. The degree of atrophy 
may vary, but however extensive it may 
be, by dipping a section in the iodine 
solution, and microscopically examining 
it with a low power, one will always 
find abundant evidence of amyloid ma- 
terial in the degenerated vessels and 
tubes. 

Etiology. — The primary cause of amy- 
loid degeneration is still a vexed ques- 
tion. It never occurs in those who 
are in perfect health, and the circum- 
stances under which it almost uniformly 
occurs determine to a certain extent its 
causation. It is most frequently met 
with in syphilitic subjects. Another 
frequent cause is prolonged suppura- 
tion, especially when associated with 
diseases of bone. A long-continued empyema may give as a result an amy- 
loid kidney. It is not infrequently met with in those who die of pulmonary 
phthisis, consequently chronic suppurative diseases of the lungs must be 
ranked among its causes. Caries of bone, ulcers of the intestines, cancer, 
and chronic rheumatism mav induce it. 




Fig. 147. 
Waxy Kidney. 

Vertical Section from the Medullary Portion of 
a Kidney in advanced Waxy Degeneration. 

A, A. Collecting tubules containing fatty gran- 
ules, B, and colloid matter, C. 

D, J). Wall of tubules showing thickening and 
irregularity, the result of waxy chan ge. 
E. Transverse and F longitudinal sec- 
tion of blood-vessels with lumen nearly 
obliterated by amyloid degeneration 
of the coats. G. Ascending limb of 
HenWs loop, x 350. 



WAXY KIDNEY. 



619 



Symptoms. — The symptoms which attend the development of amyloid de- 
generation of the kidney are never well marked. The usual manner of its 
development is as follows : an individual who is suffering from tertiary 
syphilis or some exhausting form of disease, notices that he is losing 
strength, that he is becoming more feeble than usual, and that he has less 
mental and physical vigor than he is accustomed to have ; that he is trou- 
bled with shortness of breath on exertion ; that he has an unusually pallid 
countenance, and that there is a great increase in the quantity of urine 
passed. He is obliged to rise two or three times during the night to pass 
urine, and at times he passes large quantities. He also notices a fulness 
of the abdomen which he has never before observed, and sometimes there 
is a sense of weight in its upper portion. He may have detected a tumor 
in the right and perhaps in the left hypochondrium. When he assumes 
the recumbent posture, he must have the upper portion of the body ele- 
vated to prevent dyspnoea. Doubtless the dyspnoea is partially due to the 
insemia and partially to the pressure caused by an enlarged liver and spleen. 
Perhaps there is slight oedema about the ankles, especially at night. The 
patient does not perspire readily, but when he does the perspiration has a 
urinous odor. Certain articles of food, especially fatty substances, which 
never before have disagreed with him, now give rise to dyspeptic symptoms 
and he may have occasional vomitings. 

This train of symptoms coming on in one who has been the subject of 
any of the forms of disease to which I have referred, leads to the suspicion 
that amyloid degeneration of the kidney is taking place. If, upon further 
examination, a marked enlargement of the liver and spleen is found, and 
the surface of the liver is smooth and its edges sharp, it is almost certain 
that the amyloid form of Bright's disease exists. With these symp- 
toms there will also be more or less fluid found in the abdominal cavity, 
but its presence will be due to changes which have occurred in the liver and 
not to changes in the kidneys. The blood is slightly altered ; the white 
corpuscles are somewhat increased in number, and the red are diminished 
and ill-defined ; in a large proportion of cases there is a peculiar cachexia 
present which is almost characteristic. The patient has a pale, waxy com- 
plexion, with little pigmentary deposits in the skin, particularly about the 
eyelids. This cachexia is usually most marked in syphilitic subjects. 

As in the other forms of kidney disease, there are three important symp- 
toms to be considered. First, abnormal changes in the urine ; second, 
dropsy ; third, nervous phenomena. 

The urine is increased in quantity, the patient perhaps passing as much 
as one hundred ounces in twenty-four hours. It is light colored, looking 
very much like clear water, or it may have a slight amber color. It is of 
low specific gravity, sometimes as low as 1.005. When tested for albumen 
it will be found always to contain an appreciable quantity, never a large 
quantity. The amount of urea excreted is but little if at nil diminished ; 
the urine will always contain casts, either large hyaline or fine granular, or 
both, but the hyaline predominate. Oasts of either variety usually are 



620 



DISEASES OF THE KIDNEYS. 



not abundant, and several examinations may be required before their pres- 
ence or absence can be positively determined. Epithelial and fatty casts 
are sometimes found. 

Dropsy is never very marked in this form of Bright's disease. The gen- 
eral anasarca which is so frequently met with in connection with paren- 
chymatous nephritis, is never present. There may be slight oedema of the 
feet, especially at night, and there may be fluid in the abdominal cavity. 
The nervous symptoms are never very prominent. This class of patients 
do not usually suffer very much from headache, and rarely have convulsions 
or pass into coma. They usually die from exhaustion, or from some com- 
plication, or, in other words, die from amyloid degeneration of other organs, 
diarrhoea, the result of amyloid changes in the mucous membrane of the 
intestine, or ascites. 

Differential Diagnosis. — The diagnosis of this form of Bright's disease is 
not difficult when it occurs as a late manifestation of syphilis. A copious 
secretion of urine of low specific gravity containing little albumen and few 
casts, in one who has a syphilitic history with an enlarged liver and spleen, 
leaves little doubt as to the character of the kidney change. It is hardly 
possible to confound the cachexia which attends this form of Bright's 
disease with that of any other chronic disease, for a urinary examination 
will give positive evidence of the renal disease, and it only remains to de- 
termine its character, which is usually readily reached by the history of 
the case. The large quantity of urine passed often causes the patient to 
consult the physician with the idea that he has diabetes, but the urinary 
examination soon settles this question. 

Prognosis. — The duration of this form of Bright's disease is uncertain ; 
it undoubtedly takes many years for the anatomical changes in the kidney 
to reach the stage of atrophy, yet when waxy changes are once established 
recovery is impossible. Resulting as it does from a grave constitutional 
cachexia, the causes which produce it are so often continuous that they are 
only in a slight degree influenced by treatment. 

The progress of the disease may sometimes be temporarily arrested, but 
its usual course is steadily progressive to a fatal termination. Amyloid 
degeneration of the kidneys may exist for many years, and yet the patient 
enjoy a comparatively good degree of health. I now have the care of a 
medical gentleman in whom the disease has existed certainly eight years, 
yet he is in such good health as to be able to discharge the duties incum- 
bent upon a large country practice. 1 An exhausting diarrhoea or an ab- 
dominal dropsy is often the direct cause of death. Most of the com- 
plications which occur are degenerative in character. Patients are not 
especially liable to have pneumonia, bronchitis or pericarditis, or any of 
the acute inflammations which occur in connection with other forms of 
kidney disease. Cardiac hypertrophy is rarely present in any stage of the 
amyloid kidney. Its early symptoms are so obscure that it is difficult to 
determine its average duration. 



1 Bartholow records a case where there was complete recovery from the waxy kidney. 



PYELITIS. 



621 



Treatment. — This is an incurable disease ; there are no known means for 
arresting it or preventing its development. The same general principles are 
to govern its treatment as govern the treatment of waxy degeneration in 
other organs. First, if possible remove its cause, as diseased bones, pro- 
longed suppuration, or purulent accumulations. If it occurs with syphilis 
anti syphilitic remedies are indicated, always remembering that waxy de- 
generation occurs only as a tertiary manifestation of syphilis, and that all 
measures which have a tendency to debilitate the patient must be avoided. 
Iodide of potassium and mercury are the most reliable remedial agents. 
Both of these agents have gained some favor as remedies in the treatment 
of Bright's disease, and there are those who employ indiscriminately one or 
the other or both of them. The benefit derived in certain cases from their 
use is undoubtedly due to their power over syphilitic manifestations. In 
such cases, the long-continued use of small doses of mercurials will gen- 
erally be followed by marked improvement, but care should be exercised 
that their use be not continued until the specific effect of the drug is 
produced. 

When these patients are in a debilitated condition iodide of potassium 
with cod-liver oil will be of greater service. The form of iodine which I 
have found most serviceable to this class of patients is pil. ferri iodidi. 
One of these pills given three times a day, at the time of taking food, is 
often followed by the most beneficial results. Diuretics and hydragogue 
cathartics will rarely be required. The tincture of the perchloride of iron, 
quinine, nux vomica, and sirups of the phosphates are often beneficial. 

PYELITIS. 

Pyelitis is an inflammation of the mucous membrane of the pelvis and 
calices of the kidney, and may run an acute or chronic course. It may in- 
volve the pelvis and infundibula of one or of both kidneys. Some describe 
an acute catarrhal, pseudo-membranous, and calculous pyelitis and a 
chronic purulent pyelitis that may or may not result in pyonephrosis. 

Morbid Anatomy. — In acute pyelitis the mucous membrane of the pelvis 
of the kidney is at first more or less reddened. When very hyperaemic the 
surface will be dotted here and there with little dark-red spots which are 
minute ecchymoses ; the epithelium of the mucous surface -is more or less 
removed ; sometimes it is entirely removed, at others it is removed in 
patches. The peculiar " tailed" cells of the pelvis are thrown off in great 
quantity. As the inflammation progresses the mucous surface becomes 
covered with more or less muco-pus. The urine in the pelvis- will contain 
numerous desquamated epithelial and lymph cells. 

In some cases a membranous exudation may be developed upon the 
mucous membrane of the pelvis, called "pseudo-membranous" pyelitis. 
It is a diphtheritic exudation occurring in connection with diphtheritic 
exudations in other parts of the body, and should be called diphtheritic 
pyelitis. This diphtheritic membranous exudation is liable to become de- 



622 



DISEASES OF THE KIDNEYS. 



tached and block up the ureter. Sloughs may form, and after their re- 
moval an ulcerated surface may be left. 

In chronic pyelitis the mucous membrane of the pelvis of the kidney is 
congested and thickened, and its surface presents small vascular granula- 
tions. It assumes a grayish white or slate color and is traversed by dilated 
veins ; the pelvis and infundibula and ureter are dilated and more or less 
thickened. Pus is more or less abundantly formed, and if there is no ob- 
struction it passes off with the urine. Calculi or fragments of calculi may 
be found mingled with the pus. 

Should there be an impediment to its escape it accumulates in the pelvis, 
which it distends more and more, and at last gives rise to a condition 
known as pyonephrosis. This dilatation as it progresses encroaches first 
upon the papilhe, which become flattened and obliterated, next on the 
pyramids, and finally, by the pressure it causes, the cortical portion of the 
kidney disappears. The apices of the pyramids may suppurate and ulcer- 
ate. In such cases only a sacculated pouch remains containing from one 
to several ounces of fluid, which may be mixed with inspissated pus, broken 
down calcareous matter, ammoniacal products and calculi. 

If a renal calculus is present, and the cause of the pyelitis, more or less 
extensive ulcerations may be established. These ulcerations may cause 
perforation of the pelvis, and give rise to extravasation of urine into the 
adjacent tissues. In this (so-called) calculous pyelitis the kidneys are al- 
ways the seat of interstitial nephritis, cysts, marked atrophy, etc. The 
ureter of the kidney which is the seat of the pyelitis may be completely ob- 
structed, and pus, blood, and urinous material may accumulate behind the 
obstruction. If these obstructions are permanent an opening may be made 
through the dilated ureter and the contents of the sac discharged into the 
adjacent tissues, into some hollow viscus or into the abdominal cavity, or 
by an adhesive inflammation reach the surface and be discharged externally. 

When the obstructions are temporary the contents of the sac are dis- 
charged into the bladder through the ureter when they give way, and such 
obstructions or accumulations may occur repeatedly. Sometimes these re- 
tained accumulations undergo entire absorption, and there remains a thick 
cicatricial tissue, with the normal kidney tissue entirely obliterated, and 
the ureter becomes transformed into a tendinous cord. Under such cir- 
cumstances if the fellow kidney is healthy it becomes increased in size and 
performs in a yery satisfactory manner the function of both kidneys, and 
the patient may live for many years. Again, in certain cases, the accumu- 
lation in the kidney is changed into a cheesy material, and presents an ap- 
pearance resembling what is known as tubercular kidney. Mingled with 
this cheesy mass may be found the urine-salts which cause it to have a 
sandy feel The kidney may be changed into a fibrous shell containing 
pus and debris. 

Etiology. — Pyelitis is seldom, if ever, a primary disease. Its most fre- 
quent cause is the presence of calculi or some foreign substance in the 
pelvis of the kidney, and the pyelitis is then secondary to mechanical irri- 



PYELITIS. 



623 



tation. Pyelitis may result from extension of inflammation from the 
bladder or ureter, or from acute interstitial nephritis, rarely from perine- 
phritic abscess. It may result from the irritation produced by the decom- 
position of urine retained in the pelvis of the kidney, as a consequence of 
some obstruction to its normal outlet. For instance, an enlarged prostate 
gland, a tumor pressing on the ureter, paralysis of the bladder, or an 
urethral stricture which causes obstruction to the passage of urine from 
the bladder. As a result of retention of urine in the bladder, cystitis is 
developed, and the inflammation of the mucous surface of the bladder may 
extend to the ureters, and from the thickening of their mucous lining and 
the diminution of their calibre, the passage of urine from the kidneys to 
the bladder is obstructed, and there is not only retention of urine in the 
bladder but also in the pelvis of the kidneys. As a result of such retention 
the urine undergoes decomposition, the urea is changed into carbonate of 
ammonia and water, the carbonate of ammonia acts as an irritant and ex- 
cites inflammation of the lining membrane of the pelvis, and thus pyelitis 
is developed. 

The absorption of the ammonia resulting from the decomposition of the 
urea may be sufficient to give rise to a condition which has received the 
name of ammoncemia. This condition is not infrequently mistaken for 
uraemia, yet they differ widely in their manifestations and the dangers 
which attend their development. In ammonaemia the urine when voided 
isammoniaeal, as are also the breath and perspiration. The mucous mem- 
brane of the mouth is dry and shining; the complexion is sallow and there 
is increasing emaciation ; no dropsical accumulations are present. Con- 
vulsions and vomiting are rare ; chills are frequent. Death is usually pre- 
ceded by coma. The development of the train of symptoms indicative of 
ammonaemia, accompanied by the evidence of obstruction to the normal 
outlet of the urine, should cause one to hesitate before performing any 
operation, especially an operation for relief of stricture of the urethra. 

'Pyelitis not infrequently occurs in connection with that class of diseases 
which depend upon blood poisoning — pyaemia, diphtheria, and typhus 
fever. In this connection it is generally a complication of acute Bright's 
disease, which is not severe in character, but which causes bloody urine. 
It is an almost diagnostic complicating symptom of myelitis. Pyelitis 
occasionally occurs in consequence of over-doses, or the prolonged use, of 
certain irritating drugs, as turpentine, cantharides, and other stimulating 
diuretics. In very rare instances it seems to come on idiopathically from 
exposure to cold and wet, or from some unknown cause. 

Symptoms.— In the majority of cases the development of pyelitis is pre- 
ceded or accompanied by symptoms clue to the causes which produce it, 
such as renal calculi, diseases of the bladder, etc. 1 Prominent among those 
symptoms which directly attend its development is pain in the back. This 
is present in the mild as well as in the severe cases. Thi s pain may haxe 

i It is said (Klebs) that bacteria may be carried into the bladder on unclean catheters or other instru- 
ments, and that these, making their way into the pelvis, cause pyelitis. 



624 



DISEASES OF THE KIDNEYS. 



its point of maximum intensity over one or both lumbar regions. It is 
often of an aching character, and shoots down along the course of the 
ureters. This pain is usually accompanied by frequent micturition, and 
when it is very intense the voiding of urine is almost incessant and is 
attended by severe pain. The commencement of acute pyelitis is usually 
marked by rigors, and in that chronic form in which temporary obstruc- 
tion of the ureter occurs, rigors are frequent. 

Symptoms of hectic fever may also mark the occurrence of permanent ob- 
struction of the ureter and the development of that condition termed pyo- 
nephrosis. There is usually considerable lassitude attending the progress 
of pyelitis, and when the disease is due to the presence of a calculus, the 
patient ordinarily suffers more or less pain on motion. 

All of these symptoms are accompanied by changes in the urine, and 
these changes are its most reliable signs ; — in its early stage the urine con- 
tains blood mixed with mucus and epithelial cells from the pelvis and in- 
fundibula : the presence of these epithelial cells, which are readily distin- 
guished from epithelium of any other portion of the urinary tract by their 
characteristic shape and appearance,is its most certain diagnostic indication 
The specific gravity of the urine ranges from 1.025 to 1.030, and it usually 
retains its acid reaction. In the more advanced stages the characteristic 
epithelium is to a great extent replaced by an abundance of pus cells, but 
the urine retains its acid character. If sacculation of the kidneys is devel- 
oped, the urine will become ammoniacal. More pain and hemorrhage at- 
tend calculous pyelitis than the other forms. Albumen is present in pro- 
portion to the amount of pus and blood. In the advanced stage of pyelitis, 
if the urinary channels remain free the discharge of pus is constant. If the 
ureter becomes blocked, for a time the urine may be quite normal, but the 
removal of the obstruction is followed by a copious flow of purulent urine. 
This may be repeated from time to time, at intervals varying from a few 
days to a few months. If the pelves of both kidneys are affected, and there 
is partial or complete obstruction of one side, the accumulation of pus in the 
urine is diminished, but not entirely prevented. If the obstruction is long 
continued or becomes permanent, a tumor develops in the lumbar region. 

The development of a, pyonephrotic tumor indicates complete obstruction 
of the ureter. The existence of the tumor is determined by the presence of 
bulging between the crest of the ilium and the false ribs on the right or left 
side, according as the right or left kidney is involved. As a consequence 
the outline of the abdomen is rendered unsymmetrical. On palpation, deep- 
seated fluctuation is felt over the tumor, which usually is tender on press- 
ure. The area of percussion dulness will correspond to the outline of the 
;umor, except where it is crossed by the colon. With these physical signs 
present, and a history of pyelitis, one will be justified in resorting to the 
exploring trocar to complete the diagnosis. 

Differential Diagnosis. — The diagnosis of pyelitis in its first or acute stage 
rests almost exclusively on the presence in the urine of the characteristic 
epithelium of the pelvis and infundibula mixed with blood globules and 



PYELITIS. 



625 



mucus. If the urine contains pus cells mixed with these epithelial cells, it 
indicates a more advanced stage of the disease. The presence of pus and 
acid urine, with pain in the lumbar region, accompanied by the develop- 
ment of a tumor at the seat of pain, which tumor gradually increases in 
size and suddenly disappears at the same time that a copious discharge of 
pus takes place from the bladder, which discharge is attended by a sense of 
great relief to the patient, renders the diagnosis of pyonephrosis very cer- 
tain. If the ureter of the affected kidney is permanently obstructed, the 
lumbar tumor is liable to be mistaken for hydronephrosis, an hydatid cyst, 
or a perinephritic abscess. 

In perinephritic abscess neither pus, blood, mucus, epithelia nor albu- 
men will be found in the urine ; in pyonephrosis they are common and 
constant. Pain on motion, the occurrence of slight oedema over the tumor, 
the delayed appearance of fluctuation — these are in contrast to the symp- 
toms of pyonephrosis. The mass of tumor in perinephritic abscess may be 
tilted forwards by pressure in the renal region, which is never the case with 
pyonephrosis. 1 Fever is a marked symptom in abscess, and slight or absent 
in pyonephrosis. In women a pyonephrotic tumor has been confounded 
with an ovarian cyst. The exploring trocar will very quickly remove all 
doubts. 

Pyelitis is distinguished from cystitis by absence of vesical pain and fre- 
quent micturition, by lumbar pain, and by the intimate admixture of for- 
eign materials in the urine. Pelvic epithelial cells are not found in the 
urine of uncomplicated cystitis. In pyelitis the urine is acid ; in cystitis 
it is alkaline. When pyelitis occurs as a complication of chronic cystitis, 
an enlarged prostate gland, or urethral stricture, it is often impossible to 
diagnosticate its existence if there is no tumor in the lumbar region. Under 
these circumstances the character of the urinary constituents is not of much 
assistance, if, however, the quantity of pus is large, the urine slightly 
acid, the loins painful on pressure, and the febrile movement constant, 
with rapid loss of flesh and strength, there is good reason to believe that 
chronic pyelitis has been added to disease of the bladder and. urethra. 

Prognosis. — The prognosis in pyelitis depends upon the nature of its ex- 
citing cause. In simple catarrhal pyelitis, not connected with extensive 
disease of other portions of the urinary apparatus, the prognosis is good, 
unless the disease affects both kidne} r s and has reached the purulent stage; 
then, whatever may have been its cause, the prognosis is bad. When the 
disease is confined to one side, recovery is possible, although one kidney 
may be completely destroyed. We suspect unilateral pyelitis with calculi 
and with tumors that compress an ureter ; but following a cystitis, ure- 
thritis, prostatitis, etc., the affection is usually bilateral, and the prognosis 
is unfavorable. 

Pyelitis may be regarded as a hopeless disease when it is secondary to an en- 
larged prostate gland, extensive chronic cystitis, urethral stricture, or cancer 
of the kidney. It is exceedingly grave when it depends upon renal calculi or 



1 London Lancet, January, February, March, 1879. 

40 



626 



DISEASES OF THE KIDNEYS. 



hydatids, although it is not necessarily fatal. The issues of a pyonephrosis 
are uncertain ; the various directions in which a sac may burst determine 
to a great extent its termination. Rupture into the peritoneal or tho- 
racic cavity is speedily fatal. Recovery is possible if the rupture takes 
place externally or into the intestine. Sometimes, when the sac does 
not rupture, patients die from the exhaustion caused by the long-con- 
tinued discharge. Recovery may be reached by a gradual diminution 
of the discharge and a final contraction and obliteration of the sac, pro- 
vided the other kidney is unaffected. Death may occur from uraemia or 
ammonsemia, 

Treatment. — The first thing in the treatment of pyelitis is, if possible, 
to remove its cause. If the attack is an ac ate one, and at the onset of 
the disease the fever is considerable, the pain in the lumbar region severe, 
and the urine bloody, wet cups should be freely applied to the loins, fol- 
lowed by a hot bath, and a sufficiently large hypodermic of morphine to 
entirely relieve pain. The patient should drink freely of alkaline fluids 
and should be kept in bed. 

In chronic pyelitis, when the secretion of pus is abundant, astringents 
may be employed to diminish the purulent secretion. Balsams are here 
indicated. Attention should be paid to the general health of the pa- 
tient. Cod-liver oil and quinine should be administered with a nutri- 
tious and non-stimulating diet. A residence at, and prolonged use of 
the waters of some alkaline spring will often be found of great service. 
Diluent alkaline drinks and milk should be the sole articles of diet in the 
acute stage. 

When a tumor exists and can readily be reached through the integument, 
aspiration may be performed, after which the question of a free perma- 
nent external opening will present itself, and must be decided by the pecu- 
liarities of the case. 

HYDRONEPHROSIS . 

Hydronephrosis is a chronic, non-inflammatory affection of the pelvis 
of the kidneys. Whenever the flow of urine through the ureters into the 
bladder is permanently obstructed, the urine collects in the pelvis and in- 
fundibula, compressing the renal substance, which becomes partially or 
completely atrophied, so that after a time the kidney is converted into a 
sac or pouch. This condition has received the name of hydronephrosis, 
or dropsy of the kidney. The dilatation may affect the ureter and pel- 
vis, or only the pelvis. 

Morbid Anatomy.— In a kidney that is the seat of moderate hydronephro- 
sis following simple dilatation of the pelvis, the papillae will become flat- 
tened, hardened and shrunken, and gradually disappear. The remaining 
portion of the renal substance gradually diminishes from the pressure and 
becomes more or less tough and resistant. In extreme cases the kidney 
substance finally entirely disappears and the kidney is converted into a large 



HYDRONEPHROSIS. 



627 



multilocular cyst ; sometimes it is unilocular. At times such a cyst at- 
tains a size as large as a child's head ; there is a case recorded where the 
whole abdominal cavity was occupied by an enormous tumor containing 
sixty pounds of fluid. Some healthy kidney substance will nearly always 
be found in its walls. That portion of the ureter which is the seat of dila- 
tation may reach the size of a small intestine, has a blue-white color, its 
walls become greatly thickened, and it may become convoluted. 

The fluid contained in hydronephrotic cysts is generally altered urine. 
It is much more watery than normal urine, containing more or less of the 
urinary salts ; it may also contain blood, pus, epithelium and some albu- 
men. Sometimes it is perfectly clear ; it is usually alkaline. Adhesions 
frequently form between the enlarged kidney and neighboring organs. 

Etiology. — Closure of a ureter which gives rise to hydronephrosis may 
be due to compression by a tumor external to its walls, especially rectal or 
uterine, or to the impaction of a calculus, blood-clot, or mass of echi- 
nococci within it, or to inflammation which has caused adhesion of its 
walls and complete obliteration of its lumen. A moderate degree of dila- 
tation of the ureter sometimes results from obstruction to the free dis- 
charge of urine from the bladder ; when this is the case the pelvic dilata- 
tion is bilateral, and can never become very extensive without destroying 
life, for when the pressure becomes equal to that within the blood-vessels 
the urinary secretion is entirely suppressed. Congenital defects often 
cause it. 

Symptoms. — The symptoms of hydronephrosis depend upon the nature 
of its cause and the extent of dilatation. If the sac is small and the op- 
posite kidney healthy, there may be no symptoms to indicate its existence ; 
there will be no diminution in the urinary secretion, as the healthy (usu- 
ally hypertrophied) kidney performs the work of its diseased fellow. 
There may be pain in the lumbar region. 

As soon, however, as the tumor attains sufficient size to be readily felt, 
the existence of hydronephrosis may be determined by it. This tumor 
causes no pain or inconvenience except by its pressure. With double hy- 
dronephrosis ursemic symptoms may develop suddenly. The nephritic 
tumor is fluctuating, usually lobulated, and gives a tympanitic resonance 
in front on percussion unless the colon has been pushed aside. If the ob- 
struction to the escape of urine from the kidney is temporarily removed, 
its removal will be followed by a sudden diminution and disappearance of 
the tumor, coincident with a sudden discharge of a large quantity of pale 
urine. Such au occurrence is almost pathognomonic of hydronephrosis. 
Constipation, from pressure of the tumor on some portion of the intestine, 
is not infrequent. 

Differential Diagnosis. — Hydronephrotic tumors may be confounded with 
ovarian cysts, ascites, hydatid cysts, and pyonephrosis. 

They are distinguished from ovarian cysts by the presence of the colon 
in front of the tumors, by the absence of tympanitic percussion in the lum- 
bar region, and by a vaginal and rectal examination. 

Single hydronephrosis is distinguished from ascites by the non-existence 



628 



DISEASES OF THE KIDNEYS. 



of dulness in both lumbar regions. In ascites, when the position of the 
patient is changed, there is a change in the level of dulness, which never 
occurs in hydronephrosis, 

It is quite impossible to distinguish hydronephrosis from an hydatid 
cyst, unless the hydatid vesicles are found in the urine, or the hydatid fre- 
mitus is present. 

It is distinguished from pyonephrosis by the non-purulent character of 
the urine, and by the absence of constitutional symptoms. An aspirating 
needle will generally decide the diagnosis, for the watery urine withdrawn 
differs, chemically and microscopically, from the fluid obtained from hy- 
datid or ovarian cysts or the pus of a pyonephrosis or a perinephritic ab- 
scess. 

Prognosis. — The prognosis is more favorable in this than in any other 
form of renal tumor; yet it is always serious. When only one kidney is 
involved, life may be indefinitely prolonged, and there is always a possibility 
that spontaneous evacuation of the sac may occur. But cases are rec rded 
where — one kidney only being involved — it caused death by pressure on 
neighboring parts. If the healthy kidney becomes the seat of any form of 
nephritic degeneration, the prognosis becomes unfavorable ; complete sup- 
pression of the urine may then occur at any moment ; or if the impedi- 
ment which has obstructed one ureter extends so as to prevent the flow of 
urine from both kidneys, uraemic symptoms will be developed, and death 
speedily follow. 

Treatment. — In hydronephrosis the principal thing to be accomplished is 
the evacuation of the tumor. To accomplish this result it should be care- 
fully manipulated. This can readily be done, as the tumor generally causes 
no pain. If this does not cause its evacuation, aspiration should be re- 
sorted to. I now have a case under observation in which aspiration has 
twice been performed with complete relief to the patient, and the aspira- 
tion has not been followed by any unpleasant symptoms ; nothing is to be 
expected from medicinal treatment. 

CYSTIC KIDNEYS. 

Cysts of the kidneys are very frequently met with at autopsies, but they 
are of very little clinical importance, for if the cysts are of small size 
they give no symptoms during life. Cystic degeneration may have a con- 
genital origin, and both kidneys may be converted into a mass of cysts of 
sufficient size to entirely fill the abdominal cavity ; such conditions are 
usually associated with other congenital malformations. It is claimed that 
cysts originate in the epithelia or even in the fibrous stroma of the kid- 
ney. They are often found scattered through kidneys that are otherwise 
healthy. It is difficult to make any practical distinction between the 
cysts of a true cystic kidney and those occurring with cirrhotic kidney. 
They are usually situated in the cortical substance near the surface. 
Colloid cysts of the glomeruli are frequently surrounded by laminae of 
fibrin from hemorrhages within the capsule. 



KEK"AL CALCULI. 



629 



The contents of kidney-cysts vary in character even in the true cyst. 
They may contain a clear albuminous fluid ; sometimes it is gelatinous, 
containing phosphates, carbonates, cholesterin, and very rarely urea and 

uric acid. The vascular tuft 



in 

transformed 



a glomerulus 

into a cyst, is flattened against 
wall of the thickened capsule, and 
the cyst may be lined with pavement 
epithelia. 




Fig. 148. 
Cystic Kidney. 
Drawing showing a Vertical Median Section of a 
Kidney containing Cysts. 



Fig. 149. 
Cystic Kidney. 
Section from the Cortex of a Cirrhotic Kidney, show- 
ing the Epithelial lining of a small Cyst. 

A. Cirrhotic intertubular tissve. 

B. A small artery in transverse section showing the 

thickened coats. 

C. Cavity of a small cyst. 

D. Epithelial lining of the last, partly detached. 

(The extreme 'tenuity of this lining cannot be 
tvell shown in a wood-cut.) x 300. 



The origin of these cysts is obscure, although there is reason to believe 
that they are the results of dilatation of the kidney tubules and Malpighian 
bodies. Congenital cysts have their origin, as a rule, in the Malpighian 
bodies. Serous cysts are often found in kidneys that have undergone senile 
atrophy. They may be developed in the connective-tissue by an enlarge- 
ment of a lacunar lymph -space. 



EENAL CALCULI. 

Renal concretions vary greatly in shape and differ in their composition. 
They may be deposited in the tubes of the pyramids, in the cortical sub- 
stance, or in the pelvis of the kidney. Their development occurs at any 
age ; they are met with in the kidney of the foetus in utero and in the 
kidneys of the very aged. 

Morbid Anatomy. — In the kidneys of infants dying within forty-eight 
hours .after birth, brownish strise of amorphous urates will invariably be 
found running from the papillae to the base of the pyramids. In adults, 
urate of soda, in the form of crystals, may be found deposited in the 



630 



DISEASES OF THE KIDNEYS. 



white lines in the pyramids and cortical substance, both in the tubular and 
intertubular structure ; this is always associated with a gouty diathesis. 
Carbonate and phosphate of lime may be found deposited in the tubes and 
pyramids of the kidneys of old people, or in connection with diseases of the 
bones. By far the most frequent variety is uric acid. Some think that 
oxalate of lime forms the starting-point of uric acid deposits. Cystine, 
ammonio-magnesian phosphate, or urate of ammonia and the mixed urates 
may form nuclei of renal calculi. Mixed calculi are not uncommon. 

These different varieties of urinary concretions may be permanently im- 
pacted in the uriniferous tubes, and render them impervious and cause 



Drawing showing an" Impacted Renal {Mulberry) Calculus, A. The anatomical changes 
JB. Ousts. ^ 



vary: they may cause pyelitis, pyonephrosis, hydronephrosis, or abscess, 
or they may excite parenchymatous nephritis. 

Etiology. — The causes of the ditferent concretions found in the kidneys 
are very obscure. Uric acid is most frequently met with in infants. The 
deposits of lime and triple phosphates are most frequently met with in 
adults. They are caused by the precipitation (in the nascent state) of uric 
acid or oxalate of lime due to renal excess of insoluble uric acid, or to de- 
ficiency in water of the urine. A colloid material composed of mucus or 
blood globules or other animal base exists in all. They increase by accre- 
tion. Certain constitutional conditions are supposed to be favorable to their 
development, but the exact nature of the urinary changes has not as vet 




Fig. 150. 
Renal Calculi. 



cysts to be developed, or they 
may be washed down the tubes 
by the urine, and finally de- 
posit in the infundibula and 
pelvis of the kidney. They 
vary in number and size. A 
kidney may contain one or a 
large number of concretions. 
They usually vary in size from 
a pin's head to a hazel nut ; 
the larger ones may fill the 
whole pelvis ; the smallest con- 
stitute " kidney gravel" If a 
concretion becomes impacted 
in the pelvis, it may attain a 
very large size, weighing one 
or two ounces. The smaller 
calculi pass through the 
ureters into the bladder and 
are discharged ; the larger 
ones may permanently ob- 
struct the ureters and become 
the cause of pyo- or hydro- 
nephrosis. 



produced by renal concretions 



RENAL CALCULI. 



631 



been determined. In most cases, calculi that develop in the pelvis of the 
kidney have some foreign substance as a nucleus. These nuclei may be 
pus, blood, epithelium, or grains of pigment. The composition of the re- 
maining portions of the calculi depends upon the varying conditions of the 
urine which attend their development. 

Symptoms. — The symptoms which indicate the presence of renal calculi 
vary. In some instances they are well marked, in others very obscure. 
Usually, the existence of renal calculi is indicated by an aching pain in the 
lumbar region and loins, which frequently shoots into the testicles or labia 
and down the thighs, — by an itching at the end of the penis, and by a fre- 
quent desire to urinate. The urine often contains pus, blood and " tailed '■' 
epithelium from the pelvis of the kidney. These symptoms are usually 
aggravated by anything that disturbs the position of the calculus, espe- 
cially by violent exercise, or by jolting in driving or horseback riding. 

The symptoms often assume the characteristics of "renal colic," due to 
the passage of the calculus along the ureter to the bladder ; this may occur 
after violent exercise or without any assignable cause. The attack may be 
sudden, or there may have been uneasiness in the loins for some time. The 
passage of a calculus along the ureter into the bladder is marked by sudden 
and intense pain in the region of the affected kidney. This pain radiates 
in various directions, but mainly toward the hypogastrium, testis, inside of 
the thigh and end of the penis. There is a constant desire to micturate, — 
"tenesmus of the bladder," — but the urine is scanty or suppressed, and 
what is passed is of a smoky, high color, often bloody, and is discharged in 
drops, the individual at the time experiencing a painful burning sensation. 
When hemorrhage is profuse, elongated blood clots are not infrequently 
found in the urine. The testicle of the affected side is retracted. As the 
pain increases in severity the patient rolls from side to side and shrieks 
with pain. His countenance becomes pale and the surface of the body is 
covered with a cold perspiration. The pulse is small and the hands and 
feet are cool. The severe paroxysms of pain are often attended by violent 
and frequent vomitings. There is great anxiety, and if the patient is of a 
very nervous temperament convulsions may occur. If the attack is pro- 
longed there is a slight rise in the temperature. Syncope is common dur- 
ing the attack. 

The duration of these attacks varies. Sometimes they are only of a few 
hours' duration, at other times they may be prolonged for days ; again, 
temporary remissions may occur, followed by violent exacerbations. 

As the calculus reaches the bladder the pain suddenly subsides, with a 
sense of relief, and the patient is often conscious of its passage into the 
bladder. After the passage of a calculus into the bladder it will soon be 
found in the urine voided. Occasionally calculi become impacted in some 
portion of the ureter. In such cases the subsidence of the pain is more 
gradual and less complete, and signs of hydronephrosis follow, and a tumor 
may be felt in the region of the kidney. By placing the patient on his 
back with his knees drawn up, the enlarged kidney may be pressed forward, 
and with the other hand in front it may be pressed backward and below 



632 



DISEASES OF THE KIDNEYS. 



the margin of the ribs. In the young and in those who are thin this 
method will aid very much in the diagnosis. Renal calculi may attain a 
large size and destroy extensive portions of the kidney, and yet not a single 
symptom may be present to indicate their existence. Again, the signs of 
renal calculi may exist for a long time, and finally atrophy of the kidney 
occurs, or they may become encysted and cease to give any indication of 
their presence. 

Differential Diagnosis. — Renal calculi may be confounded with neuralgia; 
the seat of pain is the same, and the neuralgic pains are often severe and 
paroxysmal ; but the urinary symptoms and an examination of the urine 
will make the differential diagnosis. 

The passage of blood-clots or hydatids through the ureter, causing renal 
colic, cannot be distinguished from the passage of renal calculi, unless the 
antecedent history is known and appreciated, and a subsequent urinary 
analysis is made. 

The irritation produced by an impacted calculus on the right side will 
not long be mistaken for perityphlitis, if careful and repeated examinations 
of the urine are made. Frequently, the abnormal conditions of the urine 
which indicate the presence of renal concretions are present only after vio- 
lent exercise. 

Prognosis. — The prognosis in renal calculus is good, unless the calculi 
become impacted and obstruct the ureter, or are of too large size to pass 
through the ureter to the bladder. In these conditions the prognosis is 
the same as in similar conditions in pyelitis, pyonephrosis and hydro- 
nephrosis. Should both kidneys be involved, the prognosis is exceedingly 
unfavorable. 

Treatment. — Since the tendency to the formation of renal calculi is usu- 
ally persistent and develops in patients of a gouty or rheumatic diathesis, 
the most important indication for treatment is found in the constitutional 
condition. All the directions given for the constitutional treatment of 
gout and the uric acid diathesis apply with equal force here, and there is 
reason to believe that the faithful use of alkaline waters not only delays, 
but often arrests, the formation of renal concretions. It is claimed that 
some of the natural waters exert within the body something of that solvent 
action upon calculi which they are known to possess under experimental 
conditions. Solutions of carbonate of soda, or, better, lithia or the Carls- 
bad, Vichy, or Ems natural waters, are among the more valuable agents. 
The American lithia waters are also efficacious. 

The paroxysms which attend the passage of renal calculi, or so-called 
nephritic colic, must be relieved by the careful administration of morphine 
hypodermically, warm baths, and the application of hot poultices to the 
loins and abdomen. The danger of opium poisoning developing upon the 
sudden cessation of pain attending the passage of a calculus from the ureter 
into the bladder must be borne in mind. In most instances, when the pain 
is intense and the vomiting constant, inhalation of chloroform will be found 
to give the most speedy and sometimes permanent relief. Change in the 
position of the patient, and manipulation of the abdomen along the course 



NEW GROWTHS IX THE KIDNEY. 



033 



of the ureters, may sometimes dislodge a calculus aud facilitate its 'passage 
iuto the bladder. The treatment during the interval between the parox- 
ysms which mark the passage of renal calculi will depend upon the changes 
which have occurred in the kidne*ys; the surgical treatment alone is appli- 
cable to cases of impacted calculus associated with pyelitis or pyonephrosis. 
The means to be employed for the relief of these conditions when not 
associated w r ith obstruction of the ureter have been considered under 
Pyelitis. 

]STEW GROWTHS IN THE KIDNEY. 

{Renal Cancer.) 

Renal Cancer may occur as a primary or secondary affection. When sec* 
ondary, its developments usually are of small size, and may occur in both 
kidneys. When primary, it is limited to one kidney, which soon forms an 
enormous tumor. 

Morbid Anatomy. — Both primary and secondary cancer of the kidney are 
generally of the medullary variety, and develop in the form of circumscribed 
nodules in the cortical substance, or occur as a diffuse infiltration. The 
medullary cancer, however, may be nearly as hard as scirrhus. Colloid can- 
cer is rare. It develops from the fibrous stroma of the cortical substance. 
Sometimes a whole kidney is transformed into a cancerous mass, which at- 
tains an enormous size, filling up a large portion of the abdominal cavity. 
The average weight of a cancerous kidney is over eight pounds; it has 
weighed thirty-one pounds in children. Secondary cancer (bilateral) never 
reaches a yery large size. The kidney tissue is always intensely congested ; 
it is often associated with cancer of the testicle. 

The pelvis, ureters, the veins, the peritoneum, colon, and even the skin 
adjacent to the neoplasm may be involved. The lymphatics and adjacent 
glands are always enlarged. With the growth of the cancer all traces of 
renal structure become obliterated and the diseased organ becomes adher- 
ent to the adjacent tissue. Hemorrhages occurring in the mass at varying 
points give an appearance called "fungus haematodes." Sometimes a can- 
cerous kidney is movable, • no adhesions taking place with surrounding 
parts. The minute anatomical changes that take place in cancerous devel- 
opments in the kidney, are similar to those which occur in cancerous devel- 
opments in the other organs of the body. 

Etiology. — The etiology of renal cancer is as obscure as the general eti- 
ology of cancer. In a large proportion of cases it depends either upon 
hereditary taint or local infection. Primary cancer' occurs oftenest before 
the tenth and after the fiftieth year of life. 1 Secondary cancer may occur 
by continuity or from metastasis; e.g., mamma, uterus, liver, stomach, 
testis or supra-renal capsules. Males suffer oftener than females ; the right 
kidney oftener than the left. 



1 Oat of Rohre's 107 cases of primary renal carcinoma, 37 were under ten ; 30 were over fifty years of 
age. 



634 



DISEASES OE THE KIDNEYS. 



Symptoms. — Cancer of the kidney often remains latent for a long time. 
Its development is marked by gradual emaciation, for which no cause can 
be assigned. It may not be attended by pain in the lumbar region ; if 
pain is present it is not characteristic. There may be no change in the 
renal secretion ; but as the disease advances more or less profuse hemor- 
rhages occur ; sometimes the blood appears in the urine in clots, in which 
elements of the neoplasm may be found. 

As -the disease advances, and the cancerous mass reaches a large size, it 
can be felt through the abdominal walls. The form of the tumor and its 
immobility will enable one to distinguish it from enlargements of the liver 
or spleen. Very large cancers of the right kidney may displace the liver 
upward. The tumor is usually nodulated and firm, gives a dull or tym- 
panitic note on percussion, and can be tilted forward. The colon lies in 
front of it. Aortic impulse may cause it to pulsate. When hematuria is 
present it is constant. In its advanced stage the countenance assumes the 
characteristic cancerous cachexia. 

Differential Diagnosis. — Cancer of the left kidney is distinguished from 
splenic tumors by its lower site, absence of splenic notch, absence of blood 
changes, by its nodulated outline, and by hematuria. 

From perinephritic abscess it is distinguished by absence of febrile 
symptoms, by its slow growth, and absence of fluctuation. 

Cancer of the right kidney may be distinguished from hepatic tumors by 
an area of tympanitic percussion between the liver and the tumor. Reli- 
ance is also to be placed on signs peculiar either to hepatic or renal 
lesions. 

Tumors of the liver or spleen are carried down on full inspiration ; renal 
cancer is not. Faecal and ovarian tumors have peculiar characteristics. 1 

Abscess and hydatid tumors are distinguished by introducing an aspirat- 
ing needle, which withdraws either pus or a saline fluid containing por- 
tions of the echinococci. 

An ovarian tumor when tapped is found to contain a peculiar ovarian 
fluid ; fluid from a hydronephrosis contains some urinary elements. • 

Prognosis. — The prognosis is always bad. But cancer of the kidney is 
tolerated longer than that of any other organ. Death is reached either by 
the exhaustion produced by repeated and profuse hemorrhages, or as a con- 
sequence of some intercurrent disease, as parenchymatous nephritis in the 
unaffected organ. The lungs, retro-peritoneal glands, and liver may be 
secondarily invaded. A year in children and two years in adults is its 
average duration. Intestinal fistulae may be formed, and the skin may be 
ulcerated, as sequelae to cancer of the kidney. Dropsy may result from 
compression of the vena cava. The vertebrae may be eroded. 

Treatment. — Its treatment is palliative. The principal things to be ac- 
complished are to relieve pain by hypodermatics of morphine and to sustain 
the patient. 

1 See " Intestinal Obstruction.'''' 



TUBEECULAB DISEASE OF THE KIDNEY. 



635 



Of the new growths met with in the kidney, cancer is the only one which 
has any special clinical significance. 

Leukcemic tumors are occasionally met with as small whitish masses, de- 
veloped in the intertubular tissue. They are composed of lymphoid cells, 
and are always associated with similar growths in the other viscera. These 
" lympJiadenomata " are developed in connective-tissue ; the liver is usually 
simultaneously involved. 

Syphilitic gummata are also met with in the kidneys in the form of small 
nodules, in connection with similar developments in the other organs ; 
cicatrices may be left, usually in the cortex, but sometimes in the medulla 
of the organ. G-ummata destroy the tubules. Patches of "fibrous tissue" 
independent of gummata occur in kidneys of those who are syphilitic. 

Fibromata may appear in the pyramids of kidneys in the form of small, 
white, fibrous nodules. The remaining portion of the kidney will be nor- 
mal, or the seat of parenchymatous nephritis. 

Lipomata include those accumulations of fatty tissue which are some- 
times developed around the capsule of the kidney and in the pelvis of 
atrophied kidneys ; sometimes in the cortical substance beneath the cap- 
sule small, rounded, fatty tumors are found. Growths of bony, muscular, 
and glandular tissue have also been met with in a few instances. 

Sarcomata have been found in young children. 



TUBEKCULAE DISEASE OF THE KIDIS^Y. 

Tubercles are developed in the kidneys as an advanced lesion of gen- 
eral tuberculosis. Primary tuberculosis of the kidneys is occasionally met 
with in young subjects. 

Morbid Anatomy. — At first, gray miliary tubercles are found throughout 
the affected kidney, principally in the pyramids. The tubercles may origi- 
nate in the stroma or in the cortex, in the arterioles separating the pyra- 
mids of Perrein, or on the surface of the kidney. Later, solid, cheesy, yel- 
low masses are found in the pyramids and in the cortex. The organ is en- 
larged and lobulated. The mucous membrane of the pelvis and ureters is 
thickened, infiltrated, and often ulcerated. When the ureter is involved 
diminution of its lumen may result in hydro- or pyonephrosis. The larger 
yellow masses are found at the junction of the cortex and medulla ; they 
are usually softened at their centres, containing a puriform debris ; the pel- 
vis and calices are also dilated and filled with caseous pus or with a semi- 
fluid pulp rich in cholesterin. The tubules are compressed, and their epi- 
thelium undergoes granular and fatty change. An inflammatory process 
may coexist (strumous nephritis, of English authors), and the entire mu- 
cous membrane of the geni to-urinary tract may be involved. Calcareous 
nodules and incrustations are found mingled with tubercle granules. Every 
portion of the genito-urinary tract, especially in the male, may show tu- 
bercle granulations. 



636 



DISEASES OE THE KIDNEYS. 



Etiology. — Eenal tuberculosis generally occurs in the young. Men are 
far oftener affected than women, the right kidney oftener than the left. 
It may occur as a primary tuberculosis, as part of acute miliary tuberculo- 
sis, or it may complicate chronic pulmonary phthisis. 

Symptoms. — The symptoms are essentially those of pyelitis ; such as pain 
and tenderness in the loins, an irritable bladder, and scalding urine, which 
contains mucus, pus, and blood. As the disease advances, hectic fever de- 
velops, with the coexistent symptoms of intestinal or pulmonary tubercu- 
losis. The urine will contain albumen (no casts), and under the microscope 
it is found loaded with fatty granules, lymph cells, blood corpuscles, 
and debris of connective-tissue infiltrated with small and fatty granular 
cells. A flaky, cloudy deposit always occurs in this urine, unless the 
ureter from the affected side is impermeable. If masses of cheesy mate- 
rial or bacilli are found, they establish the diagnosis. A renal tumor may 
■sometimes be detected. 

Differential Diagnosis. — The diagnosis rests upon the hereditary history, 
the presence of tubercles in lungs or prostate, on lymphatic enlargements, 
cheesy, puriform urinary debris, and the presence of a painful renal 
tumor. 

Prognosis. — The prognosis is very unfavorable ; the complications are 
tubercle in any or all of the other organs of the body, cystitis, pyelitis, 
pyelo-nephritis, abscess, hydro- and pyo-nephrosis, waxy kidney, peritoni- 
tis, and urinary suppression. 

The Treatment is altogether palliative. 



PARASITES IIS" THE KIDNEY. 

Eenal parasites are occasionally met with ; the most frequent is the echi- 
nococcns. The cysticercus cellulosus, strongylus gigas, pentastoma den- 
ticulatum, distoma haematobium, spiroptera hominis, and dactylus aculea- 
tus are parasites of rare occurrence. They are sometimes found embedded 
in the kidney. The symptoms which attend their development, and the 
manner in which they gain entrance intc the kidney, are obscure. 



HYDATIDS OF THE KIDNEY. 

While hydatids of the kidney are less common than hydatids of the 
liver, the affection occurs under similar conditions. 

Morbid Anatomy. — A kidney the seat of hydatids is sometimes enormous- 
ly enlarged ; as a rule, a spherical cyst projects from the surface whose 
fibrous wall is derived from the kidney. The inner cyst wall may or may 
not be covered with daughter vesicles containing scolices, but a clear saline 
fluid always distends it ; the pressure of the cyst causes atrophy of the kid- 



PERINEPHRITIS. 



637 



ney structure. These cysts may suppurate and be changed into a shriv- 
elled cyst with caseous contents in which are embedded echinococci hook- 
lets. They may rupture into the perinephritic tissue and give rise to a 
lumbar abscess, or into the lungs, intestine, stomach, peritoneum, or pel- 
vis of the kidney. 

Symptoms. — A nephritic tumor is the first noticeable sign. A vesicle 
passing from the pelvis to the bladder gives rise to the symptoms of renal 
colic. An examination of the urine may reveal echinococci hooklets. In 
all cases the exploring trocar will withdraw a clear saline fluid containing 
hooklets. 

Percussion may elicit the hydatid fremitus. If pus or blood appears in 
the urine it results from complicating inflammation or suppuration set up 
by the cyst or its contents. 

Prognosis. — This is always uncertain. It is possible for a cyst to grow 
so rapidly as to cause death of the echinococci by pressure, or the fluid 
necessary to their life may be insufficient, or it may become so altered that 
calcareous changes will occur and then a calcareous mass may remain for 
life and cause no further harm. An' echinococcus may be the nucleus of 
a stone in the bladder or in the pelvis of the kidney. 

Treatment. — Aspiration should always be practised, and if it is not fol- 
lowed by adhesive inflammation, iodine should be injected into the cyst. 

PERINEPHRITIS. 

{Perinephritic Abscess.) 

This is an inflammation of the connective- tissue surrounding the kidney : 
it may terminate in suppuration, or in the formation of fibroid tissue. 

Morbid Anatomy. — The cellular tissue about the kidney becomes cede- 
in atous and the seat of inflammatory exudation, causing the cellular, adi- 
pose and adjacent retro-peritoneal tissues to become solid and firm. Sup- 
puration may commence at the centre of the mass, leading to the formation 
of one large abscess ; or, if it commences at numerous points and gradu- 
ally extends, a number of circumscribed abscesses are formed. The tu- 
mor formed may become so large as to reach from the level of the liver or 
spleen to the iliac fossa, and may project forward and cause bulging of the 
abdominal wall. The pus contained in the abscess may be odorless, or thin, 
fetid and ichorous, especially if mixed with urine. The pus may have an 
odor of faeces independent of perforation from the toivel into the abscess 
cavity. This process may end in gangrene. The peritoneum over the tu- 
mor is thickened. 

A perinephritic abscess may open into the lung, pleural cavity, or bron- 
chi, by extending into the retro-peritoneal tissue and then through the dia- 
phragm. The pus may burrow along the psoas muscle and appear as a 
psoas abscess on the thigh, or abdomen. Spontaneous opening usually 
occurs, externally, in the lumbar region. The bladder, ureter, pelvis of the 
kidney, peritoneum, and colon have all been perforated by perinephritic 
abscesses. Sometimes inflammation of the perinephritic tissue is not fol- 



638 



DISEASES OF THE KIDNEYS. 



lowed by suppuration, but at the autopsy a thick, tough, fibrous mass is 
found occupying the place of the (so-called) adipose capsule of the kid- 
ney. The same result may follow discharge of the abscess and cicatriza- 
tion. 

Etiology. — Perinephritis may be caused by pyelitis, suppurative nephri- 
tis, blows, falls, strains, parasites, or wounds of the kidney or the tis- 
sue about it. It may occur in pyaemia or in the course of any of the ex- 
anthems or specific fevers. It may also complicate pelvic cellulitis, psoas 
abscess, and perityphlitis. It occurs more frequently in men than in 
women. 

Symptoms. — Eecurring rigors are among the first symptoms, followed or 
accompanied by pain in the lumbar region — which is increased by move- 
ment and firm pressure — shooting down toward the testicle. The pulse is 
rapid and feeble. The temperature rises to 100°-105° F. The skin at first 
is dry, but later it is covered with a profuse perspiration. There is ano- 
rexia, great thirst, and constipation. The urine is usually slightly dimin- 
ished in quantity ; otherwise it is normal, unless pyelitis or nephritis should 
coexist. 

Physical Signs. — A tumor forms in, or a little below, the lumbar region ; 
it rapidly increases in size ; at first it is hard ; later it gives signs of deep 
fluctuation. The skin over it is cedematous and pale. The tumor is im- 
movable and cannot be separated from the kidney, but can readily be dis- 
tinguished from the spleen or liver enlargements. An exploring trocar 
will establish the diagnosis. 

Differential Diagnosis.' — The differential diagnosis between perinephritic 
abscess and pyonephrosis and hydronephrosis has already been given. 

It is distinguished from suppurative nephritis by the presence of a tumor, 
and by the absence of casts, albumen, blood or mucus in the urine. 

From extravasation of blood due to rupture "of an aneurism, it is distin- 
guished by fever, rigors, & fluctuating tumor, and the absence of the causes 
and physical signs of aneurism. 

Prognosis. — A perinephritic abscess is always serious. Its duration is 
usually from two to four weeks ; in some cases several months have elapsed 
before the tumor has subsided. Its discharge into the intestine or bladder, 
or the establishment of an external opening, may be regarded as favorable. 
With an early diagnosis and prompt surgical interference the prognosis is 
good. Some regard many " cures" of hip-joint disease without deformity, 
as in reality cases of suppurative perinephritis. 1 

Treatment. — A free opening should be made as soon as the diagnosis is 
established. Grainger Stewart states that early counter-irritation by blister- 
ing is useful, and that iodide of potassium internally and iodine externally 
may prevent suppuration ; my experience does not sustain this statement. 
Yet incision is safer than aspiration ; after an opening is made the finger 
should be introduced into the abscess- cavity and any adhesions that may be 



1 Amer. Jour. Med. Sciences, April, 1877, and Oct., 1878. V. P. Gibney, M.D. 



FLOATING OR MOVABLE KIDNEY. 



639 



present should be broken down. Then a drainage tube should be intro- 
duced. Antisepsis should be practised during the operation and with 
subsequent dressings. Stimulants and concentrated fluid nutrition should 
be freely administered. 

FLOATING OR MOVABLE KIDNEY . 

As a congenital peculiarity one or both kidneys may be movable, and in- 
stead of occupying their normal position may lie upon the brim of the 
pelvis, or be freely movable in the loose retro-peritoneal connective-tissue 
which surrounds them, and the peritoneum may be so reflected in front 
and behind them as to allow their free motion. The displacement of the 
kidney under any one of these conditions may follow parturition or a severe 
shock from a fall. It is met with more frequently in females than in males. 

Morbid Anatomy. — A congenital displacement is distinguished from an 
acquired displacement by the abnormal arrangement of the vessels of the 
kidney and its peritoneal coverings. The extent of the mobility in any 
case is determined by the length of the vessels which form the pedicle. 
Movable kidneys are almost always surrounded by connective-tissue forma- 
tions, and after having been once movable they may become firmly fixed 
again in their normal or in an abnormal position. 

Symptoms. — A displaced kidney is usually felt midway between the free 
border of the ribs and the umbilicus. If the right kidney is displaced it is 
apt to make its appearance just below the liver ; it may be pushed upward 
and backward into its normal position, but it will return as soon as the 
support is withdrawn. 

If a displaced kidney can be grasped its pressure causes a sickening sen- 
sation. If it gets compressed or otherwise injured, it may become painful, 
tender, and swollen. Otherwise it may give rise to no symptoms and be 
recognized only by accident. 

Differential Diagnosis. — Its diagnosis rests — 1st, on the shape and size of 
a tumor corresponding to that of a normal kidney ; 2d, when the tumor 
can be felt in front there will be an abnormal tympanitic resonance over 
the normal position of the kidney ; 3d, the tumor can be pressed back into 
the normal kidney region ; 4th, the peculiar sickening sensation produced 
by its manipulation. 

Prognosis. — Such kidneys are never a cause of death. Many observers 
have doubts in regard to the probable occurrence of a floating kidney. 
There is little post-mortem evidence in its favor. I have never made but 
one diagnosis of this condition during life that was sustained bv a post- 
mortem examination. 

Treatment. — When a movable kidney is painful, rest is indicated, and a 
concave abdominal pad so adjusted as to fit the form and position of the 
kidney tumor should be worn, 



640 



DISEASES OF THE KIDNEYS. 



HEMATURIA. 

Hematuria is the passage of urine containing blood. The blood may 
have its origin at any point from the Malpighian tuft to the orifice of the 
urethra. As it is a symptom, it has no morbid anatomy ; its causes con- 
stitute its pathology. 

Etiology. — Local causes. — (1) In the kidney the conditions which induce 
hematuria are active and passive hyperemia, acute (rarely, if ever, chronic) 
suppurative nephritis, or surgical kidney, infarctions (including embolism 
and thrombosis), tuberculosis, a single or multiple pyaemic abscess, pyeli- 
tis (especially when the pyelitis is calculous), stone in the kidney, or in the 
pelvis of the kidney, and, in a few cases, hydro- and pyonephrosis. Crystals 
in the tubules may induce it. Among kidney causes may be included the 
drugs which cause hematuria, e. g., turpentine, cubebs, copaiba, canthar- 
ides, etc. 

(2) The causes that have their seat in the ureters are ureteritis, cancer, 
polypi, ulcers, and calculi. 

(3) The Madder causes are cystitis (but only when very acute and accom- 
panied by erosion and ulceration), cancer, abscesses in the vesical walls, poly- 
pus of the bladder, stone in the bladder, rupture of the bladder, tubercu- 
losis, specific or non-specific ulcers. Dilatation and varicosity of the vesical 
veins may cause it, called oftentimes i( hemorrhoids of the bladder." 

(4) The urethral causes are many : urethritis (non-specific and specific), 
peri-urethral abscess, chordee, cancer, fracture of penis, rupture of prostatic 
abscess, an enlarged prostate, urethral, polypi (especially in females), caustic 
injections, chancre and chancroids, phimosis, impacted stone, and new 
growths in the prostate. 

The general causes of hematuria are acute infectious diseases, fevers, 
especially malarial, scurvy, purpura, the condition known as haemophilia 
(the bleeders), and certain central nervous diseases (see Myelitis). 1 

Symptoms.— The urine may be almost black and loaded with clots, or it 
may be only slightly smoky or pinkish in color. It is albuminous ; under 
the microscope swollen or shrunken corpuscles are found, the degree of al- 
teration depending on the time they have remained in the urine. If equal 
parts of tincture of guiacum and oil of turpentine are shaken together to 
form an emulsion, an intense blue color will arise when bloody urine is 
slowly added to it. 

To determine the source of the hemorrhages the following rules may be 
observed : — urethral hemorrhages are independent of micturition, as only 

1 There is a variety of hematuria which occurs in tropical countries (Egypt, Brazil and Cape of Good 
Hope especially) caused hy a fluke called Bilharzia hsematobia, a parasite (atrematodc hasmatozoon), which 
is endemic. Dr. John Harley discovered this parasite in the blood of a patient in South America. It is 
one-ralf to three-quarters in. long, and is found chiefly in the vessels of the portal system and of the blad- 
der. The eggs are found in the urine ; they are 1-100 to 1-189 in. in length, and are peculiarly pointed at 
one end, the whole contour, however, being ovoid. This parasite causes thickening, ulceration, ecchy- 
moses and large blood extravasations in the mucous membrane in whose vessels it is lodged. 



HEMATURIA. 



041 



a residue of blood is washed out at the beginning of the flow of urine. The 
history will aid and inspection will probably reveal the true state of affairs ; 
albumen, casts and epithelial cells are not often found in urine when it 
becomes bloody in the urethra. The Madder may be suspected as the seat 
of the hemorrhage when blood flows only at the time of micturition, and 
follows the discharge of urine ; should the stream suddenly cease, a stone 
or blood-clot blocks up the opening of the urethra into the bladder, and 
this will be well-nigh diagnostic. Clots following the flow of urine indicate 
cystic disease. When they precede the flow or occur with it, urethral dis- 
ease is indicated. Should blood globules, albumen, casts, and blood moulded 
in the form of renal tubules be found in the urine, renal disease may be re- 
garded as the cause of the hematuria. In renal hemorrhage blood is 
mingled with the urine, and is commonly as profuse at the commencement 
as at the end of micturition. 

Should hematuria be combined with the symptoms of stone in the blad- 
der, of pyelitis, or of cystitis, the source of the hemorrhage is then no longer 
a matter of doubt. Sir Thomas Watson states "that slender cylinders of 
fibrin in the ureter indicate renal disease or commencing inflammation of 
the ureter." 

In "endemic" haematuria the diagnosis rests on discovering the trema- 
tode or its ova in the urine or fasces ; it causes pain along and over the 
genito-urinary tract. 

In the so-called false haematuria the urine contains only haemoglobin, 
the microscope failing to discover any corpuscular elements in the urine. 
It is also called Immoglobinuria, hcematinuria, and (when occurring peri- 
odically), intermittent or paroxysmal hcematuria. The haemoglobin of the 
blood is set free in one of two ways : either the extravasated corpuscles dis- 
integrate or the haemoglobin escapes without rupture of the capillary walls. 
Once free in the blood the kidneys eliminate the haemoglobin. Fevers, 
poisons, gases, and cold are said to cause this condition. 

When intermittent it is usually dependent on malaria, but a malarial 
cause need not necessarily exist for the paroxysm to occur. Chills, sweat- 
ings, and, at times, a rise in temperature attend the discharge of the red- 
dish urine, which soon shows a granular, brownish sediment. Albumen, 
and hyaline and granular casts are very often present, independent of renal 
disease. In severe cases the patient becomes anaemic and cachectic. 

Quite recently a disease has been described called "melaenic fever," 
resembling somewhat in its constitutional symptoms acute yellow atrophy 
of the liver and yellow fever. The urine is brown-black and contains al- 
bumen, casts, and a large quantity of blood cor}:>usc]es (not haemoglobin 
alone). Suppression often occurs, and the case ends fatally. 1 

Differential Diagnosis. — The points of differential diagnosis have been suf- 
ficiently considered in its etiology. First, care must be taken by micro- 
scopical examination and spectrum analysis to positively determine that 
blood corpuscles or haemoglobin are actually present in the urine. Then 



41 



1 Virginia Med. Monthly, February, 1880. 



642 



DISEASES OF THE KIDNEYS. 



a study of its causes and accompanying symptoms renders the diagnosis 
comparatively easy. 

Prognosis. — The prognosis in hematuria depends on its cause. Endemic 
haematuria is never the direct cause of death, but it may lead to extreme 
anaemia. Paroxysmal haemoglobinuria is rarely fatal. 

Treatment. — When the hematuria is slight and of short duration no 
special treatment is required ; if profuse or persistent the patient should 
be placed in a recumbent position, ice-bags applied over the seat of the 
hemorrhage, and haemostatic remedies used, such as gallic or tannic acid, 
ergot, acetate of lead, and astringent ferric preparations. If the haema- 
turia is of parasitic origin prophylaxis demands that the drinking water 
be filtered and boiled ; to expel the parasites male-fern or chloroform may 
be given internally. Harley advises belladonna and henbane. Quinine is 
indicated in all forms of paroxysmal haematuria or haemoglobinuria. If 
the hemorrhage is from the bladder persistent weak astringent injections 
may be employed. 

CHYLUEIA. 

Chyluria is characterized by the occasional or continuous discharge of 
urine which resembles milk when passed and coagulates into a jelly mass on 
standing. 

Morbid Anatomy and Etiology. — The kidneys are usually found free from 
disease, and the affection is attended by no known constant pathological 
lesions. At one time it was regarded as a disease of defective assimilation 
which permitted the chyle to mingle with the blood; at another, a fault of 
the kidneys which allowed the unchanged chyle to be transuded with the 
urine. Neither of these explanations has been sustained by observation. 

There are at present many theories in regard to its causation : first, that 
there is a direct communication between the chyle-carrying vessels and the 
urinary tract ; second, that it is a symptom of piarrhaemia due to a de- 
ranged liver function ; third, that it is caused by an eczema along the 
urinary tract ; fourth, that it is due to hypertrophy of the lymph channels 
and their subsequent assumption of glandular functions ; fifth, that it is 
due to a parasite, but whether the action of the entozoon is on the function 
of the liver or causes irritation and rupture of the lymph and chyle chan- 
nels is not determined. 

Symptoms. — No disease pursues a more irregular course : no two cases 
exactly resemble each other. There may be pain in the loins and along the 
geni to-urinary tract, depression of spirits, and debility, before the urine 
becomes chylous ; or, the first sign may be a sudden flow of milky urine, 
having a whey-like or milky odor, made more perceptible by warmth. It 
soon coagulates on standing, but the trembling, jelly-like clot breaks down 
and the urine decomposes in a few hours. Bloody coagula, usually shreddy, 
may also form. White and red blood discs are found in varying quantity. 
Clots may form in the bladder, and during micturition the flow may sud- 



CYSTITIS. 



643 



denly stop from blocking of the urethra. The sp. gr. of the urine varies, 
(1.007-1.020). Heat and nitric acid cause a precipitate. Shaken with 
ether the urine loses its milkiness. Fat, albumen, and fibrin are all present. 

Blood analyses vary ; but when the filaria sanguinis hominis is not found 
in chylous urine it is found in a drop of blood taken from the finger, and 
vice versa. Hoppe-Seyler says blood in this disease resembles human 
lymph in its composition. Chylo-serous discharges take place also from 
axilla, groin, scrotum, and surface of the abdomen or inner comer of the 
eye. Chyluria is an intermittent disease, but there is no periodicity or 
regularity to it. 

Prognosis. — The disease runs a chronic course. Men have suffered on and 
off for fifty years. Change of climate does not seem to improve the out- 
look when the disease is once established. Sudden death may occur at any 
moment, even in those with fair health. Elephantiasis, phlebitis, hema- 
turia, " lymph-scrotum," craw-craw, leprosy, and furuncles are not infre- 
quent complications. 

Treatment. — This has been unsatisfactory. Turpentine and gallic acid 
are recommended. Iodide of potash and perchloride of iron are claimed to 
be highly beneficial. Mangrove and nigella sativa are used by the natives 
in places where chyluria prevails; sometimes they effect a cure, oftener not, 
however. Prophylaxis demands care in drinking water in a tropical re- 
gion, and first boiling or filtering it. 

CYSTITIS. 

Cystitis is an inflammation of the mucous membrane lining the urinary 
bladder. It is acute or chronic ; and it may be either catarrhal, croupous, 
or diphtheritic. The whole or part of the bladder may be involved j 
when "partial," it is limited to the neck and bas-fond. 

Morbid Anatomy. — In acute catarrhal cystitis the appearances are in no 
wise different from those observed when any mucous surface is inflamed. 
The small glands at the base of the bladder are enlarged and filled with a 
pearly secretion. The interior portion of the trigone is also studded with 
these pearly masses. They may form a circle about the neck of the blad- 
der. Intense (acute) cystitis may end in suppuration of the submucous 
connective-tissue, and ulceration of the mucous membrane may allow 
these submucous abscesses to empty into the bladder. 

When cystitis results in paralysis of the bladder, gangrene of the mu- 
cous membrane may occur ; then browuish-black, irregular patches are 
seen mingled with debris and phosphatic incrustations on the surface of 
the bladder. When the mucous layer is thus destroyed by gangrene, the 
urine infiltrates the neighboring tissue, and local or general peritonitis may 
result. An acute cystitis may lead to a pyelo-nepkritis. Ulcerating cys- 
titis occurs in typhoid and low eruptive fevers, in diphtheria, pyaemia, 
etc. It is called by some diphtheritic. ' The lesions in this form and in 



644 



DISEASES OF THE KIDNEYS. 



croupous cystitis are similar to those which take place in diphtheritic 
exudations on other mucous surfaces. (See Inflamtnation.) 

In chronic cystitis the mucous membrane is thick, blue-gray in color, 
and very tough. Muco-pus and viscid mucus are formed in large quanti- 
ties upon its surface. As the disease progresses a peri-cystitis consolidates 
the bladder with the neighboring organs and parts. Chronic catarrhal 
ulcers may form, and perforation of the bladder may result, and the 
vagina, rectum, or abdominal cavity may be entered, or an external open- 
ing may be formed through which pus is discharged. The muscular wall 
of the bladder may sometimes be half an inch thick, and the fasciculi 
give a ribbed appearance to the internal surface, called the "columnar 
bladder." The hypertrophy of chronic cystitis may be eccentric or con- 
centric. In some cases diverticuli are formed, in whose walls are dilated 
and tortuous veins. Some of these cysts are in the form of hernial protru- 
sions. In nearly all cases bacteria are found in abundance. 

Etiology. — • Acute cystitis is rarely idiopathic. 

It may result from the presence of foreign bodies, especially calculi. 
Blows may cause it. Protracted retention of urine has set up a rapidly 
fatal cystitis. 

It may be caused by some unknown blood condition, such as occurs in 
scarlet, typhus, and typhoid fevers, pyaemia, septicaemia, small-pox, and 
diphtheria ; it is a frequent complication of certain grave lesions of the 
nervous system, especially myelitis. 

Cystitis may result from the extension of an urethritis, a pyelitis, or a 
pelvic cellulitis. 

Chronic cystitis may be the sequela of acute cystitis or result from the 
retention of urine caused by an enlarged prostate or urethral stricture. 
Over-distention, atony or paralysis of the bladder, calculi, polypi, and 
neoplasms of all kinds cause it. Gout and some forms of kidney disease 
are accompanied by chronic cystitis. 

Symptoms. — Acute cystitis is always accompanied by frequent micturi- 
tion, only a few drops being voided at each attempt. After its passage 
the patient strains (as in the tenesmus of dysentery) to pass what he 
imagines is still retained in the bladder. There are dull, aching pains 
over the pubis ; sometimes the pains in the vesical region are agoniz- 
ing, and there is a constant burning sensation along the urethra. These 
local symptoms are not infrequently accompanied by rigors, and the tem- 
perature rises to 100°-101° F., with loss of appetite, sleeplessness, and a 
feeling of great anxiety or depression. 

The urine is cloudy, deposits mucus on standing, is alkaline, and some- 
times fetid. Microscopically, epithelium, pus and red blood-corpuscles 
are found. Membranous exudations may be found, especially in females. 
Niemeyer states that in the "croupous cystitis following cantharides 
poisoning and forcible forceps deliveries large tenacious false membranes 
are discharged " with the urine. 

Chronic cystitis is often only indicated by a frequent desire to pass urine. 



CYSTITIS. 



645 



Usually there is a constant;, dull, aching pain, or a sense of weakness oyer 
the bladder. The bladder is nearly always intolerant of its contents, no 
matter how long the catarrh has persisted. Hence only a small amount of 
urine will be passed with each act. Distention and muscular hypertrophy 
of the bladder often give rise to an abdominal tumor reaching as high as 
the umbilicus ; it may contain from two to eight pints of urine j as large 
a quantity as this, in some cases, may constantly remain in the bladder, 
only so much urine being passed as exceeds this amount, and then a patient 
will be passing yery nearly a normal quantity, and the introduction of the 
catheter may remove a quart of stinking, alkaline urine, which, when it 
stands, divides into two parts, a lower thick, turbid, gelatinous, coherent 
and opaque mass — the supernatant layer being clear. The " glairy mucus " 
so frequently described in this connection is only met with when the urine 
is ammoniacal and also contains pus ; it is formed by the reaction of the 
alkali upon the pus. Chronic cystitis accompanied by enlargement and 
atony of the bladder often eventuates in ammonaemia, and then typhoid 
symptoms are developed. Great local pain, emaciation and occasional 
bloody urine indicate ulceration. Acute suppurative inflammation of the 
bladder, accompanied by hectic, rigors, and extreme exhaustion, may accom- 
pany acute suppurative nephritis. 

Differential Diagnosis. — Pyelitis often resembles cystitis closely in its sub- 
jective symptoms ; there may be the same pain referred to the bladder, 
and the same frequent desire to micturate. In pyelitis the lumbar pain, 
the "tailed " cells in the urine, the even admixture of pus with the urine, 
the acid reaction, and the absence of ropy, gelatinous mucus, are symptoms 
in marked contrast to those of cystitis. 

Prognosis. — The prognosis depends upon the cause ; in general it is good. 
Chronic cystitis may continue for years ; the longer it continues the less 
chance there is of recovery. Acute cystitis is usually recovered from in 
about a week. 

Treatment. — In acute cystitis the patient must have. perfect rest. Warm 
hip-baths give relief. Leeching or cupping over the bladder is often of 
service. Suppositories of opium and belladonna, or rectal injections of 
the same, are always indicated, with large poultices and very hot fomenta- 
tions over the bladder. The bowels should be kept free with the mildest 
cathartics. An anodyne internally may be demanded for the relief of 
pain ; I have found chlorodyne the best. Twenty minims of liquor po- 
tassae in mucilage may be given three times in the twenty-four hours. 
Half-drachm doses of fluid extract of Indian hemp are highly recom- 
mended. The diet should be nutritious ; milk is to be preferred. No 
form of alcohol should be allowed ; the patient may drink freely of flax- 
seed or linseed tea, barley water, or decoction of triticum repens. In all 
cases the cause should be sought for and if possible removed. 

In chronic cystitis the catheter is to be regularly and persistently used. 
The bladder should be washed out with weak solutions of borax. Very 
weak solutions of salicylic acid, carbolic acid, permanganate of potash, 



646 



DISEASES OE THE KIDXETS. 



and chloride of sodium are also recommended. The daily use of a min- 
eral water, like Vichy, is beneficial iu many cases of chronic cystitis. I 
have found great benefit from the daily use (drachm doses after each meal) 
of the "Lafayette mixture." 1 All stimulating drinks are forbidden. 
The injection of quinine into the bladder has recently been very success- 
fully practised for the cure of chronic cystitis. 



1 R Bals. copab. 



Spts. eth. nitros. a5 

Liq. potass 

Mucilag. acaciie 



. . . 1 88. 

.... 3i. 
ad 5iv. 



M. 



SECTION IV. 



ACUTE GENERAL DISEASES. 

Modern pathology has demonstrated the specific nature of some patho- 
logical processes and their dependence upon the entrance and development 
within the system of micro-organisms. 

The pathological and clinical resemblances which many diseases bear to 
conditions known to be of bacterial origin are so numerous and striking 
that we are compelled to believe that they also depend upon a similar 
cause. All these conditions are classed under the general term of Infectious 
Diseases. In the present state of bacteriological study the proper classifi- 
cation of some diseases is still unsettled. I shall include in this section 
only such as are generally accepted as of undoubted bacterial origin. A 
few, on the other hand — as acute hydrocephalus and pneumonia — whose 
specific nature is established, are better described in connection with other 
diseases of the organs which they principally affect. While not scientific- 
ally accurate, such a classification is the one generally adopted. 

Although the specific bacteria of comparatively few of the infectious 
diseases have been isolated and recognized, they all present, clinically, 
certain well-defined class characteristics. First: Their pathogenic action 
is specific and invariable, so that, under similar circumstances, the patho- 
logical processes which any particular germ incites are always identical 
in kind, although several germs may have the power to produce a given 
morbid condition. Second: They possess the power of indefinite repro- 
duction when placed under favorable circumstances, and their resulting 
diseases are therefore often endemic where permanent sources of infection 
have become established, or epidemic when the poison affects large num- 
bers at the same time, rather than sporadic. The infective element in 
all infectious diseases, whether it be the bacterium itself or its ptomaine, 
is termed a virus, and is always developed, so far as we know, either in 
the bodies of diseased living beings or in connection with vegetable organic 
matter. 

Every virus is more or less diffusible and may be conveyed by air, fluids, 
or solids ; while in some diseases it becomes so localized that it can be 
transmitted by inoculation. These morbific agents give rise to distinctive 
diseases either by changes which they produce in the blood or by their 
direct action upon the cellular elements of the different organs and tissues. 

When a virus originates and attains its full development only in a living 
animal, and is excreted in an active state, it is called a contagion, and the 
disease which it produces is contagious. 



648 



ACUTE GENEKAL DISEASES. 



When the morbific agent originates and is developed in decomposing 
organic matter, it is termed a miasm, and the affection it develops is a 
miasmatic or malarial disease. Contagions may be transmitted mediately 
or immediately, and are reproduced with each infection. Miasms are con- 
veyed only by diffusion, generally through air or water, and their activity 
is limited to a single infection. 

Many clinical facts have given rise to the belief that some of these 
poisons are not thrown off from the affected person in an active state, but 
require a period of development outside the body to attain infective powers. 
The diseases in whose development such a poison is supposed to be the 
etiological factor are termed miasmatic-contagious. It seems probable, 
however, that even in these diseases the pathogenic bacteria are excreted 
in an active condition, and that their clinically noncontagious character is 
due to the physical conditions under which their excretion takes place 
rather than to any lack of infective power. Strictly speaking there are no 
degrees to contagion. All diseases whose infectious element is thrown off 
in an active condition are equally contagious. Clinically, however, the 
term is used to imply the power of communicability which any patho- 
genic germ possesses, so that we may still retain the term miasmatic-conta- 
gious for those contagious diseases whose bacteria are commonly commu- 
nicated through a stage of extra-corporeal development. With this preface 
I shall continue the etiological classification of infectious diseases. 

I. Miasmatic Contagious Diseases, due to a virus originating in a living 
being and developed in decomposing organic matter. 

1. Typhoid Fever. 4. Cerebro-spinal Meningitis. 

2. Yellow Fever. 5. Septicaemia. 

3. Cholera. 6. Pyaemia. 

II. Acute Contagious Diseases, due to a virus originating and developed 
solely in a living being. 

1. Diphtheria. 8. Scarlet Fever. 

2. Erysipelas. 9. Measles. 

3. Acute Miliary Tuberculosis. 10. German Measles. 

4. Typhus Fever. 11. Miliary Fever. 

5. Eelapsing Fever. 12. Influenza. 

6. Small-pox. 13. Whooping Cough. 

7. Varicella. 14. Hydrophobia, 

III. Malarial Diseases, due to a virus originating and developed solely 
in decomposing vegetable matter. 

1. Intermittent Fever. 4. Pernicious Fever. 

2. Eemittent Fever. 5. Dengue Fever. 

3. Continued Malarial Fever. 6. Chronic Malarial Infection. 

These diseases, with but few exceptions, are commonly known as " The 
Fevers," on account of their most prominent clinical feature. A general 
description of the febrile condition and the methods of treatment may be 
given which will be applicable to all these conditions. 



FEVER. 



649 



FEVER. 

The term fever is one of those elastic words which it is impossible to 
define accurately. 

By it is generally understood any increase of the internal bodily tempera- 
ture above a recognized normal standard, which is induced by some patho- 
logical condition. Xo fixed degree of heat can be affirmed as the dividing 
point between normal conditions and febrile temperatures. A temperature 
of 100° F. is strictly febrile when caused by septic poisoning, while a tem- 
perature of 100.5° F. is equally non-febrile if caused by a hearty meal, or 
the establishment of the lacteal secretion after parturition. 

Since non-febrile temperatures are confined within comparatively narrow 
limits, it is essentially true that temperatures ranging from 98° F. to 100° 
F. may be considered as normal or sub-febrile, w T hen there are no other evi- 
dences that pathogenic conditions are present. Temperatures above 100° 
F. must always excite suspicion, even if unattended by the usual symp- 
toms of fever. The pathological processes concerned in the production 
of fever are all included in a disturbance of the normal ratio between heat 
production and heat dissipation. 

Three prominent factors largely determine this ratio : 

First : Processes of oxidation resulting in the production of heat, urea, 
and carbonic acid principally. Heat production takes place most promi- 
nently in the muscular tissue and glands, and less abundantly in the blood 
and other tissues. In the lighter degrees of fever the elements involved 
are probably the excess of nutritive material in the blood and that stored 
in the cells. With more severe forms and higher temperatures, and even 
in prolonged fevers of low grade, the parenchymatous elements of the tis- 
sues undergo oxidation, and the parts suffer degeneration with wasting 
and atrophy. 

Second : Vasomotor control of peripheral circulation. In the early stages 
of fever, peripheral circulation is often decreased, and the surface radiation 
falls below normal ; later vasomotor dilatation allows of free circulation 
and an increased radiation, although not in proportion to the increase of 
heat production. 

Third: Activity of the sweat glands. 

While radiation of heat takes place in increased degree, even when the 
skin is dry and the glands inactive, the decrease of surface temperature 
goes on much more rapidly when the surface is kept bathed by perspira- 
tion. The marked relief experienced by fever patients when sweating 
takes place has suggested the presence of some other factor than evapora- 
tion and heat absorption, and led to the belief that the febrile poison was 
and could be eliminated by a critical sweat. It is more probable that the 
sweating is primarily the result rather than the cause of the febrile re- 
mission. 

It is clearly established that the last two factors are under the control 



650 



ACUTE GENERAL DISEASES. 



of ganglionic centres in the medulla, and recent experiments have deter- 
mined with almost equal certainty that heat production, as it depends 
upon oxidation in the tissues and glands, is regulated by a thermogenic 
centre. The exact location of this centre has not been definitely deter- 
mined, but all investigators agree in placing it aboye the medulla, thus 
differentiating it from the vasomotor centre. 

It is believed that this centre acts both by stimulation and inhibition of 
oxidation. 

Etiology. — The demonstration of thermogenic centres seems sufficiently 
conclusive to warrant the assumption that fever is always primarily depend- 
ent upon some form of irritation of several correlated nervous centres, the 
thermogenic, vasomotor, and perspiratory being the most important. Set- 
ting aside physiological conditions, such as functional activity of glands 
and organs, which are attended by rise of temperature, we find that clini- 
cally the causes of fever may be classed as : 

I. Nervous: under which are classed conditions mechanically affect- 
ing some portion of the nervous system un associated with inflammatory 
changes. 

II. Hmmic : including all those conditions in which irritating elements 
are known or supposed to be present in the blood. 

Nervous Causes. — Both direct and reflex irritation of the nervous centres 
are known to produce rise of temperature without coincident inflamma- 
tion. A temperature of 120° F. has been reported in a case of fracture 
of the spine which ended in recovery. Cerebral tumors affecting the pons, 
optic thalami, or crura cerebri, or hemorrhages in the same locality, are 
often attended by temperatures reaching 105°-106° F. The marked fall 
of temperature which is at times associated with these conditions gives 
equally strong evidence of the relations w r hich these centres bear to the 
body temperature. The variations of temperature attendant upon irrita- 
tion of peripherar nerves, even when they form part of a state of shock, will 
bear a similar interpretation. 

Hcemic Causes. — Those pyrogenic elements which are found in the blood 
are at present divided into four classes : 

First: Elements developed>by perversion in the nutritive processes. 
This perversion may be in the primary digestion ; in secondary metabol- 
ism ; in the retrograde changes or in excretory functions, and results both 
in the production of new and the accumulation of normal poisonous ele- 
ments in the blood. 

Second : Leucomames ; poisons developed from inflammatory and exuda- 
tive products as already described. 

Third : Ptomaines ; or the bacterial elements with which they are asso- 
ciated. 

Fourth : Chemical, mineral, or vegetable poisons, as alcohol, opium, etc. 
The infectious fevers are believed to depend upon the third class of 
hsemic poisons, whose action, therefore, require special consideration. 
The development of ptomaines by bacterial growth has already been con- 



FEVER. 



651 



sidered, but the exact relations which bacteria and their poisonous products 
bear to pathological change are not fully determined. It seems probable, 
however, that in most cases the ptomaine is the active poison, although many 
bacteria do penetrate the tissues and are found in the blood and substance 
of organs. The question is an important one as regards prognosis and 
treatment, since destruction of living germs in the body can hardly be 
hoped for without severe injury of the tissues, while neutralization of 
chemical elements in the blood is known to be possible. 

At present we are ignorant of the exact manner in which these poison 
elements excite those metabolic processes which are productive of fever. 
The existence of a thermogenic centre does not preclude the possibility that 
bacteria or their ptomaines may act directly upon parenchymatous elements 
to increase metabolism, unless we assume at the same time that all proto- 
plasmic action is under the control of the nervous system, a supposition 
which I am inclined to accept, although it is as yet unproven. Many 
clinical facts, and the action of some drugs as antipyretics, also lend sup- 
port to such a supposition. The term thermogenic, however, must not be 
considered in this connection as implying anything more than a nerve 
centre which controls, either by way of stimulation or inhibition, those 
metabolic processes in the tissues which result in heat production. 

The general drift of opinion at present is toward the belief thatpyroge- 
nic elements act primarily upon such a centre, to produce fever ; and sec- 
ondarily upon the tissues, through perversion of the nutritive elements of 
the blood, to cause degenerative changes. 

Results of Fever. — All the infectious diseases are characterized by more 
or less extensive changes in the blood and tissues. The fibrine factors and 
albuminous elements are decreased ; the white cells are increased ; the 
corpuscles swollen, crenated, or even broken down, and their pigment 
thrown into the serum, while parenchymatous elements throughout the 
body suffer varying degrees of cloudy swelling, granular or fatty degen- 
eration. 

Formerly all these changes were supposed to be the. direct result of the 
high temperature, and other causes to have little if any connection with 
their development. Although our knowledge upon this point is still unsat- 
isfactory, it is now more generally believed that the hsemic changes are 
the direct result of the action of the poison element upon the blood, 
while the parenchymatous degeneration depends upon decreased or per- 
verted nutrition and the excessive metabolism which causes the increase 
of heat. Those cases, however, in which extreme degenerative changes 
are associated with low temperature or are developed with extreme rapidity, 
suggest a more direct action of the poison factors upon the tissues them- 
selves. 

Such a view doe's not entirely exclude the increase of body temperature 
as a factor in the causation of these degenerative changes. The effects 
of high temperatures upon the nervous system also appear to have been 
overestimated. It seems determined, both by clinical observation and 



652 



ACUTE GENERAL DISEASES. 



physiological experiment, that there is a point at which increase of body 
temperature causes collapse of nervous force and speedy death ; but such 
temperatures are seldom attained in the specific diseases, notwithstanding 
the decreased resisting power which we must assume the nerve centres pos- 
sess, in common with other tissues, under the influence of the systemic 
poison. 

Direct irritation of the nervous tissues, by the specific poison or its pro- 
ducts in the blood, is more generally regarded as the important element in 
the causation of those sensorial disturbances so characteristic of the specific 
diseases. 

Febrile temperatures of moderate intensity, not exceeding, say, 105° F., 
have thus come to occupy a position of secondary importance with most 
clinicians, among the unfavorable symptoms of disease, while many care- 
ful observers even regard fever as purely a conservative process. 

Treatment. — Our treatment of fever, per se, will vary with our views as 
to its dangers. To my mind there is little if any evidence that a tempera- 
ture of 106° or 107° F. causes any serious injury to the body, nor do I 
recognize any necessary relation between the other febrile symptoms and 
the temperature range. Those who follow the teachings of Liebermeister, 
and believe that all the grave symptoms of febrile conditions are referable 
to the high temperature, will employ antipyretics early and persistently 
in most diseases, and endeavor to maintain a temperature range below 
103° F. 

A temperature of 105° F., however, has come to be quite as generally 
regarded as the indication for the use of antipyretic measures as was 103° 
F. formerly. The temperature range, however, is not to be the sole guide 
to the use of antipyretics. If a temperature of 105° or 106° F., in a case 
of fever or pneumonia, is rapidly reduced by mild antipyretic measures, 
the patient at the same time being made more comfortable, with decrease 
in the nervous symptoms, I should most certainly recommend their em- 
ployment. But when powerful measures have but a slight effect upon the 
temperature, their use were better omitted. 

Many authorities still insist, however, upon the employment of extreme 
antipyretic methods in certain diseases, who would not extend this treat- 
ment to febrile processes in general. They must believe either that the 
effects of high temperature are not constant, or that the methods of tem- 
perature reduction have some other effect than simply to decrease the body 
temperature. 

Antipyretics are of two classes : 1st. External applications, which are 
known to abstract heat from the surface, and thus decrease the actual body 
temperature. Clinical facts suggest that such applications also have a 
reflex action upon the nervous system, not only acting as a sedative to 
nervous irritation, but also tending to restore nervous control of the ther- 
mogenetic processes in the tissues. It is certainly true that a cold bath 
will often produce a greater and more prolonged reduction of temperature 
than can be accounted for simply by heat abstraction. This sedative ner- 



FEVER. 



653 



vous effect is a more valuable guide in their use than the temperature 
range alone. When external abstraction of heat is followed by decrease 
of nervous irritability, as evidenced by decrease of muscular twitchings, 
cessation of delirium, clearing of the mind, or the advent of sleep after 
prolonged wakefulness, one may be assured that the applications are of 
value, whatever has been the effect upon the temperature. When, on the 
contrary, the opposite condition follows, with evidences of nervous shock 
or irritation, no reduction of temperature which they may accomplish can 
justify the continuance of such measures. Unfortunately, only trial can 
show what patients will be benefited and what injured. 

The means employed for abstracting heat are baths, packs, spongings, 
ice-bags, and the coil. Of these, the sponging may be done with ice-water 
in extreme cases ; the pack wrung from water at 60° or even 40° F. ; while 
the bath is best started at a temperature of 65°-70° F. , which may be 
gradually or rapidly reduced to 50° or 40° F., according to the effects 
obtained. Cold spongings may be repeated every twenty minutes to half 
an hour until the desired reduction is obtained. Cold packs should be re- 
newed as soon as they cease to give a sensation of coolness to the patient, and 
this repetition kept up until the same result is gained. When a patient is 
put in a bath, its duration is determined by its effects. If the skin becomes 
blanched, the face pinched, the pulse disturbed in force or rhythm, and the 
respiration impeded, he must be removed at once, and reaction established 
by the usual means. If, however, the bath is grateful, if the pulse is 
quieter and the circulation well maintained, the bath is continued until 
the patient's temperature is 101° F. if it falls rapidly, or 100° F. if it 
comes down very slowly. On removal, reaction in the cutaneous circula- 
tion should be obtained as before. When successful, such baths may be 
repeated as often as necessary to maintain the desired temperature. Ice- 
bags are solely for local abstraction of heat, and are now entirely superseded 
by the coil when it can be obtained. While intended more particularly for 
local use, the persistent application of a large cold coil will exert a decided 
effect upon the general temperature, and in many cases will render the 
more difficult applications unnecessary. 

2d. Internal antipyretics include all those substances which have been 
found capable of reducing body temperature when taken into the system. 
Unfortunately we have no rules to govern their use except those gained by 
clinical observation. In the light of our present knowledge of fever, it 
seems probable that these remedies may be of two classes : those which act 
primarily on the thermogenic centres ; and those which neutralize or in 
some manner render inert pyrogenic substances in the blood. At present, 
however, w r e have no definite knowledge upon this point. Clinically, we 
know that in different conditions different antipyretics have unequal 
therapeutic values, and the above suggestion simply offers an explanation 
in accord with our present ideas regarding fever. Another decade may 
prove them all wrong. The more important antipyretics are quinine, anti- 
pyrin, antifebrin, salol, salicylic acid, phenacetin, opium, and other seda- 



654 



ACUTE GENERAL DISEASES. 



fives. Other remedies have been employed, but are all represented by these 
given. Substances which, stimulate the flow of bile are also regarded as- 
antipyretic in diseases where intestinal absorption is an element in the pro- 
duction of fever. 

There can be no question as to the superiority of quinine in all malarial 
fevers, whether the malarial poison be the sole cause or only one factor in 
the etiology. Quinine is also generally considered preferable in surgical 
fever attended by suppuration, and in septic conditions, or simple inflam- 
matory fever. At present antipyrin and antifebrin are the favorite anti- 
pyretics in the specific fevers and conditions where nervous irritation is 
prominent. Personally I prefer antifebrin. Salol and the salicylates are 
employed rather for their primary antiseptic action upon the intestinal 
contents, and only secondarily as antipyretics. Phenacetin is not so favor- 
ably regarded as the others of this class. Opium and sedatives probably 
act as antipyretics simply through their effects upon nervous irritation. 
They are used more in combination with other more active remedies than 
alone. Finally, it must be repeated that the above statements are to be 
taken in the most general manner, and that experience alone can deter- 
mine which antipyretic is most suitable to any given condition. 



TTPHOID FEVER. 055 



TYPHOID FEVER. 

This is the most prevalent of all fevers except malarial. So far as we 
know, there is no place where it may not be developed and spread. It more 
frequently prevails in the temperate zones than in the torrid or frigid, but 
it is possible for it to be developed in all latitudes and in all countries. 
This disease, which is essentially the same in all countries, is designated by 
different names. American writers describe it under the name of typhoid 
fever. The French call it the typhoid affection, or dothinenteria. English 
writers describe the same form of disease under the head of enteric fever. 
The Germans call it abdominal typhus, or gastric fever. I prefer the name 
typhoid fever. 

Morbid Anatomy. — As soon as the disease is fully established a change in 
the blood occurs. It becomes darker in color, coagulating imperfectly, and 
the serum is of an unnaturally yellow color. The question arises : — did 
these changes take place in the blood prior to the occurrence of the fever, 
between the exposure and the period of attack ? It is certain that as 
soon as the characteristic symptoms of the disease are present, the diminu- 
tion in the fibrin of the blood is in exact proportion to the severity of the 
fever, and the number of white globules is increased in a similar ratio. 

In connection with these blood changes, a series of changes take place in 
those organs and tissues of the body in which the process of waste and re- 
pair are most rapidly going on. They are of the nature of parenchyma- 
tous degeneration, the essential constituents of the affected organs and 
tissues being involved. Similar parenchymatous changes are met with to a 
greater or less extent in other acute infectious diseases. 

Spleen. — The organ in which parenchymatous degeneration occurs ear- 
liest and most extensively is the spleen. We find this organ undergoing 
three distinct changes : — 

First. It is increased in size, sometimes enormously. The enlargement 
commences soon after the beginning of the disease, and goes on rapidly 
until the third week, after which it ceases, and within a few days begins to 
diminish. If recovery takes place, by the time it is reached, the spleen will 
have returned to its normal size. The splenic enlargement is apparently 
due to congestion and to an increase of normal elements. 

Second. As soon as the spleen reaches its maximum size, its consistency 
diminishes, and this softening is sometimes so marked that, if a post-mortem 
be made at the end of the third week, it will present the appearance of a 
dark, jelly-like mass, which is easily broken down. 

Third. The organ becomes almost black in color, owing to the intense 
congestion which attends its enlargement, and to the deposit of a brown 
pigment in its substance. These changes in the spleen take place, in a 
greater or less degree, in ninety-eight cases out of every hundred. At the 
post-mortem of those who have died of typhoid fever infarctions are some- 



G56 



ACUTE GENERAL DISEASES. 



times found, although there is nothing peculiar about them. In rare in- 
stances, rupture of the spleen occurs without infarctions. 

Liver. — Changes in the liver are by no means as common as those in the 
spleen. The liver may be found presenting its normal appearance, or it 
may be soft and flabby. When soft and flabby, a microscopic examination 
shows the liver cells more or less granular and fatty ; the nuclei of the cells 
can no longer be seen, and the degeneration may become so extensive that 
the outline of the hepatic cells is lost, and nothing but a mass of granules 
remains. Occasionally there will be found in the liver small grayish nod- 
ules situated along the course of the small veins ; these bodies consist of 
lymphoid cells. The lining membrane of the gall-bladder sometimes pre- 
sents evidences of catarrhal or diphtheritic inflammation, when there has 
been no evidence of its existence during life ; cases are recorded where it 
has been found ulcerated. 

Kidneys. — degenerative changes in the kidneys are of not infrequent oc- 
currence in the course of typhoid fever ; they vary in extent with the dura- 
tion and severity of the fever. When present, they are more marked in 
the cortical than in the medullary portion of the organ. In some cases 
they are confined to the epithelial elements, while in other cases degenera- 
tion of all the anatomical elements of the organs can be found. Such ex- 
tensive changes are less liable to occur in typhoid than in typhus fever. 
Small gray nodules, similar to those referred to as occurring in the liver, are 
sometimes found. If the epithelial degeneration of the cortical substance 
is extensive, the cells finally break down into a granular detritus, and the 
cut surface assumes a yellow color and is softer than normal. Infarctions 
are sometimes met with in the kidneys of those dying of typhoid fever. 

Heart. — The parenchymatous changes which take place in the heart are 
more marked than those in any other organ except the spleen. In a large 
proportion of cases it becomes soft and flabby, and is of a grayish or brown 
color. Sometimes it is so much changed that its tissue is easily broken 
down by moderate pressure ; it loses its normal outline, and when removed 
from the body the walls of its cavities readily fall together. When its mus- 
cular tissue is examined microscopically, in many instances it will be found 
that granular changes, affecting the ultimate muscular fibres, have oc- 
curred ; this granular muscular degeneration may be general or local. Oc- 
casionally the muscular fibres are infiltrated with brown pigment. If, as 
is sometimes the case, the heart retains its normal outline, is friable, and 
its cut surface glistens, the muscular fibres will be found to have undergone 
a change which closely resembles amyloid degeneration ; they will be filled 
with a material which presents the same shining appearance as the amy- 
loid substance, but on applying the iodine test the amyloid reaction does 
not take place. It is a form of degeneration which is not confined to the 
muscular tissue of the heart, but is found to a greater or less extent in the 
voluntary muscles throughout the body. Thrombi are sometimes found in 
the heart, and vegetations adhering t® the valves and chordae tendineae. 
These may give rise to infarctions in the different organs. The existence 
of these degenerative changes in the heart may be recognized during the 



TYPHOID FEVER. 



657 



life of the patient, for the heart-sounds become feeble according to the ex- 
tent of the degeneration, and in some cases the first sound of the heart will 
be absent. 

Langs, — The lungs undergo changes which have received the name of 
splenization, from the close resemblance which the affected portion of lung 
then bears to the spleen. The affected tissue is of a darker color than nor- 
mal, and scattered through its substance will be seen minute red or yellow- 
ish-white points ; these points are scanty blood extravasations. It is of a 
reddish-blue, brown, or black color ; its consistence is firmer than normal, 
it crepitates less freely, has a more homogeneous appearance upon its cut 
surface, and is less moist than normal lung-tissue ; a dark fluid will some- 
times ooze from its cut surface, but not as freely as in hyperemia, and the 
fluid is more watery in appearance. A microscopical examination of lung- 
tissue in this condition shows the capillary vessels filled with blood, and the 
alveoli containing a variable number of cells. It is a condition closely re- 
sembling that condition known as static pneumonia, but no inflammatory 
process exists ; it is simply a stasis in the capillary circulation, accom- 
panied by a slight increase in the cell elements in the alveoli. 

So constantly is catarrhal bronchitis present in this fever, that Dr. Stokes 
proposed to call typhoid fever bronchial typhus. In most cases this catarrh 
is not extensive, but affects only the larger bronchi ; it may, however, ex- 
tend to the smaller tubes and give rise to capillary bronchitis and broncho- 
pneumonia. Pulmonary infarctions are frequently found in the lungs of 
those who have died of typhoid fever. They are sometimes quite numerous, 
are usually of small size, and vary in appearance according to the stage of 
their development. When recent they are of dark color, and feel like con- 
solidated lung-tissue ; later, the color changes to yellow ; they may soften 
and break down. 

Larynx. — The larynx, as well as the bronchial tubes, is frequently the 
seat of catarrhal inflammation ; less frequently it is the seat of diphtheritic 
inflammation. In connection with these laryngeal inflammations, ulcers 
appear in the larynx ; these have received the name of il typhoid ulcers of 
the larynx : " sometimes they give rise to quite extensive hemorrhages. 
In connection with, or independent of, these laryngeal ulcers, ulceration of 
the mucous membrane of the mouth and pharynx may occur ; at times it 
involves the epiglottis in such a manner as to clip off its edges. These 
ulcers may develop on the mucous membrane of the Eustachian tubes. In 
those cases where permanent deafness follows an attack of typhoid fever, 
it will usually be due to ulceration of the mucous membrane of the Eus- 
tachian tube. 

Brain and Nervous System. — As yet we have not been able to determine 
whether there are any structural changes in the brain or nervous system 
so constant that they may be regarded as lesions of typhoid fever, although 
it is reasonable to infer that in a disease where such severe functional dis- 
turbances of the cerebro-spinal system exist there must be constant and 
definite parenchymatous changes. (Edema of the pia mater and of the 
brain substance, with occasionally quite extensive adhesions of the dura 



658 



ACUTE GENERAL DISEASES. 



mater to the cranium, not infrequently exists. Punctate extravasations 
into the brain substance are found in a certain number of cases, but even 
in severe cases they are not always present. 

Stomach. — The changes which occur in the stomach are equally impor- 
tant with those which occur in the other internal organs, and are degenera- 
tive in their nature. Softening and degeneration of its glandular struc- 
ture are sometimes so extensive that, if recovery from the fever takes place, 
a very long time must elapse before the organ can perform its normal func- 
tion. It is the existence of these degenerative changes that gives rise to 
the disturbance in digestion whicli is present in so many cases, not onty 
during the continuance of the fever, but during convalescence. 

Muscles. — Muscular degeneration is of .two varieties -.—first, a granulai 
degeneration, which corresponds to ordinary fatty degeneration. Secondly, 
a waxy or vitreous degeneration, which consists in the conversion of the 
contractile substance of the primitive bundles into a homogeneous, waxy 
shining mass. Often both forms of degeneration occur together, one or the 
other predominating. In both forms of degeneration the muscular fibres 
become thicker and more brittle than normal. In the highest degree of de- 
generation the muscular fibres are entirely lost, and the muscle may present 
a yellowish or whitish appearance, so that hardly any traces of its normal 
color remain. This muscular degeneration, however, is not peculiar to 
typhoid fever, but is met with in all severe infectious diseases. The want 
of muscular power, which is so prominent a symptom during the height 
of the fever, may depend on the disturbances of the nervous system, but 
the excessive loss of muscular power which is so often present during con- 
valescence is due almost entirely to the muscular changes. The physical 
strength returns gradually during convalescence as the muscles are re : 
generated, and it may be months before it is fully re-established. The 
muscles of the tongue undergo degeneration in the same way as the other 
voluntary muscles, which accounts in some degree for the interference 
with the function of that organ, so often a prominent phenomenon of the 
disease. 

The salivary glands enlarge, become firm and tense, and assume a more 
or less brown-yellow color. They have the consistence of cartilage. Late 
in the disease the hardness diminishes, and they assume a red color. These 
changes are due to a parenchymatous degeneration, which has been pre- 
ceded by a cellular hyperplasia. It accounts to a certain extent for the 
diminution of the salivary secretion, which is so marked and constant an 
attendant of the fever. Similar cellular and parenchymatous changes take 
place in the pancreas. Changes similar to these occur in other febrile 
diseases, so that they cannot be regarded as characteristic of typhoid 
fever. 

Intestines. — The essential and characteristic lesions of typhoid fever are 
found in the lymph structures of the intestines. They vary only in degree 
and not in character with the duration of the fever and their proximity to 
the ileo-caecal valve. Although changes closely resembling them may be 
present in other diseases, there is no other disease in which they follow a 



TYPHOID FETER. 



C59 



regular course of development, with stages limited by days and weeks. 
These changes in typhoid fever correspond very closely in their different 
stages with the four weeks of the disease. During the first week they are 
confined to a catarrhal inflammation of the intestinal mucous membrane, 
most marked about the Peyerian patches, with a medullary infiltration of 
these and the solitary glands, which extends in some cases into the adja- 
cent tissues. The infiltrated cells are mostly lymphoid cells, though large, 
round and polygonal cells with multiple nuclei are also present. These lat- 
ter are swollen epithelial cells from the reticulated tissue of the mucous 
membrane and lymph follicles. As a result of these processes, there is 
hyperemia and swelling of the mucous membrane, and the affected glands 
become enlarged and elevated from one to two lines above the mucous sur- 
face. They assume a dark red or reddish-gray color marked with fine white 
striations, and present the so-called 
"shaven beard" appearance. Their 
consistence varies with the severity oJ 
the process. When moderately swollen, 
they are soft and present a spongy ap- 
pearance, but in the severer types the 
entire gland becomes hard and smooth. 
These changes begin and are most ex- 
tensive in the glands nearest the ileo- 
cecal valve ; they are generally well 
marked within forty-eight hours after 
the commencement of the disease, but 
are not fully developed until the end of 
the first week, when all the glands are 
involved which are likely to undergo 
change. The number of patches in- 
volved varies from four to five near the 
valve to twenty or thirty throughout 
the whole intestine. The solitary fol- 
licles do not participate in the infiltra- 
tion and swelling to the same extent as 
the agniinated glands. 

In the second week the hyperemia 
and catarrh of the mucous membrane 
subside, leaving the agminated and solitary glands more elevated ; the 
white lines upon their surface disappear, and they assume a uniformly red 
color. An unusually rapid cellular hyperplasia takes place in the follicles, 
by which they become swollen in all directions. Usually the new cell 
growth extends beyond the limit of the follicles, so that the adjoining 
mucous membrane is also infiltrated with cells. The new cells distend the 
glands, and a vertical section of a patch in this stage shows the villi in- 
creased in length and width, and fused together at their bases or through- 
out their entire length by the embryonic tissue. These newly formed 
cells may wander through the muscular coat or penetrate the sub-serous 




Fig. 151. 

Mucous surface of a portion of the Ileum 
during the first week of Typhoid Fever. 

A. Peyer's patch, showing the reticulated or 

shaven-beard appearance. 
Tlie mvcovs membrane is hypercemic, and the 
solitary follicles, B, are only slightly involved. 



660 



ACUTE GENERAL DISEASES. 



tissue. 



Thus hyperplasia of the adenoid tissue is the essential patho- 
logical change in the second week. 
By the middle or latter part of the 
second week the process passes into 
its third stage, and necrotic changes 
are established in the newly formed 
tissue. 

These morbid changes may ter- 
minate in three ways : first, the new 
elements in these ductless glands may 
become disintegrated and undergo 
absorption, and in this way they may 
gradually undergo resolution ; second, 
either the tissue between the follicles 
remains infiltrated and elevated while 
their contents are absorbed, or indi- 
vidual follicles of the agminated 
glands rupture and discharge their 

Mucous surface of the Ileum during the second week Contents into the intestine, leaving 
of Typhoid Fever. 

A. Peyer's patch thickened and raised— from hyper 
plasia. 

B. Solitary follicles much enlarged. 




depressions which give the gland a 
reticulated appearance ; third, the 
most frequent and characteristic ter- 
mination of the typhoid process is the separation of the dead tissue as a 
slough, or by ulceration and the 

formation of the typhoid ulcer. ^=~=^-~ — _ ^ 
Ulceration which begins at the 
most elevated portion of a patch, 
already stained yellow or yellow- 
ish green by intestinal fluids or 
darker by sanguineous infiltration 
advances gradually until a small 
irregular ulcer has enlarged to 
one covering the whole gland, or 
the entire gland may slough uni- 
formly, and at once form the com- 
plete ulcer. 

Usually the sloughing and re- 
moval of the necrotic tissue does 
not take place until the third 
week of the disease. As the 
sloughs gradually loosen and fall 
off, there is a loss of substance 
which extends to the deeper 
layer of the mucous membrane, 
removing the entire gland and 
the mucous tissue surrounding it, 
laying bare the muscular coat of 




Fig. 153. 

Mucous surface of a portion of the Ileum in the third week 
of Typhoid Fever. 

A. Beyer's patch, ulcerated, showing the overhanging 

edges and the roughened base. 

B. Solitary follicles ulcerated at their apices. 

C. A small oval vlcer. 

D. Perforation of the intestine. 



TYPHOID FEVER. 



061 



the intestine. The necrotic process may extend and involve the muscular 
tissue, and end in perforation of the peritoneal covering. These ulcers 
may be developed in the jejunum, the ileum, the stomach, and the large 
intestine. In the lower part of the ileum, at the ileo-caacal valve, they are 
usually of large size — so large that only small portions of healthy mucous 
membrane are left between them ; in the jejunum, stomach, and large 
intestine they are usually round and of small size. The form of the 
ulceration corresponds to that of the necrotic tissue ; if an entire 
Peyerian patch is necrotic, an elliptical ulcer is formed, with its long axis 
corresponding to that of the intestine. In the jejunum and large intes- 
tine, the ulcers are usually small and round. The edges of the ulcer are 
sharp, tumid, and overhang the floor of the ulcer. Sometimes the ulcers 
are hemorrhagic. 

In the fourth week the process of cicatrization is commenced. Gradually 
the swollen edges of the ulcers subside, granulation-tissue springs up from 
their base, connective- tissue membrane is formed, and the edges of the ul- 
cer become united by a cicatrix which is covered with a layer of epithelium. 
The gland structure is never regenerated. The cicatrix which is formed 
by the healing of these ulcers is slightly depressed, and less vascular than 
the surrounding mucous membrane. During the healing process the cica- 
trix becomes more or less pigmented, and these pigmented scars may be 
recognized years after cicatrization has taken place. They seldom cause any 
puckering or diminu- 
tion in the calibre of the 
intestine. In many cases 
the process does not 
pursue this regular 
course ; while one por- 
tion of the ulcer is 
cicatrizing, ulceration 
in another part may 
be extending ; such 
long-continued ulcera- 
tion prolongs convales- 
cence, and may even 
cause death from ex- 
haustion. 

Mesenteric Glands. — 
Associated with these 
intestinal changes, anal- 
ogous processes take 
place in the mesenteric 
glands. These mesen- 
teric changes are also 
most marked in the 
glands situated nearest 
the ileo-caecal valve ; they are secondary to the changes in the intestinal 




Fig. 154. 

Sketch showing Enlargement of the Mesenteric Lymphatic Glands 
in Typhoid Fever. 
A, A. Portion of Small Intestine. 

B. Mesentery. 

C. Glands enlarged. At Da gland is shown in section. 



602 



ACUTE GEJSTEEAL DISEASES. 



glands, and usually in a degree corresponding to the extent of the intestinal 
lesions. The glands are first congested, then there is a production of lym- 
phoid and large cells similar to those which are found in the enlarged 
intestinal follicles ; the glands become enlarged, and are the seat of an 
acute cellular hyperplasia. When the enlargement has attained its full 
size, the hyperemia diminishes, and the cellular elements begin to disin- 
tegrate and are absorbed. In about one-half the cases the enlargement 
reaches its maximum size by the middle of the second or at the commence- 
ment of the third week. The enlarged glands vary in size from that of 
a hazel-nut to a small hen's egg. In the stage of retrogression some of 
the glands simply shrink and return to their normal condition; in others, 
partial softening takes place and afterward absorption, leaving a fibrous 
cicatrix. If the glands reach a very large size, absorption is incomplete, 
and dry, yellow, cheesy masses are left, which after a time become calca- 
reous and enclosed in a fibrous capsule. In rare instances the glands be- 
come fluid, their capsules are destroyed, and the softened masses escape into 
the peritoneal cavity and cause peritonitis. A calcareous condition oi 
the mesenteric glands, like the pigmented cicatrices of the solitary and 
agminated glands, gives evidence of a previous severe attack of typhoid 
fever. 

Another lesion of typhoid fever occurring during convalescence, is sup- 
purative inflammation in the subcutaneous cellular tissue. The inflamma- 
tion is not of an active type, but is accompanied by some redness and pain. 
Gradually a tumor is formed at the seat of the inflammation, usually where 
there has been the greatest amount of pressure, and after a time fluctuation 
becomes distinct as the swelling increases ; sometimes two or more of these 
swellings coalesce, and finally an immense abscess may be formed contain- 
ing a pint or more of pus. Eetro-pharyngeal ulcers are the result of sup- 
purative inflammation of the connective-tissue. 

Etiology. — Among the bacilli which are known to be connected with spe- 
cific diseases, the bacillus of Eberth is generally recognized as the specific 
cause of typhoid fever. By inoculation with this bacillus, Gafifky has suc- 
ceeded in producing a fever, and the characteristic lesions of typhoid fever, 
in animals. Very many clinical facts also support the claim that the excit- 
ing cause of the disease has been determined. I have included this fever 
in the class of miasmatic contagious diseases because a period of extra-cor- 
poreal growth has seemed necessary for the complete development of the 
bacillus. It is possible, however, that the circumstances attending its 
expulsion from the body, rather than inactivity of the virus, determine its 
classification, and that while it is clinically miasmatic-contagious, it is 
strictly, according to our definition, a contagious disease. The generally 
accepted meaning of the word contagious, however, makes it desirable to 
continue this classification. Usually it has been regarded as an endemic 
form of disease. There seems to be no connection between its develop- 
ment and destitution. It may occur as an isolated case, or whole house- 
holds and neighborhoods may be stricken down with the disease. It is 



TYPHOID FEVER. 



GG3 



possible for it to prevail as an epidemic, but it must first have been 
endemic. 

Persons sick with, this fever are now admitted into our general hospitals, 
and are placed by the side of patients with pneumonia or any form of chronic 
disease, without endangering the lives of such patients. This fact shows how 
generally the profession regard this disease as non-coritagious. Typhoid- 
fever patients are no longer restricted by quarantine regulations. The his- 
tory of epidemics of typhoid fever leads to the conclusion that the poison 
is contained in the f meal discharges of the sick. When such excrement is 
in fresh condition the poison is not active ; it must go through a stage of 
development outside of the body. This may take place in the excrement 
itself, but it goes on more rapidly and abundantly if the excrement is col- 
lected in privies, or in earth that is already saturated with organic matter. 
In this way we can readily explain how a typhoid-fever patient coming into 
a locality previously free from the disease can establish there a focus of 
infection, from which many persons may become diseased. It is supposed 
that this poison is not active in its fresh state, from the fact that the dis- 
ease is not carried directly from one individual to another ; attendants, 
nurses, and physicians are no more liable to the disease than those who are 
not thus directly exposed to the disease. 

It is difficult to determine the period of incubation, or length of time 
the poison must remain in the body before symptoms of the disease are 
manifest. The histories of isolated cases would lead to the conclusion that 
the period varies from fourteen to twenty days. Undoubtedly there are 
two principal channels of infection, namely, the air we breathe and the 
water we drink. This poison may be contained in gases which emanate 
from privies, sewers, etc.. which have been the receptacle of excrement 
from typhoid patients, and also in drinking-water from springs and wells 
which have become contaminated by matters from adjoining privies and 
cess-pools. It is an established fact that water remains contaminated, 
though far remote from the point where it came in contact with a defective 
sewer or water-closet. Soil pipes and sewerage may be defective for a 
long time and no case of typhoid fever occur, when suddenly an endemic 
of typhoid fever breaks out, and careful investigation shows that its de- 
velopment was preceded by the introduction of the excrement of a single 
individual sick with the disease. It is the belief of some that milk may 
convey the typhoid poison, and there is evidence in favor of this opinion ; 
but there is stronger evidence that the water used to dilute the milk, and 
not the milk itself, is the medium through which the poison is transmitted. 

This poison has great vitality. Typhoid fever frequently occurs in the 
same locality year after year, when the surrounding conditions are favor- 
able to its development. Those conditions are more frequently present in 
the autumn than in any other season of the year, and for this reason it 
has been called autumnal fever. Usually it makes its appearance in a 
locality, each year, at about the same time ; case after case is developed 
until entire households and neighborhoods become its victims. Individu- 



664 



ACUTE GENERAL DISEASES. 



als who come to care for the sick may contract the disease, and even per- 
sons who visit houses in which the disease is prevailing may afterward de- 
velop the fever, contracting it, not from the sick, but from the infected 
atmosphere of the locality. 

Age must be regarded as a predisposing cause of typhoid fever. It is 
much more likely to occur in young than in old persons ; it occurs most fre- 
quently between the ages of fifteen and twenty-five, and is rarely met with 
in persons over fifty. There are also individual idiosyncrasies which seem 
to predispose to this fever. Some contract it upon the slightest exposure 
to the influence of the poison, while others, frequently brought in contact 
with it for a long time, escape. Again, an individual may have repeated 
attacks of typhoid fever. 

Symptoms. — I shall first consider the prominent symptoms of a typical 
case, and discuss in detail these symptoms, without special regard to the 
time of their occurrence. 

This fever is usually insidious in its approach, and comes on with a cer- 
tain degree of uneasiness throughout the system ; the patient feels uncom- 
fortable, has no pain, but feels that he is about to be sick. He complains 
of a grumbling headache, more or less aching of the limbs, " a tired feeling 
all over," chilly sensations, alternating with flashes of heat and loss of 
appetite; — not infrequently nausea and vomiting are present. The pre- 
monitory symptoms gradually increasing in severity, by the fifth or sixth 
day the patient is compelled to take to his bed. At this early period there 
may be a slight diarrhoea. In very mild cases the disease comes on so in- 
sidiously, and with symptoms so mild, that the patient is often able to 
pursue his ordinary avocations, complaining only of an undefined indispo- 
sition. In very many severe cases it is impossible for the patient to accu- 
rately fix upon the time when the fever commenced ; and in no case will 
an early positive diagnosis be possible. Typhoid fever may be suspected, 
but that is as far as one can safely go. 

In all cases variation in temperature is one of the most important early 
symptoms. Such variations in temperature in a typical case may be divided 
into four periods, of one week each, which correspond to the four weeks of 
the disease. In the first week there is a gradual and steady rise in tem- 
perature, with regular morning and evening variations, each evening tem- 
perature being about 2° F. higher than that of the morning, and 1° F. 
higher than the previous night, so that at the end of the first week it 
is at its maximum, — 104° or 105° F. This is one of the most character- 
istic features of the disease. This gradual rise of, and these variations in, 
temperature are not present in every case, but when they are present 
they will greatly assist in making an early diagnosis. It has been said that 
t}'phoid fever is the only disease, except double quotidian intermittent 
fever, that gives two full thermometrical curves within twenty-four hours ; 
that is, two remissions and two exacerbations. If this is true, it helps to 
explain certain high temperatures in the morning, and affords valuable 
assistance in making a diagnosis. 

During the second week the variations in temperature are slight, retain- 



TYPHOID FEVER. 



665 



ing, however, the same maximum as was reached at the end of the first 
week. The variations during the third week are remittent in character. 
During the fourth week they become intermittent, and the range of tem- 
perature in the exacerbations is lower. The variations in pulse correspond 
to those in temperature. During the first week the pulse gradually be- 
comes more and more frequent, and remains at the height reached at the 
end of the first week ; throughout the second and third weeks there are 
distinct morning and evening remissions ; during the fourth week it falls 
to its normal standard. Diarrhoea generally comes on during the first 
week or is continued from the prodromal stage. In some cases it may have 
ceased by the second week. 

On the seventh day, or between it and the twelfth day, the characteristic 
eruption appears. About this time the headache abates and more or less 
somnolence and delirium come on. The delirium at first is slight, and is 
only observed during the night. Day by day the patient loses flesh and 
strength, and becomes more and more unconscious, and all the phenomena 
of the typhoid state are developed, viz. : a dry brown tongue, feeble pulse, 
low muttering delirium, stupor, tremors, subsultus, involuntary evacua- 
tions, and the other phenomena of great prostration. If the disease is to 
terminate favorably, the amendment is usually gradual. The first sign of 
improvement is a decided remission of the fever. 

Such, in brief, are the phenomena which attend the ushering-in and de- 
velopment of an ordinary case of typhoid fever ; they are, however, sub- 
ject to numerous modifications. Some cases are mild throughout their 
entire course ; some are severe at first and mild afterward ; some are mild 
at first and severe afterward ; while others are severe throughout their en- 
tire course. 

The Physiognomy. — As a rule, the countenance has nothing peculiar in 
its appearance ; but if the disease is of a severe type, by the second week 
the countenance assumes a characteristic appearance — there is a pale, olive, 
leaden look, the eye becomes dull and the conjunctiva congested, and usu- 
ally there is a small, rose-colored spot in the centre of each cheek. The 
face does not assume the dark mahogany color seen in typhus, but in the 
advanced stage of the fever it has more of the hectic flush of phthisis. 

Tongue. — From the very outset, the tongue is covered with a light, white 
coat, but there is nothing special in its appearance before the end of the 
first week ; then it may become red upon its sides and tip, and show a 
slight disposition to dryness in its centre. As the disease passes into its 
second and third weeks, the tongue becomes more heavily coated, the 
coating becomes brown and dry, and sordes collect upon the teeth and 
sides of . the mouth in sufficient quantities to form crusts. These crusts 
may become thicker and more abundant as the disease progresses. At any 
period in the course of the disease the tongue may suddenly clear off, and 
present a shiny red, " beef-colored " appearance. The tongue and lips may 
become dry, cracked and fissured. As the sordes are removed from the 
lips, they will often bleed ; and in certain cases, more especially in the 
severer forms of the disease, the entire mouth and tongue may be covered 



6G6 



ACUTE GENERAL DISEASES. 



with dark-colored incrustations. Such incrustations are seen early in con- 
nection with those cases where there are extensive blood changes ; when 
present they are of grave significance. One of the first indications of con- 
valescence is a moist condition of the tongue about its edges ; gradually 
its entire surface becomes moist, and by the time convalescence is fully 
established it is restored to its natural condition. 

Gastric symptoms are always more or less prominent ; loss of appetite is 
one of the earliest symptoms, and nausea and vomiting are quite common 
during the first week of the fever. The vomited matters usually consist, of 
a greenish fluid. When vomiting comes on late in the fever, it is either 
due to sub-acute gastric catarrh, or is symptomatic of local or general peri- 
tonitis. In a large proportion of cases thirst is excessive. The lips are 
parched, and in severe cases crack and bleed. In some cases hemorrhage 
from the gums occurs. 

Diarrhoea. — Although not invariably present, diarrhoea is so frequent an 
attendant of this fever that it is considered one of its characteristic symp- 
toms. It varies with the severity of the attack, the date of its commence- 
ment, and its duration. The characteristic typhoid discharges are of a 
yellowish-green color, described as " pea-soup discharges." Sometimes 
they are of a dark color, resembling coffee-grounds ; their reaction is alka- 
line. In some cases diarrhoea is present at the very outset of the disease, 
and continues throughout the entire course. In others, it does not appear 
until the third week. The second week is the ordinary time for its ap- 
pearance. When the diarrhoea appears late in the course of the disease, 
the discharges are more copious than when it appears early. A mild 
diarrhoea throughout the entire course of the fever is a favorable rather than 
an unfavorable symptom. In mild cases diarrhoea is sometimes absent, 

Intestinal Hemorrhage. — This occurs in about one in twenty cases, and 
varies in quantity from a mere trace of blood in the stools to a profuse dis- 
charge of from sixteen to eighteen ounces. The slight hemorrhages which 
occur early in the disease simply indicate a hemorrhagic tendency, the same 
as the epistaxis, which is very frequently among the early symptoms. In 
both instances the bleeding comes from the capillaries of the mucous mem- 
brane. The more profuse hemorrhages are due to the opening of an artery 
in some intestinal ulcer. Hemorrhages due to this cause may be sudden 
and profuse, and may destroy the life of the patient. The usual time for 
the occurrence of these profuse intestinal hemorrhages is the latter part of 
the second and during the third week. These hemorrhages are usually 
accompanied by a sudden fall in temperature, perhaps two or three degrees ; 
if then in a patient severely ill of typhoid fever a sudden fall in tempera- 
ture occurs during the second or third week, accompanied by extreme 
prostration, it is very conclusive evidence that intestinal henrorrhage has 
occurred, although externally the hemorrhage may not have made its 
appearance. The blood is usually fluid, rarely clotted ; generally it is of a 
bright red color, owing to the alkaline condition of the intestinal contents. 
Copious intestinal hemorrhages are more frequent in severe cases that have 
been attended by profuse diarrhoea. Patients may die of intestinal hem- 



TYPHOID FEVER. 



667 



orrhage before any blood has been voided externally. If the patient sur- 
vive a profuse intestinal hemorrhage, there is great danger of his dying 
from peritonitis. He may die unexpectedly by syncope a number of hours 
after a profuse intestinal hemorrhage. 

Abdominal pain and tenderness are not usually present at the very outset 
of typhoid fever, but generally, and almost without exception in the 
severer cases, by the sixth day of the disease some pain and tenderness will 
be present in the right iliac fossa. The pain and tenderness usually in- 
crease as the disease progresses, and in the advanced stages it is sometimes 
so marked that slight pressure over this region is unbearable. While ex- 
amining this region in order to determine the presence or absence of pain 
and tenderness, the pressure should be made with the palm of the hand ; 
the expression of the countenance will indicate the presence of ten- 
derness, long before an audible complaint is made by the patient. It is 
important to bear in mind the possible occurrence of a more severe ab- 
dominal pain arising from intestinal perforation. The following are the 
characteristic symptoms of this lesion : if in the course of a slight or 
severe form of this fever, or even when the disease has been latent and the 
diagnosis of typhoid fever has not been clear, the patient should be suddenly 
seized with diarrhoea, pain in the abdomen, aggravated by pressure, per- 
haps at first localized in the right iliac fossa, but soon extending over the 
entire abdominal cavity, attended by rapid tympanitic distention of the 
abdomen, and symptoms of great prostration, a rapid, feeble pulse, a sunken, 
anxious expression of countenance, nausea and vomiting, quickly followed 
by coldness and blueness of the extremities, and the other signs of sudden 
collapse, it is almost certain that perforation of the intestine has occurred. 
I have known this accident to occur when convalescence was apparently 
progressing satisfactorily. 

Tympanitis is another very common symptom of typhoid fever. 
Usually it is not present during the first week, but by the end of the first 
or the commencement of the second week a fulness of the abdomen will 
be noticed. As the fever advances, the distention often becomes extreme; 
this is due to a collection of gas in the large intestine, developed 
through some change in the mucous membrane, the exact nature of 
which we do not fully understand. When once it is developed it remains 
until convalescence is fully established, and is always an important diag- 
nostic sign of this fever. 

In connection with the development of the tympanitis, when firm press- 
ure is made over the right iliac fossa, a gurgling sound is produced ; but 
gurgling in the right iliac fossa cannot by any means be regarded as a 
positive symptom of typhoid fever, as it may occur in any disease where 
there is distention of the abdomen due to accumulation of gas in the intes- 
tines. In typhoid fever, so long as the abdomen remains tympanitic, no 
matter what the temperature and pulse of the patient may be, he is in 
more or less danger, for it shows that there are intestinal changes still in 
progress, and the reparative processes are not complete ; this is more espe- 
cially the case when the tympanitis has continued from the active period 
of the disease into the period of convalescence. 



668 



ACUTE GENERAL DISEASES. 



Urine. — Extended and very careful analyses of the urine of typhoid 
fever patients have been frequently made, without giving any very practi- 
cal results. Usually during the first two weeks of the fever the urine 
is diminished in quantity, and its color is dark and its specific gravity high; 
after the second week it is increased, and when convalescence is estab- 
lished, it becomes pale, and its specific gravity is lowered. The amount of 
urine excreted daily throughout the active period of the fever is increased. 
The increase is in proportion to the intensity of the fever, subject in some 
degree to the quantity and quality of the food taken. It will be greater 
when large quantities of strong beef -tea are taken than when the diet 
consists of milk. So long as the kidneys are able to eliminate the excess 
of urea, no harm results ; but if the quantity exceeds their power of elimi- 
nation, or if their function is interfered with, ursemic symptoms will be de- 
veloped, such as delirium, stupor and coma. Albumen in the urine is 
only of occasional occurrence in the course of typhoid fever. When 
present the quantity is usually small, and is only temporary. It rarely 
appears before the third week. Its appearance is often marked by the oc- 
currence of cerebral symptoms. Eenal epithelium and casts may or may 
not be present with the albumen. 

Nervous Phenomena. — The symptoms referable to the nervous system 
are not so prominent in typhoid as in typhus fever ; yet there are many 
cases in which these symptoms form an important part of the history. One 
of the most constant is headache. In the majority of cases it is one of the 
ushering-in symptoms of the disease. It is present in mild as well as in 
severe cases ; sometimes it is confined to the forehead and temples ; more 
often it extends over the whole head ; it is not violent, but a dull, heavy pain. 
It usually increases in severity until the middle period of the disease, cer- 
tainly until the close of the first week ; and generally associated with it 
there is intolerance of light and conjunctival injection, pain in the back 
and limbs, and a general aching of the whole body. 

Somnolence is present to a greater or less degree in all cases. In mild 
cases it does not appear until late, and usually is not long continued. In 
the severer cases it appears early and continues until convalescence begins ; 
in fatal cases it passes into a state of coma. It is often interrupted by de- 
lirium. In children this symptom is especially prominent, and is very val- 
uable as a means of diagnosis. 

Delirium is more frequently present than absent in typhoid fever. The 
character of the delirium varies; the usual form is known as the "low- 
muttering" delirium, and is rather characteristic of this type of fever, al- 
though in very many cases the delirium is violent in character, and may 
become maniacal to such an extent as to require physical restraint. Not 
infrequently typhoid fever patients attempt to jump out of a window, or 
injure themselves or their attendants in their endeavors to escape from fan- 
cied dangers. It is very common for the minds of this class of patients to 
be occupied with those things which engaged their attention just prior to 
their illness. The delirium rarely comes on until the second week of the 
fever, and it commences and is most active at night. After it has once ap- 



TYPHOID FEVEK. 



669 



peared, it usually continues until convalescence is established, and generally 
disappears during a sound sleep which attends the early stage of convales- 
cence. The maniacal form of delirium in typhoid fever is usually most 
marked at night. During the low-muttering delirium, if the patient is 
asked questions he will generally answer correctly. 

Muscular Prostration and Paralysis. — In all severe cases of typhoid fe- 
ver, muscular prostration is noticeable in the early stages, and increases 
with the progress of the fever. It is generally most marked during the 
third week. Where there is marked muscular paralysis, the urine and fas- 
ces are passed involuntarily, there is inability to protrude the tongue, and 
more or less difficulty in deglutition, or inability to articulate distinctly. 
Retention of the urine may also occur from vesical paralysis. 

Muscular Tremors. — Tremors of the hands, tongue, or lips are most 
often met with in young subjects and those who are addicted to the use of 
spirits. Severe tremors unaccompanied by much mental disturbance often 
attend extensive intestinal changes. Spasmodic movements, such as sub- 
sultus, hiccough, etc., and rigid contraction of the muscles of the neck or 
extremities are sometimes present in severe cases. General convulsions are 
of rare occurrence, except in very young children, and when they occur 
have no special significance. 

Special Senses. — The symptoms referable to the special senses require lit- 
tle more than enumeration. As regards the sense of sight, there is nothing 
worthy of note, except that the eye assumes a dull expression and that the 
pupil is dilated ; some patients complain of haziness of vision, which is in- 
creased when they assume a sitting posture. The sense of hearing is always 
more or less impaired. This is most marked about the middle period of 
the fever ; then it is impossible for the patient to hear ordinary conversa- 
tion. Einging and buzzing sounds in the ears are often complained of in 
the early stage of the fever. When the loss of hearing is confined to one 
ear, it is generally caused by ulceration of the mucous lining of the Eusta- 
chian tube, or by suppuration of the middle ear. The sense of taste usually 
is altered or perverted ; articles of food are tasteless, or have an unnatural 
flavor. When the tongue and mouth are covered with a heavy coating of 
sordes, the patient is unable to distinguish between bitter and sweet, and 
swallows the most disgusting doses without complaint. 

Hyperesthesia is another disturbance of a special sense. The surface of 
the body of a typhoid fever patient may become so sensitive that he will cry 
out with pain from the slightest touch. This hyperesthesia maybe present 
during the first week, or may not be present until convalescence is estab- 
lished. It is most marked over the abdomen and lower extremities, and 
usually occurs in females of an hysterical tendency. It is of importance to 
discriminate between cutaneous tenderness in the abdominal region, and 
the tenderness of peritoneal inflammation. 

Epistaxis. — When this occurs during the first week, in most cases it is 
of little importance except as a diagnostic sign of this type of fever ; when 
it occurs during the third week it becomes important as an element of 
prognosis, as it may be sufficiently profuse to destroy the life of the patient. 



670 



ACUTE GENERAL DISEASES. 



Occurring late in the disease, unless it can be promptly arrested, it always 
jeopardizes the life of the patient. 

Emaciation is perhaps more marked and rapid in this than in any other 
form of fever. It commences early and is progressive. By the time a 
patient has reached the fourth week of a typhoid fever of even moderate 
severity he is usually in a condition of extreme emaciation. In this par- 
ticular he markedly differs from a patient ill with typhus fevp'\ for in the 
latter case emaciation to any great extent does not occur. 

Temperature.— In making thermometrical observations in this as well as 
in all other forms of fever, the thermometer may be placed in the axilla, 
the mouth, or the rectum. I shall refer to axillary temperature whenever 
I speak of temperature without qualification. Usually in a typical case 
the temperature begins to rise about noon on the first day of the develop- 
ment of the fever, and continues so to do until between six and eight 
o'clock in the evening, when it reaches its maximum for that day ; then 
there is no change until midnight, when it begins to decline, and by six 
or eight o'clock in the morning it has reached its minimum, which is a de- 
gree higher than on the morning of the preceding day. After six or eight 
o'clock in the morning the temperature does not vary much until noon; 
then it again begins to rise, and by six o'clock in the evening it has reached 
its maximum for that day, which is one degree higher than on the even- 
ing of the preceding day. Again, at midnight it begins to fall, and by 
morning it has fallen a degree, which leaves the minimum, and the aver- 
age for the day a degree higher than on the preceding day. Thus it rises 
a degree each day, with regular morning and evening variations, until the 
eighth day of the fever, when, in most cases, it has reached its maximum 
for the whole course of the disease. 




Fig. 155. 

Temperature Record in a Typical Case of Mild Typhoid 
Fever. Recovery. 



During the second weeh the temperature remains at about the same maxi- 
mum degree which it has reached at the end of the first week. There are 
morning and evening variations of a degree or more, but the maximum of 
the evening exacerbation remains the same. 



TYPHOID FEVEK. 



671 



During the third week the remission becomes mere and more marked, 
while during the exacerbation the temperature retains nearly the same 
standard as during the second week. By the end of the third week the 
morning temperature during the remission will be two or three degrees be- 
low the maximum of the second week. 

By the time the fourth iveefc is reached, or at least by the middle of that 
week, the temperature becomes intermittent, and with each exacerbation it 
falls lower and lower, until by the end of the week the normal standard of 
temperature has been reached, or it may fall a little below the normal 
standard. These are the typical thermo metrical variations of typhoid 
feyer, yet they are not always present, and there are many things which 
will materially modify them. The fever does not always follow this typi= 
cal course. Marked deviations from the record may be produced by com- 
plications which would never have been discovered but for the irregular 
thermometrical variations. By treatment, the temperature can, for a time, be 
very much lowered ; but if the treatment be discontinued, it will rise again. 
In some cases it is not possible to detect the cause of the irregularity. 

Pulse. — The pulse is also subject to variations, which correspond very 
nearly with the variations in temperature, and occur not only on different 
days, but at different hours on the same day. During the first week the 
pulse becomes more and more frequent ; in the second and third weeks it 



Day. 


L 






4. 


5. 


0. 


7. 


9. 


9. 


/a 


it. 


12. /3. 










/7A/8. 


19. 


2a 


17, 






a , 


e 










c 














'n 






e 










e 












e 








-c 


m. 


& 










/03 




















































































/02° 
/Of 

/M 
99 
98°- 
97 












































# 










— 


























»* 


h 1 



i£ An intestinal hemorrhage occurred here. 

Fig. 156. 

Temperature Record in a Non-typical Case of Typhoid Fever. 



remains at its height, and during the fourth week sinks to its normal aver- 
age. Throughout the whole course of the disease it is less frequent in the 
morning than in the evening. If, at the commencement of the fever, the 
pulse is 98, by the end of the first week it will have reached 100, or 110 
per minute, and there it remains during the second week ; after that time 
it may become as frequent as 120, or 140. During the first and second 
weeks the rate of the pulse and the temperature range correspond, but 
after this time the parallelism ceases as the failure of heart-power begins 



672 



ACUTE GENERAL DISEASES. 



to manifest itself. This failure of heart-power is indicated by an increase 
in the frequency and feebleness of the pulse, which at this time may reach 
140 per minute and yet the temperature show no alarming variation. 
Under these circumstances, the pulse may become irregular and intermit- 
ting. Should these irregularities and intermissions occur during the third 
week, in most cases they are followed by death. With an irregular and 
intermitting pulse, the first sound of the heart will usually be inaudible 
oyer the precordial space, and this indicates that prompt and judicious 
means must be employed to restore the heart's normal action and to avert 
a fatal issue. 

The severity of the disease during the first and second weeks of its devel- 
opment is, to a great extent, indicated by the frequency of the pulse and 
the height of the temperature. Although delirium and extensive tym- 
panitis are important symptoms they do not determine the result ; but if a 
patient during the first, or at the commencement of the second week of the 
disease, has a pulse of 120 per minute, and a temperature of one hundred 
and six, it is very doubtful whether convalescence can ever be established. 
The pulse may increase in frequency from feeble heart-power alone while the 
temperature is steadily falling. On the other hand, the pulse sometimes 
falls almost to a normal standard, while the temperature remains high. 

Eruption. — Some have claimed that this should be considered as a lesion 
of the disease, but I prefer to class it among the symptoms. It makes its 
appearance between the sixth and twelfth days, dating from the commence- 
ment of the fever, and it is not attended by any unusual sensation. It 
remains visible from eight to fourteen days, leaving no stain or mark 
on the surface after its disappearance. It consists of isolated, lenticu- 
lar spots scattered more or less abundantly over the surface of any part 
of the body, but usually most abundant upon the chest and abdomen. 
There may be only a few spots visible at a time, or they may be so pro- 
fuse as to cover the body like a rash. Two or three well-defined spots 
of the eruption are sufficient to establish the existence of the fever. 
Each spot varies in diameter from a point to a line and a half, rarely 
reaching two lines. It is slightly elevated above the surface of the sur- 
rounding cuticle, is of a bright rose color, disappears upon slight pressure, 
and returns as soon as the pressure is removed. Each spot remains visible 
for three days, and then disappears. Sometimes, as one crop of the erup- 
tion disappears another is developed, and this may go on for eight, twelve 
or fourteen days. There are many cases in which only one crop appears. 
As soon as one spot makes its appearance, it is well to mark it with tinc- 
ture of iodine or nitrate of silver, so that observations will be always made 
upon the one point. If it is a spot of typhoid eruption, and one crop of 
eruption is to follow another, it will disappear within three days from the 
time at which it was first seen, and other spots will take its place. It is 
this feature which distinguishes the typhoid eruption from that of all other 
fevers . 

The question may be asked : — is this eruption essential to the diagnosis of 
typhoid fever ? Many observers mention that the eruption is not constant, 



TYPHOID FEYER. 



C73 



and consequently not necessary for its diagnosis ; while others, equally 
competent, maintain that, unless the eruption be present at some period 
during the progress of the disease, the diagnosis of typhoid fever cannot be 
made with certainty. Jenner states that he found the eruption present in 
one hundred and forty-eight out of one hundred and fifty-two cases. I 
would not • say that it is possible for typhoid fever to occur without the 
eruption ; neither would I affirm that scarlet fever ever exists without the 
characteristic rash of the disease ; but as regards these respective fevers, if 
no eruption was present, I would make the diagnosis with equal hesitancy 
in the one case as in the other. The eruption is usually most marked in 
cases of typhoid fever which occur between the ages of ten and thirty. Be- 
fore ten and after thirty years it is usually not as well marked, and may be 
readily overlooked unless careful search is made. 

The typhoid poison, in its operation on the human body, does not always 
effect the series of changes and symptoms just described. On the contrary, 
there are cases which run so mild a course that they can scarcely be digni- 
fied by the name of fever, and, besides, there are imperfectly developed 
cases which show a great diversity in their course, but they all can be in- 
cluded under two heads. 

First, — Mild typhoid fever, in which the symptoms are all mild. 

Second. — Abortive typhoid fever, in which the duration of the disease is 
markedly shortened. 

In the mild type, the fever runs its regular course, but is of low grade. 
The temperature rises regularly until its maximum is reached, which rarely 
exceeds 103° F., then it remains stationary for a time, generally about a 
week ; the decline follows in the same manner as in a typical case. This 
is the regular course of these cases if left to themselves, and, as a rule, 
they should be left to themselves. Some of these cases are so mild that the 
patients are not confined to the bed, or even to their rooms, and perhaps 
throughout the entire course of the disease are able to transact a certain 
amount of business. Such cases have been called walking cases" of ty- 
phoid fever. The eruption appears in these cases early, is of short dura- 
tion and only a few spots appear ; usually there is only one crop. Diar- 
rhoea is also present in most cases of this class, but it is of a mild type and 
the discharges from the bowels apparently give relief to the patient. In 
some cases the diarrhoea alternates with constipation, or constipation may 
be present throughout the entire course of the disease, and the cases go on 
exhibiting a varying amount of fever for from twenty to thirty days, until 
gradual convalescence is established. This class of cases, if properly man- 
aged, rarely prove fatal ; but if improperly managed, there is great danger. 
If a patient walks about while he is suffering from one of these so-called 
mild attacks of typhoid fever, he does it at great risk to life ; there should 
be no " walking cases " of typhoid fever. A patient sick with typhoid 
fever, however mild the type, should take to his bed and remain there 
until convalescence is fully established, as it is impossible to say just how 
extensive the changes may be that have occurred in the intestinal tract, 
and in the mildest type of the disease they may be of such a nature that 



674 



ACUTE GENERAL DISEASES. 



very little physical exertion will cause intestinal perforation which will be 
followed by a fatal peritonitis. 

The abortive- form of typhoid fever is ushered in with all the symptoms 
of a typical case — headache, lassitude, pain in the limbs, nausea, etc., — 
and the temperature during the first week follows the regular variations of 
the fever. At the onset the disease has every appearance of a severe form 
of typhoid fever ; the temperature may rise as high as 105° F. or 106° F. 
by the end of the first week ; delirium is often active, and diarrhoea is 
present. By the end of the second week, certainly by its close, if recovery 
occurs, the fever is cut short, and abruptly disappears ; the temperature 
falls to the normal standard, and the patient passes on to a state of rapid 
and complete convalescence. The eruption, diarrhoea, and all the urgent 
symptoms of the disease may be present, and yet before the end of the 
second week the patient may be fully convalescent. That it is the typhoid 
poison which thus acts upon the system, and gives rise to the characteristic 
symptoms of typhoid fever in these abortive cases, is evidenced by the fact 
that at the post-mortem examinations the characteristic typhoid intestinal 
lesions are found, and these, taken in connection with the presence during 
life of the typhoid eruption, establish the diagnosis beyond question. 
There can be no doubt but that an individual may be affected, overwhelmed 
as it were, by typhoid poison, and yet not develop well-marked typhoid fever. 
So, if only a moderate amount of typhoid poison is introduced into the sys- 
tem, a mild or an abortive type of fever will be developed. The natural 
power of the individual to resist the action of such poisons must always be re- 
garded, and should be taken into consideration in the treatment of a case. 

Differential Diagnosis. — In a typical case, after the fever is fully developed, 
the diagnosis is not difficult. The presence of febrile excitement, marked 
by evening exacerbations and morning remissions, headache, diarrhoea, ab- 
dominal tenderness, and other abdominal symptoms, and the presence of 
the characteristic rose-colored spots are sufficient for a diagnosis. In the 
mild type of the disease, or when the symptoms are developed irregularly, 
or during the first week of a typical case, the diagnosis is often difficult, 
and sometimes impossible. 

The principal diseases which are liable to be confounded with typhoid 
fever are typhus and relapsing fevers, continued malarial (so-called typho- 
malarial) fever, acute tuberculosis, pycemia, septicemia, pneumonia, gastro- 
enteritis, trichinosis, and diffuse parenchymatous hepatitis. The differen- 
tial diagnosis between typhoid fever and diffuse hepatitis has already been 
given. The points of differential diagnosis between typhoid and typhus, 
relapsing and continued malarial (so-called typho- malarial) fevers, will be 
considered in connection with the history of these fevers. 

Acute Tuberculosis. — This disease is attended by many of the symptoms 
which are present in, and supposed to be characteristic of, typhoid fever. 
The fever of acute tuberculosis is of a remittent type, attended by evening 
exacerbations and morning remissions, delirium, a dry, brown tongue, a 
tendency to stupor, great prostration, rapid emaciation, and sometimes by 
a diarrhoea, with abdominal tenderness and tympanitis. All of these are 



TYPHOID FEVER. 



675 



among the prominent symptoms of typhoid fever. More than once have 
patients in Bellevue Hospital, with the diagnosis of typhoid fever, pre- 
sented at the post-mortem examination the characteristic lesions of acute 
tuberculosis. If, therefore, patients with acute tuberculosis may go through 
a large general hospital, under the observation of diagnosticians, — who cer- 
tainly are not men of inferior ability, — and be supposed to have typhoid 
fever, there evidently is great danger of a mistake in diagnosis. The higher 
range of temperature in acute tuberculosis than in typhoid fever is one of 
the distinguishing characteristics of the disease. Usually, early in the 
progress of the disease, it reaches 106° or 107° F., while in typhoid fever 
the temperature rarely reaches 10G° F , or if it does, in most cases it is not 
before the end of the second week and after the typical rise. There is no 
eruption, neither is there enlargement of the spleen in acute tuberculosis, 
while both are very constant attendants of typhoid fever ; yet their absence 
is not positive proof that typhoid fever does not exist. Quinine will reduce 
the temperature of typhoid fever from three to four degrees, while it has 
but little influence over that of tuberculosis. Pulmonary consolidation is 
at the apex in tuberculosis, at the base in typhoid fever. According to 
Bouchut, the ophthalmoscope reveals the presence of tubercular granula- 
tions in the choroid in all cases of acute tuberculosis. In all doubtful 
cases the family history of the patient, his immediate surroundings, whether 
typhoid fever is prevailing at the time, and whether the patient has been 
exposed to typhoid poison, become important points in diagnosis ; after 
the first week of the disease, the presence of the rose-colored spots is neces- 
sary for a diagnosis of typhoid fever. 

Pycemia and Septicemia. — In most cases these diseases will be readily 
recognized, as the surface of the body has a jaundiced hue, there are no 
lenticular spots, and the febrile symptoms are irregular in their develop- 
ment. There are exacerbations and remissions, but their appearance and 
disappearance are not marked by any regularity, and usually there is more 
than one exacerbation and remission in the twenty-four hours. Not only 
are the variations in temperature irregular, but the temperature reaches a 
high degree much sooner, and ranges higher throughout its entire course 
in pyaemia and septicaemia than in typhoid fever. In pyaemia and sep- 
ticaemia there are early in the disease recurring chills followed by profuse 
sweatings, great prostration, rapid emaciation, delirium, subsultus, tym- 
panitis and diarrhoea, while in typhoid fever these do not come on until 
late in the disease. Moreover, the history which precedes and attends the 
development of pyaemia and septicaemia differs widely from that of typhoid 
fever. In pyaemia, thrombi, infarctions and multiple abscesses establish 
the diagnosis. 

There is a condition of septic poisoning occasionally met with resulting 
from the introduction into the system of septic poison through the drink- 
ing water, which so closely resembles that which is the result of typhoid 
poisoning that it is almost impossible to make a differential diagnosis. In 
these cases the absence of the rose-colored spots is almost the only distin- 
guishing feature. 



676 



ACUTE GENERAL DISEASES. 



Pneumonia. — Pneumonia, with typhoid symptoms, is sometimes mis- 
taken for typhoid fever. The pneumonia which complicates typhoid fever 
does not come on until late in the fever, and is preceded by the regular 
history of typhoid fever. On the other hand, when the typhoid symptoms 
are present from the beginning, or come on at the end of the second 
stage of the pneumonia, the physical signs of the pneumonia will attend 
or precede the typhoid symptoms. There will be cough and the character- 
istic pneumonic expectoration ; there will be no eruption, and no typical 
variation in temperature. If a patient who is over sixty years of age with 
this type of pneumonia is not seen until the second or third week of its 
progress, although evidences of lung consolidation may be present, it will 
frequently be very difficult to decide whether the pneumonia is or is not 
complicating a typhoid fever. The diagnosis must be based upon the his- 
tory of the case. 

Gastro-Enteritis. — In the adult this disease is quite readily distinguished 
from typhoid fever, as the diarrhoea and vomiting precede the febrile move- 
ment ; the fever is irregular in its development and progress, and the tem- 
perature rarely rises higher than 103° F. In a child between two and six 
years of age it is very difficult to distinguish gastro-enteritis from typhoid 
fever. The typhoid eruption is not so prominent or constant a symptom 
in the child as in the adult, and with both diseases we have diarrhoea, 
tympanitis, and typhoid symptoms. When all the symptoms precede the 
fever, and there is a history of the case, and a thermometrical record from 
the beginning of the fever, in most cases the diagnosis can readily be made ; 
but if the case is not seen until it has reached the second week of its prog- 
ress, and there is no accurate or reliable history of its development, a posi- 
tive diagnosis is impossible. 

Trichinous Disease. — This condition is not infrequently attended by 
diarrhoea, vomiting, and the development of other typhoid symptoms ; but 
with poisoning by trichinae there are almost constantly present intense 
muscular pains and oedema of the eyelids, which will be sufficient to arrest 
attention. There will be wanting the typical temperature trace and the 
rose rash, and a microscopic examination of small portions of the muscular 
tissue will afford a positive diagnosis. 

Prognosis. — Death may occur at any stage of this fever. A typhoid 
patient is not out of danger until all tympanitis, diarrhoea, and other ab- 
dominal symptoms which indicate that intestinal changes are still progress- 
ing, have disappeared. Independent of complications, the duration, type, 
and intensity of the febrile excitement have more to do than all the other 
elements in determining the prognosis in any case of typhoid fever. The 
height of the temperature on the eighth day determines the range of tem- 
perature that may be expected on each succeeding day. If upon that day 
it is not higher than 104° or 105° F., and has been regular in its devel- 
opment (independent of complications), the prognosis is good ; in uncom- 
plicated cases it very rarely rises higher than the degree it has reached at 
that time. A prolonged high temperature (above 105° F.) after the first 



TYPHOID FEVER. 



week renders the prognosis unfavorable. In mild cases, during the second 
week, a marked morning remission occurs, which begins early and continues 
until midday; the evening exacerbation is late, and by the end of the sec- 
ond week there is a marked and permanent fall in the temperature. In 
severe cases, the opposite conditions are observed. A sudden rise in tem- 
perature, or a rapid and extreme fall at any period of the fever is a very 
bad omen ; the latter often precedes the occurrence of a severe intestinal 
hemorrhage. Marked variation from the typical temperature of the disease 
indicates the existence of complications. Slight decline accompanied by 
great fluctuation of temperature, during the third week, is an unfavorable 
symptom. The natural power of an individual to resist disease, especially 
the effects of prolonged high temperature, is a very important element in 
prognosis. The organ which is the surest indicator of such power (espe- 
cially in typhoid fever) is the heart. 

If the pulse is full and regular, perhaps beating at the rate of 110 or 115 
per minute, if the cardiac impulse is good, and a distinct first sound can 
be heard, even though at the end of the second week the temperature stands 
as high as 10G° F., the prognosis is favorable. If, however, the pulse has 
risen to 120 or 130 per minute, if the apex-beat is feeble or imperceptible, 
and the first sound of the heart is indistinct or altogether obscured, with a 
tendency to cyanosis and pulmonary oedema, the indications are that the 
patient's powers of resistance are failing, and under such circumstances the 
prognosis must be unfavorable. It is not so much rapidity as irregularity, 
a sudden falling and a sudden rising of the pulse, that indicates impending 
danger. The rapid rising of the pulse upon the slightest excitement is the 
most unfavorable indication, as it shows extensive heart-failure and a rapid 
giving way of vital power. A sudden fall of the pulse from any cause must 
always be regarded as an unfavorable indication. The abundance or color 
of the eruption does not influence the prognosis. Excessive tympanitis and 
severe abdominal pains are unfavorable symptoms. Severe and protracted 
muscular tremors, with subsultus, indicate danger. Sudden collapse 
during the second and third weeks of the fever is always attended with 
danger, as it is very likely to be due to copious intestinal hemorrhages 
or intestinal perforation. It sometimes occurs independently of either of 
these causes, but nevertheless is very apt to be soon followed by a fatal 
result. 

The prognosis is always bad in those who are very fat, and in those 
who are the subjects of gout, disease of the kidney, or any other severe form 
of chronic disease. In all such persons, during the second and third weeks 
of the disease, it is necessary to be constantly on the watch for the occur- 
rence of sudden collapse. My own experience leads me to the belief that 
when intestinal hemorrhage is scanty it has little influence on the final re- 
sult. When it occurs before the twelfth day of the fever, it is often of ad- 
vantage by relieving the intestinal congestion. But when profuse, or even 
slight, after the twelfth day, it is an unfavorable symptom and renders the 
prognosis unfavorable. The occurrence of the hemorrhage renders it prob- 



678 



ACUTE GENERAL DISEASES. 



able that ulceration has extended to the vessels beneath the transverse mus- 
cular fibres of the intestine, and such ulceration is very apt to go on to per- 
foration and a fatal peritonitis. 

The influence of age is very great in determining the prognosis in any 
case of typhoid fever. It is much better in children than in adults ; and in 
persons over forty years of age the prognosis is decidedly unfavorable, even 
though the symptoms may not indicate a severe type of the disease. In the 
case of those individuals who habitually use alcoholic stimulants, whose 
power of resistance to high temperature is diminished, the rate of mortality 
is very great. The puerperal state renders the prognosis especially unfa- 
vorable. The danger to the patient is equally great, whether the fever 
comes on prior to delivery or during puerperal convalescence. The paren- 
chymatous changes which take place in the different organs of the body 
during the progress of this fever, necessarily influence the prognosis. The 
muscular degenerations of the cardiac walls, and consequent loss of heart- 
power, which favor pulmonary and other hypostatic congestions, and the 
diminished quantity of blood sent to the various tissues of the body, inter- 
fere more or less with their nutrition. Necrotic and gangrenous processes, 
sometimes met with in the cellular tissue of the surface and along the line 
of the intestines, as also the venous thrombi which so frequently develop in 
a protracted case of this fever, are, to a certain extent, the result of this 
cardiac weakness, and render the prognosis unfavorable. Excessive cardiac 
weakness also favors the development of blood-clots in the heart-cavities ; 
these may break up and cause embolism somewhere in the course of the 
general circulation, and thus lead to changes which may destroy life. In- 
testinal perforations, one of the results of the intestinal changes incident to 
the fever, render the prognosis most unfavorable. 

Complications. — Slight bronchial catarrh can hardly be regarded as a 
complication, it is so much a part of the clinical history of the disease, 
but another much more serious bronchial complication is capillary bron- 
chitis. This usually comes on during the second or third week of the 
disease, and, if extensive, greatly endangers the life of the patient. It is 
indicated by subcrepitant rales suddenly developed over the whole of both 
lungs, accompanied by great dyspnoea and an abundant expectoration of 
stringy mucus. Its advent renders the prognosis most unfavorable. Ex- 
tensive oedema of the lungs, occurring with, or independent of, capil- 
lary bronchitis and pulmonary congestion, sometimes comes on suddenly 
during the third week of typhoid fever, and indicates great failing in 
heart-power. The slightest indication of its occurrence would always be 
regarded with suspicion. It is not infrequently accompanied by more or 
less extensive hemorrhagic infarctions of the lungs. These depend on 
embolism of some of the branches of the pulmonary artery due to frag- 
ments of clots which have formed in the right side of the heart, the re- 
sult of the cardiac weakness, and often lead to gangrene of the lung. It 
is sometimes impossible to diagnosticate their existence during life. 

Pneumonia, when it complicates typhoid fever, is generally latent. It 



TYPHOID FEVER. 



679 



comes on very insidiously, and will be recognized only by the most care- 
ful physical examination. It is more frequently developed during the 
third and fourth weeks of the fever, and usually is lobular rather than lobar 
in character. At first only single lobules are involved, but after a time 
an entire lobe becomes consolidated. When irregular variations in 
temperature occur during convalescence, or during the third or fourth 
week of the fever, there is reason to suspect the development of pneumonia. 
In the majority of cases the characteristic pneumonic cough and expecto- 
ration are absent. Whenever an extensive pneumonia complicates typhoid 
fever, the prognosis is especially unfavorable. 

Pleurisy is not so frequently a complication of typhoid fever as is 
pneumonia or bronchitis. When it does occur, the almost invariable prod- 
uct of the inflammatory process is pus. Usually it comes on insidiously, 
late in the disease, and is quite likely to pass unrecognized unless frequent 
physical examinations are made. In many instances it is really a sequela 
of the fever, not developing until three or four weeks after the fever has 
run its course. Its occurrence must always be regarded as unfavorable, 
for a year, or even longer time, must elapse before recovery can take place, 
and even then complete recovery is doubtful. 

Occasionally laryngitis is a serious complication of this fever. It gene- 
rally occurs in those cases where the fever has been very protracted, and 
there is great prostration. Its presence is marked by sudden and very 
intense inflammation of the mucous membrane of the glottis, which is 
liable to become oedematous, when death may suddenly occur. It may 
lead to ulceration of the mucous membrane, Pymmia may be met with 
as a complication during convalescence from typhoid fever, but it is not of 
as frequent occurrence as septicaemia. Whenever septic poisoning is de- 
veloped, with extensive sloughs in the intestines, the prognosis is exceed- 
ingly unfavorable. Acute gastric catarrh is another complication of this 
fever. Disturbances of nerve-function have been considered under the 
head of symptoms, but not infrequently certain brain and nerve lesions 
are developed which cannot be classed under that head. Cerebral oedema 
may complicate a typhoid fever during its third week, and give rise to 
symptoms of a grave character. A decided enfeebling of the mental 
powers and a tendency to stupor announce its occurrence. Hemorrhagic 
extravasations on the surface and into the substance of the brain, the 
result of degeneration of the walls of the cerebral vessels, occasionally 
occur during the height of the fever. If the effusion is moderate, no 
marked symptoms are developed ; but if a considerable extravasation takes 
place, it gives rise to symptoms of cerebral compression. Meningeal in- 
flammation is a rare complication. The occurrence of any of these com- 
plications in any case renders the prognosis unfavorable. 

During the second and third weeks of the fever certain cerebral disturb- 
ances may occur which seem to indicate the existence of some one of 
these complications, when no cerebral lesion exists. Usually they are 
present in patients who have had a continuously high temperature, and in 
favorable cases they disappear after a few days. Various other disturb- 



680 



ACUTE GENERAL DISEASES. 



ances of the nervous system, such as hemiplegia, paraplegia, etc., which 
may simulate those due to lesions of the nerve-centres, or forms of local 
paralysis and anaesthesia which seem to be confined to individual nerves 
are met with, but as these functional disturbances do not depend upon any 
anatomical changes, the prognosis in such cases is good. Those changes in 
the kidney, due to parenchymatous degeneration, which usually attend this 
fever have already been noticed ; but occasionally nephritis is developed 
as a sequela. The urine becomes scanty, is loaded with albumen, and con- 
tains blood and casts ; the face and extremities become oedematous, and 
death may occur from urgemia. The occurrence of this complication 
necessarily renders the prognosis bad. In a few instances under my ob- 
servation, severe catarrh of the bladder has developed during convalescence, 
greatly complicating the case ; in one instance the cystitis was accompa- 
nied by pyelitis. Cellulitis, especially of the surface, often complicates 
convalescence, and in some cases causes death. Occasionally it is met with 
in the pharynx and along the line of the lymphatics. Accompanying 
this cellular inflammation, or independently of it, gangrenous inflamma- 
tions of the integument not infrequently occur, giving rise to bed-sores. 
These gangrenous processes are most frequently developed at those points 
which have been subjected to the greatest pressure, on account of the po- 
sition of the patient in bed, such as the sacrum, nates, heels, and shoulder- 
blades. In the simplest form of bedsores there is only a superficial loss 
of substance ; in more severe cases the subcutaneous cellular tissue is in- 
volved ; and in the worst cases the muscles and fibrous tissues. I have 
met with cases where the slough had involved the connective- tissue and 
muscles, and laid bare the bone. A considerable number of typhoid pa- 
tients who have lived through the fever die either from the exhausting ef- 
fects of these bed-sores or from the resulting septic poisoning. The possi- 
ble occurrence of these complications must enter into the prognosis in every 
severe case, and the earlier they make their appearance the greater the 
danger. 

The average duration of typhoid fever is from three to four weeks. It 
may terminate in death or recovery at an earlier date. A typical case ex- 
tends over a period of four weeks. The period of invasion lasts from one 
to five days. The period of glandular enlargement continues until about 
the fourteenth day. The period of ulceration extends from the twelfth or 
fourteenth day to between the twenty-first and twenty-eighth. When the 
fever is protracted beyond the middle of the fourth week, in most in- 
stances this is due to some complication, or to an extension of the intestinal 
ulceration. The period of greatest danger is at the close of the third week. 

Death rarely occurs before the fourteenth day. The prominent direct 
causes of death are : toxcemia ; asthenia ; suppression of the excretory 
function of the kidneys ; hyperemia and cedema of the lungs ; intestinal 
hemorrhage ; exhaustive diarrhoea ; intestinal perforation ; and peritonitis 
with or without intestinal perforation. In nearly all cases the failure of 
heart-power is directly or indirectly the cause of death. In no case can 



TTPHOID FEVEK. 



681 



convalescence be said to be fairly established until the temperature remains 
normal for two successive evenings. The termination, like the commence- 
ment, is gradual, and is not marked by any critical evacuation or day of 
crisis. 

Relapses. — After typhoid fever has run its course, and the patient is en- 
tirely free from fever, quite frequently there is a new development of the 
fever ; these new developments are called relapses. Their course corre- 
sponds with that of the primary attack, only they are of shorter duration. 
The temperature rises more rapidly, the eruption reappears, the spleen en- 
larges, the intestinal and abdominal symptoms return, and all the promi- 
nent symptoms of the primary fever are rapidly developed. As a rule, the 
relapse is milder than the primary attack. If it terminates fatally, the post- 
mortem examination shows, in addition to the cicatrizing intestinal ulcers 
of the primary attack, the recent intestinal changes of the relapse. The 
lesions of the relapse, although of the same character as those of the primary 
attack, are less extensive. 

It is very difficult to give a satisfactory explanation of these relapses. 
Some claim that they are the result of certain plans of treatment, especially 
the cold-water plan. This assertion lacks proof. Others hold that all re- 
lapses depend upon a new infection. Perhaps this is possible if the patient 
remains in the same locality and has the same surroundings as when he had 
the primary attack ; but it does not explain relapses in those who are re- 
moved from all the sources of the primary infection. Another explanation 
offered is that a part of the typhoid poison has remained in the system, 
undeveloped during the primary attack, and that some time after this has 
passed the poison reproduces itself and sets up a second fever. A more 
recent theory is that the typhoid poison thrown off in the faeces of the 
patient is reabsorbed and causes the relapse. Unquestionably, it is possible 
for healthy glands to become inoculated by sloughs thrown off from those 
first affected. In many cases it is impossible to account for the occurrence 
of the relapse, and all of these explanations as to the cause in any case are 
more or less unsatisfactory. In those cases which have come under my 
own observation, I have noticed that the splenic enlargement which has 
existed during the course of the fever does not subside with its decline ; 
and that the tenderness along the line of the intestines, especially in the 
right iliac region, continues during the period between the original attack 
and the relapse. In some instances, apparently, the relapse has been 
brought on by indiscretion in diet, or by injudicious exercise on the part of 
the convalescent patient. Occasionally relapses have occurred when great 
care had been taken against any indiscretion or over-exertion. There is 
little doubt but that relapses are of much more frequent occurrence in those 
cases that are treated with cathartics during the first week of the fever, 
than in those where cathartics are not employed. 

Treatment. — Since the specific poison of typhoid fever is contained in 
the excrements of typhoid patients, the first indication in prophylaxis is 
to destrojr this poison as soon as it is discharged from the body. For this 



682 



ACUTE GENERAL DISEASES. 



purpose the intestinal discharges should be received into a porcelain bed- 
pan, the bottom of which is covered with a thin layer of powdered sul- 
phate of iron ; immediately after the discharge, crude muriatic acid, equal 
in quantity to one-third of the faecal mass, should be poured over it. The 
discharges of a typhoid patient (no matter how thoroughly they may have 
been disinfected) should never be emptied into a privy or water-closet. 
Trenches should be dug for their reception, and new trenches should be 
opened every few days ; the greatest care must be taken that these trenches 
are not so situated that the drainage from them can contaminate wells or 
springs which furnish drinking-water. 

All underclothing or bed-clothing that may have become soiled by the 
discharges from the bowels should be immediately immersed in chlorine 
water or other disinfectant, and thoroughly boiled within twenty-four hours. 
These procedures will certainly destroy the infective power of the typhoid 
poison contained in the intestinal discharges, and in the majority of instan- 
ces will prevent the spread of the fever. Repeated observations show that 
when one member of a family has typhoid fever, not infrequently it is 
developed in every other member. This spread of the disease can be pre- 
vented, unless there is some local cause for its development which cannot 
be reached. When its origin is not apparent, the wells, springs, and all 
the sources from whence water is derived for drinking and cooking pur- 
poses should be carefully and thoroughly inspected. Care must be taken 
that the waste-pipes from wells and springs do not pass directly into cess- 
pools or sewers, and thus become a means for the conveyance of impure 
gases into the springs and wells. The greatest care must be exercised in 
regard to house drains and sewer pipes, that they shall be free from leak- 
age and obstruction, and that all water-closets, sinks, and other openings 
into them be provided with suitable traps. When unpleasant odors are 
constantly present in dwellings, especially in sleeping apartments, disin- 
fectants should be employed, and the house be thoroughly ventilated. 
When it is necessary to open drains and cess-pools in a dwelling for 
purposes of repairing or cleansing, the same precautions should be exer- 
cised ; they are especially of importance during the summer and autumn. 

The question naturally arises : — is it not possible to counteract or neutral- 
ize the effects of the fever-poison after it has gained admission into the sys- 
tem, and thus prevent the development of typhoid fever ? To accomplish' 
this, blood-letting, emetics and diaphoretics have all been employed ; but 
there is not the slightest proof that typhoid or any fever-poison was ever 
removed from the system by these or any other agents. A patient with 
some of the premonitory symptoms of fever may perspire, be relieved, and 
at once recover, but such a patient had not received the typhoid poison into 
the system, and was not, as is sometimes said, "threatened with typhoid 
fever." Notwithstanding the bold affirmation of the author of the cold 
affusion plan of treatment, that if it were resorted to before the third day 
of the disease, it would invariably arrest its development, it has failed to 
stand the test of practical experience. More recently, sulphate of quinine, 



TYPHOID FEYEE. 



683 



administered in large doses, has been thought to have the power of arrest- 
ing the development of typhoid fever in the same way that it arrests mal- 
arial fever, by its anti-periodic power ; but there is no evidence that it has 
any such power, and as a prophylactic remedy it has been abandoned. 

After the poison has once gained entrance into the system, no means 
has as yet been discovered by which it can be counteracted or neutralized 
so as to prevent the development of the disease. The duty of the physician 
is to guide the disease, so far as he may be able, to a favorable issue, and 
prevent injury to organs essential to life, keeping in mind that a certain 
definite period must elapse before this result can be accomplished. 

The arrangement of the sick-room of fever patients, though often over- 
looked, is a matter of no inconsiderable importance, not only as regards the 
comfort of the patient, but also the successful issue of the case. It is of 
the greatest importance that a properly qualified nurse be selected ; one 
who has had experience in the care of fever-patients is to be preferred. The 
patient should be placed in a large and well-ventilated apartment. All fur- 
niture should be removed from the sick-room except those articles which 
are necessary for the comfort of the patient and the convenience of the at- 
tendants. The carpets should be removed from the floor and the patient 
placed in a bed of moderate size in the centre of the room. Free ventila- 
tion during both day and night, is of the utmost importance. The tem- 
perature of the apartment should be kept below 60° F. The bed and body 
linen of the patient should be changed daily, and at once removed from the 
sick-room and placed in a weak solution of chlorinated soda ; especially 
is this important if the patient is having frequent discharges from the 
bowels. The apartment should be kept perfectly quiet, the light subdued, 
and only the attendants should be allowed in the room. Any medicinal in- 
terference in a mild type is unnecessary. The treatment resolves itself into 
the arrangement of the sick-room and proper diet ; milk is the most suit- 
able food, and fruits are not to he allowed in any case. Even in the mild- 
est case this care in diet is important, and the patient should be kept in 
bed until convalescence is fully established. This should be insisted upon 
in the mild as well as in the severe cases. 

The temperature in a mild type of this fever rarely rises above 103° F.; 
therefore there is no necessity for resorting to antipyretic measures ; fre- 
quent sponging of the surface with cold or tepid water, as is most agree- 
able to the patient, will be found of service. By far the larger number of 
cases of this fever, however, are of a more severe type, and though the 
treatment must be regulated by the circumstances which attend each indi- 
vidual case, more decided measures w r ill usually be necessary. Typhoid 
fever is a disease that has certain stages to pass through, and there is 
great doubt whether the physician can shorten its duration by a single day, 
but experience warrants the belief that many lives may be saved by reme- 
dial measures, used at the proper time, and combined with judicious hy- 
gienic management. 

Unquestionably one of the most important things to be accomplished is 



684 



ACUTE GENERAL DISEASES. 



the reduction of temperature, or rather the keeping of the temperature 
below a certain standard. The agents which have been employed more re- 
cently for this purpose act powerfully in reducing the temperature and lessen- 
ing the severity of the disease. It is claimed by many distinguished ob- 
servers of the present day that the parenchymatous degenerations of the 
different organs and tissues of the body which are found in those who die 
of typhoid fever are due to the prolonged high temperature which is pres- 
ent during the course of this disease ; but as yet there are no facts to prove 
this assertion, for the same parenchymatous changes are found in the bodies 
of those who have died of diseases the course of w^hich was not marked by 
high temperature, and did not extend over a period of more than forty- 
eight hours. So far as we are able to determine by analogy upon what 
these parenchymatous changes depend, we are led to believe that the spe- 
cific poison of the disease has more to do with their development than the 
high rate of temperature. One thing must be apparent to every clin- 
ical observer : that the injurious effects of a prolonged high temperature 
are early and most markedly shown by disturbances of the cerebro-spinal 
system. It is still an unsettled question whether these disturbances are duo 
to the primary changes in the constituents of the blood, which always ac- 
company a high range of temperature, or to the direct effects of the high 
temperature or of the peculiar poison on the nerve centres. Whichever view 
we adopt, the employment of those means which have the power of safely 
reducing temperature is indicated, and when judiciously used they have 
much to do with the safety of the patient. 

All those means which have been employed for the reduction of tempera- 
ture are included under the general term of antipyretics, and the treatment 
of disease by the use of these agents has received the name of antipyretic 
treatment. Unquestionably one of the most efficient and reliable of the 
antipyretic agents is the external application of cold by means of baths, 
packs, and affusions. 

At the present time the opinion prevails, to a great extent, that the ap- 
plication of cold to the surface is the great antipyretic in the treatment of 
fever. This is no new teaching. Long ago Dr. Currie recommended the 
application of cold to the surface of the body for the purpose of rapidly re- 
ducing temperature, and proved that it had such an effect ; yet it was never 
very generally practised, and soon fell into disuse, as there were no reliable 
indications to guide one in its application. As we now have the thermome- 
ter as such a guide, it has been resorted to more recently with considerable 
puccess. It is employed in the following manner. As soon as the axillary 
temperature in the evening rises above 105° F., the patient is placed in a 
water-bath having a temperature of 70° F. or 80° F., which is gradually 
lowered, by the addition of cold water or ice, until the temperature of the 
patient begins to fall. It may be necessary to lower the temperature of the 
bath to 60° F. before the temperature of the patient is affected. When the 
temperature begins to fall, therm ometrical observations should be made 
every two or three minutes, by placing the thermometer in the rectum. If 



TYPHOID FEVER. 



G85 



it falls rapidly — that is, two or three degrees in five or six minutes— as soon 
as the temperature has reached 103° F. the patient is to he removed from 
the bath; if it falls slowly, as soon as it reaches 101° F. he should be re- 
moved and immediately placed in bed. It is never safe to keep the patient 
in the bath until the temperature shall have reached the normal standard ; 
for he may pass into a state of collapse, since the temperature continues to 
fall for some time after his removal from the bath. While in the bath, cold 
should be applied to the head by means of a sponge wet in cold water, or 
by an ice-bag, The cold pack is much less effective than the bath ; but if 
the patient is too feeble to be removed, it may be employed with benefit. 
The patient is wrapped in a sheet wrung out of tepid water, and over this 
one wrung out of cold water is applied. The latter may be removed as it 
becomes warmed, and its application and removal continued until the de- 
sired fall in temperature shall be obtained. In severe cases, during the 
first and second weeks, after the temperature has been reduced by the ap- 
plication of cold to the surface, it will soon begin to rise, and continue to do 
so until it reaches its former height. Usually one to three hours will elapse 
before it begins to rise, and from two to six before it reaches its former 
height. It will then be necessary to repeat the baths or packs, and to con- 
tinue their use, both day and night, from three to six times during the 
twenty-four hours, in order to keep the temperature below 103° P., and ac- 
complish anything by this plan of treatment. 

My experience in the use of cold applications leads me to believe that 
unless it is possible to maintain a low range of temperature after four or 
five baths very little is gained by their continuance. I am also convinced 
that, after the second week of typhoid fever, cold baths should not be em- 
ployed to reduce temperature. The condition of a typhoid patient during 
the first and second weeks of the fever is very different from that during the 
third and fourth weeks. During this latter period there is great danger of 
collapse after a cold bath, and in several instances I am confident that pul- 
monary complications have been the result. In some cases when the 
patient is placed in the cold bath, the temperature will immediately begin 
to fall ; in other cases there will be a gradual reduction of temperature as 
the water is made cooler. In certain severe cases a patient may be kept 
in a bath of the temperature of 60° F. for the space of half an hour with- 
out the temperature falling a degree. These cases are exceedingly grave 
in character, and the bath should be used with great care. 

There is no remedial agent which requires greater care and judgment in 
its use than the cold bath, yet, doubtless, when judiciously employed, the 
lives of many typhoid patients may be saved, and it is equally certain that 
when injudiciously employed many lives may be destroyed. The general 
condition of a patient and the stage of the fever must be considered ; also 
the effects of the first few baths must be carefully noted. Should a pa- 
tient's temperature range at 104° F. or 105° F., it is no positive indication 
for the resort to a cold bath, or that a cold bath is the best agent to be 
employed for its reduction. If the patient after the second or third bath 
is more quiet, has less delirium (if delirium previously existed), if his 
breathing becomes easy and natural, if the heart's action is more regular 



686 



ACUTE GENEKAL DISEASES. 



and forcible, and he falls asleep and perspires, there can be no question in 
regard to the beneficial effects of the bath. If, on the other hand, the 
bath is followed by feebler heart's action, by dusky cheeks, by rapid respi- 
ration, and by coldness of the extremities, from which condition the 
patient rallies slowly and imperfectly, it is certain that, however high the 
temperature may range, harm will be done by continuing the baths. When 
the extremities are cold, or there is profuse hemorrhage from the bowels, 
or when from any cause there is great feebleness of the heart's action, and 
especially in the case of aged persons, cold baths are contra-indicated. 

In a few instances the temperature can be very rapidly lowered by the 
application of the cold coil to the abdomen, and it is my habit in all severe 
cases to apply the cold coil early and continue its use until the tempera- 
ture curve indicates that it is no longer necessary. The use of cold baths 
will thus be avoided in many cases. In addition to its beneficial effect on 
the intestinal changes which constitute such an important element in the 
history of this fever, the cold coil often has great power in reducing the 
general heat of the body. I have also in some instances found the body 
temperature rapidly lowered by injections of ice-water into the rectum. 
Care must be exercised that the cold injections are not administered too 
rapidly or in too large quantities. Although this mode of abstracting heat 
and lowering the body temperature is never so effective as by baths and 
packs, still it has this advantage, that no such compensating increase in 
the production of heat follows the use of the cold injections as follows 
the cooling of the external surface by the baths. In many cases the 
extreme obstinacy of the fever, which resists the most systematic use of 
cold, as well as the fact that some patients cannot bear a sufficiently fre- 
quent repetition of the baths to effect the desired result, or that there may 
be contra-indi cations to their use, necessitates the employment of other 
means for the reduction of the body temperature. 

The use of the internal antipyretics has undergone many changes within 
a short time. Formerly it was my practice to employ sulphate of quinine 
almost exclusively in the treatment of typhoid fever. Its antipyretic 
power is established beyond question, and I still regard it as a most valu- 
able agent in many conditions. When used as an antipyretic it must be 
given in large doses. Its use may often be combined advantageously with 
that of cold baths, the quinine being given when the patient is removed 
from the bath. Thus used it will delay the return of the previous high 
temperature. 

Antipyrin and antifebrin have recently been largely employed in the 
treatment of all forms of fever, and often with little discrimination as 
to their action. 

Of the two I prefer antifebrin, and have found it so valuable that it has 
largely supplanted quinine in my treatment of typhoid fever. I prefer to 
give it in five to ten grain doses three or four times in the twenty-four 
hours rather than in one large dose. It may be employed in connection 
with the cold baths in the same manner as quinine. It has seemed to me 
not only to lower the temperature, but to exert a most favorable influence 



TYPHOID FEVEK. 



687 



upon the cerebrospinal disturbance. The same general rules are to be 
followed as govern the use of all antipyretics. If, during the third and 
fourth weeks, these means fail to reduce the temperature, from ten to 
twenty grains of powdered digitalis may be administered within twenty- 
four hours, unless the pulse is very frequent and irregular — when its use 
is contra-indicated. 

Digitalis should be employed only when some other antipyretic is given. 
It seems to increase their power, but has little or no effect when adminis- 
tered alone. The use of all antipyretic remedies must be persisted in 
until the desired end — the reduction of temperature — is accomplished ; 
but the peculiarities of each patient must be studied, and these agents 
must be so administered as to suit each individual case. The satisfactory 
results obtained by the systematic use of these remedies justify their 
employment ; but the exact rules which are to govern one in their use, as 
to manner and time, can only be determined by experience. 

If the temperature of a patient can be kept below 103° F., during the 
first two weeks of the fever, the first and perhaps the most important 
thing in the treatment of this disease will be accomplished. 

Toward the end of the second, or during the third week, signs of failure 
of heart-power begin to manifest themselves ; although the temperature 
may not rise higher than 101° F., the pulse frequently becomes extremely 
feeble and irregular and reaches 140 per minute, while the first sound of 
the heart becomes inaudible at times ; the surface is cool and moist ; the 
patient complains of a sense of exhaustion, and perhaps is unable to turn in 
bed ; muscular tremors, dry, brown tongue, and all the symptoms which 
indicate failure of vital power are present. 

Under these circumstances the use of stimulants seems to be urgently 
demanded. 

A few simple rules govern their administration. 

First They should never be administered indiscriminately—that is, 
simply becan.se the patient has typhoid fever. 

Second. When there is reasonable doubt as to the propriety of giving or 
withholding stimulants, it is safer to withhold them, at least until the signs 
which indicate their use become more marked. 

Third. In every case, but especially when stimulants are not clearly in- 
dicated, the effect of the first few doses should be carefully noted. There 
are few wmose experience in the treatment of typhoid fever is such as to 
enable them to determine positively, from the appearance of the patient, 
when the administration of stimulants should be commenced. 

If under their use the tongue becomes dry, the patient more restless, the 
delirium more active, the temperature higher, and the pulse more fre- 
quent, it is very certain that stimulants are contraindicated. If, on the 
other hand, the pulse becomes fuller and more regular, if the first sound 
of the heart is more distinctly heard, or if, having been absent, it returns, 
if the restlessness and delirium are less marked, the tongue more moist, 
and the patient more intelligent, it is equally certain that the time for ad- 
ministering stimulants has arrived. When their use is once begun, it is of 
the greatest importance to administer them at stated intervals, especially 



6S8 



ACUTE GENERAL DISEASES. 



during the night. In a severe case of typhoid fever, free stimulation, just 
at a critical period (which may not last more than twenty-four hours), 
will often be followed by a refreshing sleep, and the patient may rapidly 
pass from an apparently hopeless condition to one of convalescence. 

The third important thing to be accomplished in the management of 
typhoid fever patients is the maintenance of nutrition. The principal 
effects of the typhoid poison are manifested in the changes which take 
place in the lymphatics of the gastro-intestinal tract. Experience has 
taught us that the enfeeblement of the digestive and assimilative powers, 
due to these glandular changes, which is manifested from the very com- 
mencement of the fever, renders the digestion of solid food impossible, and 
for a long time it has been the rule of the profession to allow typhoid fever 
patients only liquid food. There has been, and still is, great diversity of 
opinion in regard to the special articles of diet best suited to this class of 
patients. There is no disease in which a waste of all the tissues of the body 
goes on so rapidly as in typhoid fever. 

Milk is an article of diet which furnishes the elements of nutrition neces- 
sary to repair this rapid waste, and there are not the objections to its use 
which are against animal broths and gruels. Although there have been, 
and still are, in some quarters, strong objections against its use as an article 
of diet in fevers, recently it has been regarded with more favor, and those 
who have had most extended opportunities for testing its nutritive qualities 
have come to regard it as the only article of diet required by typhoid 
patients. In it we not only find all the elements required for repairing the 
rapidly wasting tissues, but they are in a condition to be most readily 
assimilated by the enfeebled digestive apparatus. In order that it shall not 
become distasteful to the patient some variations must be made in its 
preparation. It may be simply curdled, boiled, frozen, slightly fermented, 
or mixed with lime-water, seltzer, or some other mineral water, and various 
palatable preparations can be made from milk which has been partially 
digested with pepsin or pancreatin. If agreeable, buttermilk may be sub- 
stituted for a time. The quantity of milk is not limited ; the patient may 
take all his stomach will digest — usually patients will take from four to 
six pints in the twenty -four hours. After the patient has passed into the 
fourth week of the disease it may be necessary to administer cream and the 
yolks of eggs in connection with the milk. 

I now come to the treatment of the accidents of the disease. 

Diarrlma. — The poison which produces this fever unquestionably has a 
specific action upon the intestinal glands and lymphatics. It is here that 
we find the characteristic lesions of the disease, and it is scarcely ques- 
tioned that the typhoid poison, to a great extent, gains entrance to the 
system through these glands and lymphatics, and here produces the primary 
irritation. Following the irritation and inflammation of the follicles, other 
portions of the mucous membrane become involved, and a catarrhal inflam- 
mation of the mucous membrane of the intestinal tract follows. The nec- 
essary consequence of this is a diarrhoeal discharge, which is simply an in- 
dication that these intestinal changes are going on ; it is not due to the 



TYPHOID FEVER. 



6S9 



elimination of the typhoid fever poison, but to the inflammation which the 
fever poison has excited in the intestinal glands. When the diarrhoea is 
present in the earlier period of the disease, it is better to let it alone, as 
during the first and second weeks the danger is very slight. It has been 
proposed to treat this diarrhoea, which makes its appearance early in the 
disease, with alkalies, bismuth, pepsin, etc. It is claimed that if these 
remedies be administered, diarrhcea can be prevented, or, if it already 
exists, that it can be controlled. Theoretically, I see no reason for employing 
alkaline remedies, for the diarrhceal discharges are always alkaline, and 
from clinical observation, I am convinced that bismuth, pepsin, etc., have 
little or no effect either in controlling the diarrhcea or in preventing the 
intestinal changes which produce it. 

"When diarrhoea commences late in the disease (during the latter part of 
the third, or during the fourth week of the fever), it is of a very different 
character from that which occurs during the first and second weeks. Ul- 
ceration of the intestinal glands, and perhaps sloughing has been estab- 
lished, and, in addition to the extensive local changes, there is a septic ele- 
ment which enters into the causation of the diarrhoea at this stage. Be- 
sides, the increased peristaltic action of the intestines, which attends the 
diarrhoea, favors an extension of the inflammatory processes to the peri- 
toneum, esj^ecially that portion which covers Peyer s patches. In view of 
the^e facts, the diarrhoea should be arrested or held in check. For the 
accomplishment of this, there is but one remedy which can be relied upon 
— that is opium. My experience is against the use of astringents. If 
opium will not arrest it, one may expect little aid from astringents com- 
bined with opium as they are usually administered. The use of opium is 
objected to by some, who claim that it diminishes the power of the heart's 
action ; but in this disease, when administered in small doses, it seems to 
me to increase rather than diminish the heart-power. It is acknowledged 
that opium, more than any other drug, arrests the peristaltic action of the 
intestines ; and that is what we wish to accomplish when diarrhcea is pres- 
ent during the third and fourth week of typhoid fever. 

When during convalescence diarrhoea is persistent, the patient should be 
kept in bed and some of the vegetable astringents, as catechu or hsematoxy- 
lon, may be employed. 

Tympanitis. — When this has proved a distressing symptom, I have 
usually found relief to be obtained by the application of turpentine stupes 
to the abdomen. Some claim that if turpentine be administered internally 
from the beginning to the end of typhoid fever, tympanitis and the intes- 
tinal changes which lead to it and to the diarrhcea are much less severe. I 
am confident that the turpentine treatment, as it is called, does not have 
the controlling influence over this fever which has been claimed for it : but 
I am certain that it is our most reliable agent for the relief of the tym- 
panitis. 

• Intestinal Hemori'hage. — When this occurs early in the fever, it usually 
requires no treatment ; but when it occurs during the third or fourth week^ 

44 



690 



ACUTE GENERAL DISEASES. 



or after convalescence is apparently fully established, it must be arrested as 
promptly as possible. The occurrence of severe intestinal hemorrhages 
may sometimes be prevented by keeping the patient in bed. A typhoid 
fever patient should not be allowed to get out of bed from the beginning of 
the attack until convalescence is fully established. Especially is this of 
importance if the case is a severe one, and attended by symptoms that indi- 
cate extensive intestinal lesions. When hemorrhage from the intestines 
occurs during the third or fourth week of the fever, it is most surely con- 
trolled by the administration of opium in small doses at short intervals. 
Absolute rest of the body must be insisted on, the patient must not be 
turned on the side or moved in bed, and an ice-bag should be applied 
over the abdomen. I doubt if any good results can be accomplished by 
the use of astringents, either by enemata or by the mouth, as it is not 
known that they even reach the seat of the hemorrhage, although gallic 
acid and the persulphate of iron are usually recommended in cases of in- 
testinal hemorrhage occurring in typhoid fever. If the hemorrhage is pro- 
fuse, it may be necessary to keep the patient under the influence of opium 
for a week or ten days ; in such cases the internal use of turpentine in con- 
nection with the opium will be found of service. 

Peritonitis. — When perforation of the intestine occurs, the case may be 
regarded as hopeless ; death takes place usually within twenty-four hours, 
as the result of general peritonitis ; no plan of treatment avails anything. 
If the peritonitis occur without perforation, from extension of the inflam-. 
matory process from the intestinal ulcers, bringing the patient rajndly into 
a state of semi-narcotism and holding him there for five or six days may 
prevent the occurrence of the perforation, and thus save life. Such a case is 
to be treated in every respect as one of localized peritonitis. After recovery 
from an intestinal hemorrhage or a localized peritonitis in typhoid fever 
great care should be exercised in the administration of cathartics or ene- 
mata. The bowels will move spontaneously after a time, even though the 
use of opium be continued, and no harm will follow should two or three 
weeks pass before they do so. When the stomach is irritable, the hypodermic 
injection of morphine is preferable to opium administered by the mouth. 

Bronchitis. — For the catarrh of the larger bronchial tubes no special 
treatment is required ; but, if the bronchitis becomes capillary, great relief 
will be obtained from the application of dry cups to the chest and the in- 
ternal administration of carbonate of ammonia. Vapor inhalations will 
also be found of service in severe cases. 

Pneumonia.— The pneumonia which complicates typhoid. fever in nearly 
every case is lobular in character. The signs which indicate its occurrence 
are sudden rise of temperature, increased frequency of respiration, and the 
physical signs of localized pulmonary consolidation ; cough and expectora- 
tion are rarely present. Its occurrence is always an indication that stimu- 
lants should be administered. If they are being administered, they should 
be increased in quantity. To prevent or relieve the hypostatic congestion 
of other portions of the lung, which frequently accompanies pneumonic de- 



TYPHOID FEVER. 



691 



velopment, tlie heart-power must be increased, and the position of the 
patient changed. 

Laryngitis. — For the relief of the laryngitis which occasionally compli- 
cates typhoid fever, a small blister may be applied on either side below the 
angle of the jaw, and the whole neck enveloped in a poultice. If these 
measures fail, and suffocation appears imminent, tracheotomy should be 
resorted to without delay. 

Sub-acute gastric catarrh, occurring as a complication during conva- 
lescence from the fever, can only be managed successfully by giving the 
stomach rest as far as possible, restricting the diet to a single tablespoonful 
of milk at a time, and applying hot fomentations over the epigastrium. 

Bed-sores. — The severer forms of bed-sores are the most intractable com- 
plications one has to combat. Fortunately the severer forms are much less 
frequently met with under the more recent plan of treatment. Scrupu- 
lous cleanliness is the principal means for preventing their development. 
So long as there are no erosions, the parts should be frequently bathed in 
spirits of camphor, and the points of attack should be relieved from all 
pressure. If the sores penetrate the integument, they should be frequently 
washed with a weak solution of carbolic acid, or brushed over with equal 
parts of balsam of Peru and balsam copaiba, and afterward covered with dry 
lint, or lint covered with vaseline. The most unfavorable cases are those in 
which the point of pressure caused by the weight of the body becomes gan- 
'grenous. In such cases, a continuous warm bath is recommended by some. 
As soon as sloughing takes place, and the parts separate, they should be 
dressed with lint saturated with balsam of Peru and carbolic acid. 

Constipation. — As already stated, diarrhoea is usually present in the early 
period of this fever ; but sometimes there is constipation. The question 
arises : — is the administration of cathartics ever admissible in typhoid fever ? 
Quite diverse views are still held in regard to this question. Eecently, 
certain observers of extended experience have claimed that there is suffi- 
cient reason for the belief that a portion of the typhoid poison lodged in the 
alimentary tract may be expelled by the timely administration of cathar- 
tics, and thus the severity of the fever be mitigated and its duration short- 
ened. Eecent German writers claim that calomel acts beneficially only as 
a cathartic. Those who favor the administration of cathartics recommend 
their use mainly during the first week of the disease. On the other hand, 
equally competent observers maintain that the intestinal changes are aug- 
mented and rendered more extensive by the action of cathartics, that the 
normal course of the fever is interfered with, and that in a large proportion 
of cases where intestinal and peritoneal complications occur, hypercatharsis 
has been induced at an early period of the fever by the administration of 
cathartics for the purpose of shortening its duration. My own experience 
leads me to exercise the greatest caution in the administration of cathartics 
in any stage of this fever. 

I am confident that the routine practice of administering purgative 
medicines in the early stage of typhoid fever can only be followed by 



692 



ACUTE GENERAL DISEASES. 



a threefold injury : first, the patient is weakened. Secondly, the local 
intestinal lesions are increased. Thirdly, perforation and peritonitis are 
more liable to occur. 

Nervous Phenomena. — Should headache be severe, not readily relieved 
by fomenting the forehead and temples with warm water, or should it give 
place to active delirium and other severe nervous disturbances, the ques- 
tion presents itself : — shall anodynes be administered ? If they are to be 
used the most reliable is opium, and usually the condition of the pupil 
of the eye will serve to indicate whether opium shall or shall not be ad- 
ministered. A contracted or "pin-hole " pupil may be considered to contra- 
indicate its use, though there are exceptional cases in which opium acts 
favorably, notwithstanding this condition of the pupil. Opium should be 
given with great caution whenever signs of cyanosis are present. In all 
cases of typhoid fever, it is safer to administer opium in small and repeated 
doses than to venture upon the administration of one large dose. There 
are other anodynes which will sometimes be of service, such as hyoscyamus, 
chloral and the bromides. Chloral is said to have a special value in 
quieting active delirium, which is sometimes so troublesome, but my 
own experience in its use has not been favorable. 

When anodynes have failed to give relief to typhoid fever patients, who 
have been delirious and somnolent for days, they will sometimes become 
quiet and fall asleep immediately after the free administration of stimu- 
lants. Those cases in which the nervous symptoms are due to an anaemic 
condition of the brain, associated with a weak heart and a nagging circu- 
lation, are most likely to be benefited by the use of stimulants. In those 
cases in which subsultus becomes very marked, and there is general 
tremor, jactitation and restlessness, I have seen most happy effects pro- 
duced by the use of hypodermic injections of sulphuric ether. I would 
rise, as an average quantity, four drachms, given in injections of one drachm 
each, in different places. The same watchful care should be taken of a 
typhoid fever patient during convalescence as during the active period of 
the fever. The number of typhoid patients who die during convalescence 
is relatively large. 

Death is often due to the fact that the physician has laid down no 
strict rules to be observed as to diet and exercise, and frequently from the 
non-observance of such rules when they have been given. The diet of 
fever patients during convalescence should be carefully watched. Only 
small quantities of food should be taken at a time, so that the gastric 
juice secreted by the enfeebled stomach may be sufficient for its complete 
digestion. All indigestible articles of food, and those which furnish a 
large amount of waste, should be strictly forbidden. An apparently in- 
significant disturbance of the stomach, a slight vomiting, or a moder- 
ate diarrhoea occurring during the period of convalescence, should be 
regarded as dangerous, for any one of these may induce a sub-acute 
gastritis, or lead to intestinal perforation and a fatal peritonitis. It is 
obvious that while the intestinal ulcers are healing much mischief may be 



YELLOW FEYER. 



693 



done by improper diet. Notwithstanding the cravings of the patient's 
appetite, the diet must be restricted to such articles as milk, cream, gruels, 
jellies, and animal broths. Solid food must be strictly forbidden, espe- 
cially meats, vegetables, and fruits. If diarrhoea is present during conva- 
4 ^scence it is far safer to restrict the patient to milk and cream. All ex- 
ercise, except simple walking around the sick-room, should be prohibited. 

It is ot the greatest importance that this class of patients should keep in 
the recumbent or semi-recumbent posture until the cicatrization of the in- 
testinal ulcers is completed, which in some instances does not take place 
until two or three weeks after convalescence is well established. If con- 
valescence is alow, small doses of quinine, iron, and cod-liver oil are of 
service. They should be given after the patient has taken food. In many 
cases it is important to take the evening temperature for at least two weeks 
after the commencement of convalescence, for by its range it will be pos- 
sible to more accurately determine the exact condition of the patient. 
When convalescence is delayed, so that at the end of four or five weeks the 
patient has not regained strength, change of air is indicated. 

YELLOW FEVEK, 

Yellow fever is an endemic miasmatic contagious disease, which usually 
appears as an epidemic. It prevails most in tropical regions, and is char- 
acterized by a yellowish discoloration of the skin. From some of its more 
prominent symptoms it has been called typhus icterodes, Mack-vomit or 
hamw-gastric fever, febris fiava, and also mat de Siam. 

Morbid Anatomy. — The pathological changes of yellow fever have much 
that is common both to contagious and miasmatic diseases. Its most con- 
stant and characteristic lesion is to be found in the changes which take place 
in the liver. 

• The liver is usually slightly enlarged ; it may, however, be normal, or even 
slightly diminished in size. The most striking change is in its color, which 
has been described as butter-, cheese-, mustard-, or chamois-yellow. Some- 
times it is of a chocolate or bright orange color. The change in color 
may be uniform throughout the entire organ, or it may occur in ir- 
regular patches of different hues. Slight extravasations of blood are 
sometimes found on its surface. In some few instances this change will be 
confined to a single lobe or a circumscribed portion of the organ. The 
liver-tissue breaks down readily on firm pressure, and on section is drier 
than normal, containing less blood. Small points of extravasation some- 
times stud its substance. 

Under the microscope the liver cells, while unaltered in shape, are seen 
to be filled with oil-globules, so large that at times one globule occupies an 
entire cell. Sometimes the change is a granular one, the nuclei of the 
hepatic cells being obscured; or they have entirely disappeared. 1 This 
change is an acute fatty degeneration, and not an infiltration, as many sup- 



1 Yellow Fever considered in its Historical, Pathological, Etiological, and Therapeutical Relations. R. 
La Roche. Philadelphia, 1855. Yellow Fever. Fritz Eaenisch. Ziemssen's Cyc. Prac. Med., vol. i. 



694- 



ACUTE GENERAL DISEASES. 



pose. The organ in its gross as well as in its minute anatomical changes 
resembles the fatty degeneration of the drinker's liver. Cornil and Ran- 
vier 1 say this degeneration is secondary to a congested and ecchymosed 
state of the liver. 

The heart is lighter in color than normal, soft, friable and flabby. It 
breaks down readily under firm pressure, and resembles strongly in its gross 
and microscopical characters the heart of typhoid fever. The muscular 
elements undergo the same granular degeneration, which cannot be ascribed 
to prolonged high temperature, for in yellow fever the temperature is neither 
high nor does it persist above normal for a long time. As in typhoid, so here 
we are inclined to regard the degenerative changes as the result of the 
specific poison of the disease. The cavity of the pericardium usually con- 
tains one or two ounces of blood-stained serum. Long coagula or partly 
organized clots extend from the heart cavities quite a distance into the ves- 
sels. These coagula are the result of the heart-failure, and are formed 
during the few last hours of life. Sometimes the blood in the heart is fluid, 
varying in color and reaction. 

The blood-changes are similar to those of typhoid and typhus fever, yet 
are more extensive than in either ; the blood is of a darker color than 
normal, and coagulates very much more slowly and imperfectly than 
normal; a fact due either to a diminution in, or to a partial loss of the 
coagulating power of the fibrin-factors. The red blood globules are de- 
stroyed, or they are serrated and shrivelled, and in many instances broken 
down — this explains the yellow color of the surface which gave the name 
to the disease. A solution of part of the red corpuscles occurs, and 
the haematin is changed into pigment. This condition of the blood also 
explains to a certain extent the degenerations which are found in the dif- 
ferent organs of the body. Very soon after withdrawal the blood under- 
goes ammoniacal decomposition, due in part to the altered relation of its 
salty constituents. Some affirm that the blood contains free ammonia. It 
contains no free pigment. 

The mucous membrane of the oesophagus, stomach and small intestine is 
always the seat of a more or less acute catarrh. The veins are varicose and 
lurgid, often giving rise to arborescent injection of the membrane ; and 
ecchymotic spots of extravasation irregularly stud its surface. Hemorrhagic 
erosion of the stomach is sometimes present, and throughout the whole in- 
testinal tract there is often a considerable quantity of dark-colored fluid 
blood, the stomach, however, containing matters similar to those vomited 
during life. The gastric mucous membrane is abo not infrequently found 
thickened, softened, and reddened. The mucous membrane lining the 
larynx also suffers a catarrhal inflammation ; and ecchymotic spots are found 
on the lining membrane of the bladder. 

The lungs are almost constantly the seat of infarctions, and these are 
occasionally quite numerous. When diffuse, pulmonary apoplexy occurs, 
and when a large portion of a lobe is involved, the lung- tissue will be 
broken down and large blood-clots will occupy the space. 



1 Patholog. Histology. 



YELLOW FEVER. 



695 



The pleura are sometimes covered with ecchymotic spots, and occasion- 
ally there is a blood-stained serous exudation into the pleural cavity. 

The brain and cord, if at all altered, are only slightly hypereemic. Punc- 
tate extravasations may occur in the meniuges ; and some affirm that an 
abundant serous exudation is often present in the lumbar and sacral regions, 
attended by an inflammation of the membranes of the cord at the same 
point, with more or less intense inflammation of the neurilemma of - the 
nerves in the coeliac and hepatic plexuses. 

The kidneys are the seat of parenchymatous inflammation, which rap- 
idly passes to the stage of fatty metamorphosis. There are sometimes 
small abscesses in the parenchyma. On microscopical examination oil- 
globules are seen to till the tubules, whose epithelium is sometimes desqua- 
mated, or the seat of fatty or granular change. Occasionally the tubules 
are filled with broken-down epithelium. The pelves of the kidneys and 
the ureters are frequently the seat of an acute catarrh. 

The spleen may be slightly enlarged ; but is usually softer, more friable, 
and darker than normal. 

The shin varies in color from a bright golden-yellow to a dark orange. 
Petechias, ecchymoses, vesicles, pustules, and large patches of extravasation 
may be found upon the surface of the body. The mucous membranes are 
not infrequently of a distinctly yellowish tinge. 

The gall-bladder may or may not be increased in size ; it commonly con- 
tains a moderate quantity of dark-colored bile, and its mucous surface ex- 
hibits spots of punctate extravasation as well as arborescent vascularity. 

The ovaries and uterus very frequently contain a considerable quantity 
of extravasated blood. 1 

Etiology. — As yet the specific microbe of yellow fever has not been dis- 
covered, although two or three have been claimed by different investiga- 
tors as pathogenic of this disease. From its clinical history we are led to 
believe that it is to be included in the class of diseases whose microbic ori- 
gin has been determined. 

Yellow fever is rarely met with beyond the limits of 40° North and 20° 
South latitude ; it prevails in the West Indies and eastern part of the West- 
ern Hemisphere far more frequently than any other region, and the locus, 
if we may say so, of the malady is the Antilles. In these places it is en- 
demic, and to a comparatively slight extent it is so in certain portions of 
Europe and Africa. Commercial seaports are pre-eminently the starting- 
points of great epidemics ; it is sometimes circumscribed within very nar- 
row limits in the seaports. Crowding is one of the essentials to its develop- 
ment. The average temperature of the locality where it prevails must be 
at least 73° F.; there must be a certain amount of moisture ; and animal 
and vegetable matter must undergo decomposition, either on the surface or 
in the substance of the soil. On ship-board there may be the greatest un- 
cleanliness, yet the fever will not appear on the vessel till it has touched 



1 Traite des Maladies Infectieuses : Maladie des Marais, Fievre Jaune, Maladies T yphoides, Fievre 
Typhus des Aimees. Wilhelin Griesinger, Paris, 1868. 



696 



ACUTE GENERAL DISEASES. 



land in an affected port or been brought into communication with a ship 
already contaminated. 

The time of year during which the fever prevails varies with the climate 
and temperature ; in the United States it usually appears in July and 
August, to disappear with the first frost. The epidemic in New York city 
in 1795 began in August and terminated in October. When the prevailing 
winds are southeasterly, the development and spread of an epidemic are fa- 
vored ; northwesterly winds check or arrest it. As has been mentioned, a 
severe frost or a "freeze" puts an end to the further progress of the dis- 
ease when it prevails under the most propitious circumstances for its devel- 
opment. 

There is much reason in the arguments of those who contend that yellow 
fever is an "acclimation" disease. First (and here, however, it should be 
remarked that the disease is indigenous in some regions), certain islands and 
seaport towns along our Southern coast always suffer from an epidemic when- 
ever certain atmospheric conditions exist; a resident of one of these places 
where yellow fever is indigenous is far less liable to have the disease than a 
stranger, especially one from the North. One attack is usually, not ab- 
solutely, a protection against a second. The disease is especially liable to 
appear in those localities where a severe type of pernicious fever has pre- 
vailed, and after a warm, rainy season rather than after a dry, cool one. 
"Whether the fever is epidemic or endemic, and whether the locality is one 
frequently visited or one in which the disease is indigenous, sporadic cases 
are of very rare occurrence. 

The negro race has a marked immunity from this fever. Age and sex 
exercise no influence upon the etiology. Occupation seems to have some 
effect in its production, since those who work over, or near, hot fires are 
stricken much oftener than those who work in unhealthy, filthy surround- 
ings. Exposure to cold and wet, alcoholismus, and venereal excesses here, 
as elsewhere, render individuals more liable to the fever. 

In regard to the nature of yellow fever poison, some assert that it is a 
malarial miasm, modified by the person in whom it lodges. It is in many 
respects similar to the poison of typhoid, both in etiology and the manner 
of its conveyance. It is unquestionably a specific poison, which differs es- 
sentially from the poison of every other fever. Typhoid, malarial and yel- 
low fever may all prevail at the same time in the same locality, but one will 
never merge into the other; each runs its own individual and peculiar course. 
All chemical and microscopical research has, as yet, failed to discover what 
the poison is ; but we are led from its mode of conveyance and from the 
conditions of its development to believe that it has the elements both of a 
miasm and a contagion. 

There are three leading doctrines in regard to the contagious character of 
yellow fever -.—first, that it is contagious, like small -pox and scarlatina ; 
second, that it is non-contagious, and never directly transmitted from the 
sick to the healthy ; and third, that when yellow fever is prevailing in a lo- 
cality, it may be carried from one person to another in that locality. The 



YELLOW FEVER. 



697 



last is the doctrine of contingent contagion. One who has seen the fever 
in hospitals needs no argument to prove that it is not directly contagious. 
Some claim that yellow fever poison, though not directly transmissible from 
the sick to the healthy, becomes infectious when brought in contact with 
decomposing animal and vegetable matter. It is well established that epi- 
demics of yellow fever only occur in those localities where decomposing ani- 
mal and vegetable matter is present ; and when men are crowded together 
in shops and around the docks and wharves of seaports, or in the filthy 
streets and dwellings of such localities. In some few instances evidences 
exist that yellow fever breaking out in the hold of vessels has been circum- 
scribed to well-defined and very narrow limits by free ventilation. There 
are ample facts to sustain the belief that this fever is infectious only when 
the atmosphere has become loaded with the emanations of animal and veg 
etable decomposition to which has been added the specific yellow fever poi- 
son. Under stich circumstances, the disease may be propagated from the 
sick to the healthy. 

Whatever view is taken of the contagious or non-contagious character of 
yellow fever, all observers agree that it is portable, that it can be conveyed 
from one place to another by means of clothing and merchandise and in 
the holds of vessels. That whenever the poison is thus introduced into 
healthy localities which are suited by temperature to its reproduction, and. 
where there is animal and vegetable decomposition, it rapidly reproduces 
itself, and thus epidemics of yellow fever occur in localities that otherwise 
would be free from the disease. 

There is no doubt that the poison of yellow fever retains its vitality for 
a very long period ; and with favoring conditions may cause an epidemic 
in places very remote from the origin of the poison. The jooison j g a | so 
capable of great concentration, for short exposure to the contaminated 
air that often fills the holds of ships on which yellow fever is prevail- 
ing will be followed by the fever in a few hours. Ordinarily there is little 
danger in visiting those sick of yellow fever if there is free ventilation, and 
one does not remain in the infected locality for a long time. The period 
of incubation varies in duration from twelve hours to four or five days; 
when the exposure is followed in a few hours by the fever, the fever poison 
must necessarily be very concentrated. The activity of yellow fever poison 
is destroyed by cold ; one or two hard frosts will arrest a yellow fever 
epidemic. Some claim that epidemics of yellow fever are self -limiting, 
rarely exceeding sixty or seventy days in their duration. There is not, 
however, sufficient proof to establish this statement. 1 

Symptoms. — As in typhoid fever, there are mild and severe cases of yel- 
low fever ; but they differ only in degree, not in kind ; the clinical his- 
tory of both is the same. 

Prodromata may occur ; but headache, anorexia, lassitude and pains in 

i In this connection see : The Cause and Prevention of Yellow Fever, in the Report of the Sanitary Com.- 
mission of New Orleans. Dr. E. H. Barton, New York, 1857. Memoire sur la Fievre Jaune qui en 1857, a 
Decline la Population de Monteviedo. A. Brunei, Paris, 1860. Account of the Yellow Fever which occurred 
in the City of New York in the year 1822. Dr. James Hardie, New York, 1822. Remarks on the Epidemic 
Yellow Fever on the South Coasts of Spain. Dr. R. Jackson, London, 1821. 



698 



ACUTE GENERAL DISEASES. 



the limbs cannot be reckoned as characteristic of the fever, and only 
when these occur during an epidemic are they especially significant. 
Whether premonitory signs have or have not been present, the disease com- 
mences with a chill, distinct and severe. In a few instances a series of 
rigors takes the place of distinct chills. Sometimes persons while ap- 
pearing in perfect health are seized with a severe chill, and immediately 
become seriously ill and take to their beds in a most dejected manner. Fol- 
lowing the chill there is nausea and vomiting, the face is flushed, the con- 
junctivae are injected, there is circumorbital headache, and violent pains 
in the bones, back and limbs, especially in the calves of the legs. The eye 
has a peculiar lustre and a staring look. The course of the fever is the 
same in the severe and in the mild cases. 

The temperature rises rapidly after the chill to 103° or 104°F.; the limits 
vary, but yellow fever is not a disease of high temperature. In a few epi- 
demics the initial rise in temperature has been as great as 110° F., but these 
are phenomenal occurrences. At the end, or beginning, of the third day 
the maximum fever will have been attained ; in our country this is rarely 
more than 104° or 105° F. Between this period and the fourth day of the 
disease slight variations, hardly amounting to distinct remissions are pres- 
ent ; on the fourth day there is a rapid defervescence ; it is not an inter- 
mission but a remission, for the temperature only falls to 100° or 101°F. 

The period of remission lasts 
from a few hours to two or 



Bny. 



106 

m 
tor 

100 
$8 



t. 



2 



3. 



4. 



7. 



6. 



JO. 



three days, after which a sec- 
ond rise begins, one that does 
not take place quite as rapidly 
as the first, and is not usually 
preceded by a chill or rigors ; 
and a temperature of 104° or 
105° is again reached. The 
temperature now remains sta- 
tionary from one to two days, 
it then falls to normal and 
remains so. This last fall is, 
like the first, marked by a very 
sharp temperature curve. The 
range of temperature is impor- 
tant, for it divides this dis- 
ease into three parts; first, 
the stage of invasion, the 
febrile stage or period of ex- 
acerbation ; second, the stage 
of remission, calm or passive period ; and, third, the stage of the second 
exacerbation or collapse. 

The pulse in yellow fever is peculiar. It rarely exceeds 110 beats per min- 
ute, thus differing from that of other fevers in which the rule is an in- 



Ftg. 157. 

Temperature Record in a Case of Yellow Fever. 



YELLOW FEVER. 



699 



crease of five beats for every one degree rise of temperature. Indeed, in 
mild cases, the pulse-rate may only be five or six beats above the normal. 
It has been observed to fall much below the normal, as low as 40 and 
sometimes 30 in a minute. The " feel " of the pulse is as if the arteries 
were distended with gas, and hence the name, i( gaseous pulse," is not 
inappropriate. It is compressible and of an uncertain volume, offering 
no resistance, so to speak, to the touch. 

The skin, as soon as the temperature begins to rise, maybe either dry or 
bathed in a copious perspiration. Following the chill there is sometimes 
an abnormal coldness on the surface, while rectal thermometry shows a 
marked rise in the temperature. At the close of the first, or beginning of 
the second day, the body emits a peculiar corpse-like odor. About the 
third day the skin begins to assume a jaundiced hue, noticed first in the 
sclera and then spreading over the whole body. It is a dark jaundice, like 
that of pyaemia, and is to be regarded as hematogenous and not hepato- 
genous. Those who maintain that the jaundice is due to retention and 
reabsorption of bile have no proof to offer, since evidences of mechanical 
obstruction to the outflow of the bile are among the rarest post-mortem 
appearances. The true etiology is found in the change which takes place 
in the blood. The pigment thus formed is deposited in the tissues, and 
causes a true hematogenous icterus. The perspiration now stains the linen 
yellow. This jaundice is not always present in yellow fever, but when it 
becomes a symptom it does not run into the period of convalescence. In 
the third stage the jaundice assumes a mahogany hue. 

Vomiting. — Immediately following the chill, nausea and vomiting are 
present. First the contents of the stomach are voided, then a yellowish 
green matter ; when the latter color is present the vomiting becomes pro- 
jectile in character, and the ejected matter has an alkaline reaction and is 
fluid. The alkalinity is due toammoniacal decomposition. The vomiting 
is accompanied by burning pains at the xiphoid cartilage. If the vomit- 
ing continues without any other change in the matter vomited, it is an 
evidence that the fever is going on to recovery ; in severe cases the char- 
acteristic "black vomit" is present, the result of hemorrhage into the 
stomach. This vomit is brownish black, semi-fluid, with a glistening re- 
flection, and varies in amount from a mere trace to many pints. It may 
occur on the second or third day of the fever, but usually it does not come 
on until about forty-eight hours before death, or on the day of death ; it 
occurs only in about one-third of the fatal cases. It undoubtedly occurs 
more frequently in yellow fever than in any other disease, but it differs in 
none of its constituents from a similar material which is sometimes vomited 
in other diseases where small capillary hemorrhages occur in the stomach. 

Microscopically 1 it is seen to be made up of blood corpuscles, degenerated 
lymphoid cells, fat cells, epithelial cells from the mucous membrane of 
the stomach, fine granules of pigment, aggregated non-granular masses, 
and serous fluid. The action of the gastric juice is such that the color- 



1 Microscopic Researches in the Black Vomit of Yellow Fever. Dr. M. Michell. Charleston Medical 
Journal, 1853. 



TOO 



ACUTE GENERAL DISEASES. 



ing mutter escapes from the corpuscles as small granular or rounded 
masses. It is claimed that the black vomit of yellow fever is specific., in 
that it contains a peculiar microscopic vegetable organism. This is yet 
lacking confirmation. The enfeeblement of the walls of the capillary ves- 
sels results from the pathological blood-conditions, and as qualitative al- 
terations are likewise added, hemorrhagic extravasations occur in the 
stomach, and on other mucous surfaces. The hemorrhages from the nose 
and gums that so frequently occur, and fluid blood in the discharges from 
the bowels are caused by the same changes as cause the gastric hemor- 
rhages. Very rarely hemorrhagic extravasations occur during life from 
the respiratory organs, the genitals, the skin, and the meatus auditorius 
externus. 

Urine. — Early in the disease the urine is scanty, acid, and slight traces 
of albumen may be found. Later, when the jaundice appears, its reaction 
is alkaline, and bile pigment is present ; as the disease progresses it be- 
comes more abundant ; if not present before, it makes its appearance dur- 
ing the stage of remission ; in all severe cases, leucin, tyrosin and fatty 
casts will likewise be found. Entire suppression of urine is of frequent oc- 
currence in severe cases. Patients with black vomit may recover, but a 
fatal result almost certainly follows urinary suppression. In cases where 
the yellow fever poison is concentrated and the nervous symptoms are prom- 
inent, suppression of urine may exist from the onset, but it usually does 
not take place until the second exacerbation. Ursemic toxaemia is then 
added to the yellow fever poison, and the condition is almost necessarily 
hopeless. The perspiration in this condition has a urinous odor. 

The countenance in some cases is almost diagnostic : the eyes are lustrous 
and staring, the face is flushed, the conjunctivae are injected, the intense 
conjunctival congestion giving the eyes the appearance of two balls of fire 
set in a face of a dusky, deathly hue ; this gives to the countenance a re- 
markable expression of dejection and dulness. 

The tongue is covered at the outset of the fever with a thick, yellowish 
white coating, except at the tip and edges, which remain red. It is often 
indented, by the teeth ; and as the disease advances may become dry, brown, 
cracked and fissured, resembling the typhoid tongue. The buccal mu- 
cous membrane is bright red at first, subsequently becoming cedematous. 

The boivels are usually constipated, but when diarrhoea does occur, fluid 
blood is apt to be mingled with the discharges. Sometimes when intense 
jaundice is present, the stools are clay colored, but this is an accidental 
circumstance. 

The mind is usually clear to the last, but when delirium sets in it will 
be wild and accompanied by a desire to get out of bed. The patient lies 
in a state resembling collapse, his features shrunken, indifferent both to 
his own condition and to what is occurring about him. 

Pain is quite severe over the lumbar and epigastric regions which are ex- 
quisitely sensitive to pressure ; convulsive twitchings of the muscles, and 
diaphragmatic contractions are often present before death. In favorable 



YELLOW FEVER. 



701 



eases all the severe symptoms distinctly remit on the second day after the 
beginning of the stage of the second exacerbation, and then follows a pro- 
tracted convalescence, and it is with the greatest difficulty that the stom- 
ach will retain the blandest food. When death is to follow, the vomiting 
persists, the urine becomes less and less in amount and richer in albumen, 
and uraemic coma, or wild delirium ends the scene. Just before death, 
in some epidemics, the temperature falls ; hence the name algid yellow 
fever. But whether coma, algidity, delirium, suppression of urine, or 
black vomit is the predominant symptom in an epidemic, the disease is the 
same specific fever. The mortality varies as much in different epidemics 
as the prominent symptoms do. 

Differential Diagnosis. — Yellow fever may be confounded with acute yel- 
low atrophy of the liver, relapsing, bilious remittent, continued malarial 
fever, and the icteric variety of pernicious fever. 

The diagnoses of acute yellow atrophy of the liver and yellow fever have 
already been considered. 

Relapsing fever is an inland disease, as a rule, while yellow fever is 
essentially a coast disease. In relapsing fever the temperature rises to a 
high point, often 107° or 108°, the pulse keeping pace and running up to 
140 or 150 beats per minute ; in yellow fever a pulse of over 110 is very 
rare, and the temperature averages 104°, often lower. Jaundice and the 
peculiar-colored " yellow fever face" are early symptoms in this disease; 
while there is no change in the face in relapsing fever and jaundice is a 
very late symptom. Relapsing fever has a true intermission, while yellow 
fever has only a remission. The spleen is markedly enlarged and tender 
in relapsing fever ; in yellow fever it is normal. During the pyrexial 
period spirilli are found in the blood in all cases of relapsing fever, and are 
absent from yellow fever. Bronchitis is a very common complication of 
relapsing fever, while pulmonary complications are very rare in yellow 
fever. Finally, relapsing fever is propagated by contagion, and yellow is 
not. 

Yellow fever is a portable disease, and usually prevails in cities and 
along the coast ; bilious remittent fever is not portable, and is a disease of 
the country and inland towns. The pulse-rate is 120 or 130 in bilious re- 
mittent; in yellow fever it is rarely over 110 ; the temperature is 105° or 
106° in bilious remittent, and rarely exceeds 104° in yellow fever. The 
liver is enlarged in yellow fever, and normal in size in bilious remittent ; 
the spleen is invariably enlarged in remittent and unchanged in yellow 
fever. There is projectile vomiting in yellow fever, while in bilious re- 
mittent it is retching in character. In twenty-four hours a remission 
occurs in bilious remittent, while in yellow fever the remission does not 
occur until the fourth day. The urine is rarely albuminous in remittent 
fever, while even in mild cases of yellow fever albumen is rarely absent. 
The mind is clear in yellow fever, while a patient with bilious remittent is 
dull and delirious. The difference in the invasion of the two diseases, the 
countenance, the existence of the hemorrhagic tendency, and the history of 



702 



ACUTE GENERAL DISEASES. 



the epidemic are sufficient to distinguish yellow fever from the so-called 
yellow type of remittent fever. 

In continued malarial (so-called typho-malarial) fever the temperature 
is higher than in yellow ; there is diarrhoea, which is absent from yellow 
fever, and the spleen undergoes marked enlargement. Yellow fever, on the 
other hand, is attended by albuminuria and a peculiar facial aspect that 
are both absent from all cases of continued malarial fever. There is 
periodicity in the variations in temperature in continued malarial fever, 
and the disease is continuous over two or three weeks ; while in yellow 
fever there are slight and irregular variations in the fever, and a distinct 
remission on the fourth day, which removes all doubt. Pain in the right 
iliac fossa is much more marked in continued malarial than in yellow 
fever. The history of the epidemic, the portability, and other etiological 
points will also often greatly aid in making the diagnosis. 

Prognosis. — The mortality-rate differs in different epidemics ; the high- 
est mortality is given as one out of every three ; while in mild epidemics 
only one out of fifteen or twenty dies. The average duration is six 
days, but in cases where a concentration of the poison overwhelms the 
system at the very onset, death may occur within twenty-four hours, and 
between this time and six days there is a varying number of fatal cases. 
The conditions that render the prognosis unfavorable are early high tem- 
perature, a severe period of invasion, deep jaundice, scanty urine contain- 
ing albumen and casts, black vomit, intense pains over and irritability of 
the stomach, a gaseous pulse, delirium, and, worst of all, suppression of 
urine. 

Among the favorable signs are diminution in the quantity of albumen, a 
quiet stomach, slight and late jaundice, a moderate degree of fever, and 
fewer attacks of black vomit. A positive prognosis is best withheld ; but 
" black vomit " and complete suppression render a case hopeless. Yellow 
fever, in some epidemics, is complicated by numerous boils and abscesses, 
and by cellulitis and inflammation of the parotid gland, perhaps termi- 
nating in suppuration. Regarding convalescence, it may be said, however 
quickly it may be established, it is longer than in any other disease in 
proportion to the length of the fever. Indeed it is often two weeks after 
the final fall in temperature before the patient begins to mend, and five 
or six months may have to elapse before he is entirely well. Death may 
result from rapid overwhelming of the system with the poison, i.e., from 
the effects of the blood change, from uraemia, black vomit, suppression, 
exhaustion or asthenia. 1 

Treatment. — Prophylaxis is, in a great measure, summed up in the word 
quarantine. A strict quarantine, that should include not only individuals 
but also all articles that have been near the infected person or spot, would 
be very desirable. This does no harm to the sick ; they may be removed 
to a hospital at once, after disinfection, for the disease is not contagious. 
To go into the details of quarantine, of ship and hospital disinfection, 

i " Relation de la Fievre Jaune survenue a Saint-JSfazaire en 1861." M. F. Melier, Paris. 



YELLOW FEVER. 



703 



would be out of the domain of this work. A person who is in the yellow- 
fever region can take the best prophylactic measure — removal from the 
neighborhood. When this is impracticable, sulphate of quinine may be 
taken, and all predisposing causes avoided as far as possible. Mercury is by 
some regarded as an efficient means of prophylaxis. 1 The variability of the 
mortality-rate has been referred to. Blood-letting, mercurials, stimulants, 
and quinine, — these are the four chief methods that have been tried. 2 
Blood-letting, even to the extent of 180 ounces at a time, was formerly 
practised, but has been abandoned, as not only wrong in theory but harm- 
ful in practice. Mercurials are exhibited to-day only for catharsis at the 
commencement. Stimulation is bad in excess ; and quinine is of no avail 
for any but prophylactic measures, if even here it possesses as much 
efficacy as theory attributes to it. Recently carbolic acid has been added 
to this list, but it has had so slight a trial that nothing can be said^ro or 
con, except that it is likely to go the way of all specifics. 

The plan of treatment which seems, at the present state of our knowl- 
edge, most reasonable, may be called a diaphoretic and expectant plan, the 
diaphoresis looking toward the relief of the grave kidney trouble, and 
hence tiding over the most serious point in the fever. When a patient is 
stricken with the fever, apply counter-irritation over the kidneys, and at the 
same time administer ten grains of quinine along with fifteen or twenty 
grains of calomel. The body should be covered with flannel and slightly 
heated, moderate diaphoresis being continually kept up by these methods. 
At the same time the air must always be fresh ; close quarters are always 
contraindicated. The nausea and vomiting may be controlled by eating 
cracked ice, drinking milk and lime-water, or by small hypodermic doses 
of morphia. The restlessness, tossing, and jactitation which are so ex- 
hausting in some cases, and which probably arise from the action of the 
urea in the circulation on the nerve centres, are best controlled by hypo- 
dermic injections of morphine. Full doses of opium, producing as they do 
free diaphoresis, may also be administered, unless the kidney lesions are 
very grave. Suppression is treated by the usual methods, large doses of 
turpentine being given. In the last epidemic 3j of turpentine in sugared 
water was given every four hours in the case of a negro, and recovery 
followed. 

In copious haematemesis styptics can be given cautiously, and cold com- 
presses may be applied over the epigastrium. When the various discharges 
have caused much exhaustion the judicious use of stimulants is often 
beneficial. When the opportunity offers, it might be well to try hypo- 
dermic injections of the sulpho-carbolate of quinine. Yellow fever runs its 
course in five or six days ; hence the vital powers must be sustained until 
the defervescence, and this is found to be extremely difficult on account of 

1 Yellow Fever; its origin, improper treatment, prevention, and cure. Dr. W. A. Shubert, Savannah, 
1860. 

A dissertation on the sources of malignant, bilious, or yellow fever, and means of preventing it. Dr. W. 
G. Chalmell, Philadelphia, 1799. 

2 Das Gelbe Fieber beurtheilt und behandelt nack einer neuen Aussicht vom Wesen der Fieber in Allge- 
meinen. G. Eichborn, Berlin, 1833. The history of yellow fever, toith the most successful method of treat- 
ment. Dr. J. Mackrill, Baltimore, 1796. 



704 



ACUTE GEN"EEAL DISEASES. 



the extreme gastric irritability. A bland and highly nourishing diet is to 
be prescribed as soon as convalescence occurs, and tonics form an essentia] 
part of treatment at this period. 1 

EPIDEMIC CHOLERA. 

Epidemic cholera is an acute general disease, which prevails epidemically, 
and in certain localities is endemic. It is characterized by copious watery 
discharges from the alimentary canal, by cramps, and by suppression 
of the excretions. It has also received the names of cholera Asiatica, 
cholera asphyxia, and epidemic, malignant, algid, or Hue cholera. 

Morbid Anatomy.— The post-mortem appearances vary with the period at 
which death takes place ; in the stage of collapse or in that of reaction, 
there is usually marked emaciation ; the extremities are noticeably shriv- 
elled, and the surface of the body in the dependent portions is bluish or 
mottled ; sub-conjunctival ecchymoses are often observed. The face has a 
pinched and drawn expression, and the eyes are deeply sunken. The body 
cools slowly after death, and frequently there is a post-mortem rise in tem- 
perature of two or three degrees Fahr. 

Rigor mortis is marked immediately after death, and muscular contrac- 
tions often cause changes in the position of the limbs and body. The skin 
is often so shrivelled as to resemble the condition called "parboiled," 
which is best marked upon the extremities. Putrefaction commences much 
later than in other diseases, on account of the withdrawal of large quantities 
of fluid from the body. 

The visceral lesions are as follows. The small intestine is distended and 
of a bright red color; its muscular coat is somewhat relaxed. Its mucous 
membrane is injected with a fine aborescent vascularity ; it is sometimes 
©edematous and its folds are often prominent, especially around the lower 
part of the ileum. Peyer's patches and the solitary follicles are at first en- 
larged, the latter more than the former ; if the solitary glands rupture, the 
membrane presents a reticulated appearance. The comma bacilli are found 
in the intestinal contents, in the mucous membrane and glands throughout 
the canal. Ulcerations resembling typhoid ulceration may occur, the glands 
become flattened and pigmented. There is an almost complete detach- 
ment of the epithelium ; if any patch is left nndenuded there is a sub- 
epithelial exudation which loosens its attachment to the villi. The intes- 
tine may be partially or completely filled with a " rice-water," whey-like 
fluid, alkaline in reaction, which contains an abundance of cast-off epithe- 
lium, and the cholera bacilli, and varies in consistency from the ordinary 
cholera stool to that of putty. The mucous surface may be of a bright 
red, grayish, or, rarer than all, a greenish color. In some instances the in- 
testine contains a moderate quantity of dark grumous blood. During the 
fever of reaction gray diphtheritic patches, very difficult of removal, which 
later become dry, brown sloughs, are sometimes found in both the small and 

1 Yellow Fever in Charleston, 1871, with Remarks upon its Treatment. Dr. F. P. Porcher, Charleston, 
1872. (Trans. S. C. Med. Asso.) 



EPIDEMIC CHOLERA. 



705 



large intestine. Similar patches have also occasionally been observed upon 
the mucous membrane of the biliary passages, vulva, and vagina. In 
severe cases the basement membrane is wholly denuded. 

The peritoneum of the small intestine is of a rosy color and dry, or is 
covered with a thin layer of plastic matter. 

The intestinal glands are congested, swollen, and prominent ; while the 
mucous surface has large ecchymoses and patches of extravasation upon its 
substance. Diphtheritic ulcerations may be present in the colon. 

Tlie oesophagus is sometimes congested and ecchymosed, and its glands 
are swollen. It may have its epithelium detached, and at times it is cov- 
ered with a diphtheritic exudation. 

The stomach is at first distended and filled with fluids similar to those 
which are found in the small intestine ; later its mucous lining is hyper- 
a?mic, swollen, often relaxed and ecchymotic. Still later it is collapsed 
and empty. 

The kidneys are intensely congested and enlarged, the capsule is adher- 
ent, the surface presents a stellate or "marbled " vascularity, and on longi- 
tudinal section both cortical and medullary portions exhibit punctate or 
striped blood injections, and numerous ecchymoses. The small veins, es- 
pecially around the glomeruli, are engorged, and the cortical portion of 
the kidney is more or less discolored. The uriniferous tubules have their 
epithelium loosened, and the cells are cloudy, swollen and filled with a 
granular albuminoid material; often transparent cylinders fill the lumen 
of the uriniferous tubes. For the most part the lesions resemble those of 
acute croupous nephritis. All these changes may occur during the first day 
of the choleraic attack. Later, during the secondary fever, the discolora- 
tion and tubular changes are increased ; the size of the kidney being one- 
sixth to one-third greater than normal, and the epithelial cells undergo pro- 
gressive fatty degeneration, and the whole organ becomes soft and friable. 
Chemical examinations have shown the kidneys to contain an abnormal 
quantity of urea, uric acid, leucin, and some bile-pigment. 

The bladder is at first contracted and empty ; but later it may be par- 
tially filled with albuminous, milky urine. Its mucous membrane and 
that of the ureters and pelvis of the kidneys undergo changes similar to 
the other mucous surfaces ; — viz. : hyperemia, ecchymoses, and perhaps 
diphtheritic processes. 

The lungs are engorged at the entrance of the pulmonary artery ; but 
the parenchyma of the lung is collapsed and exsanguinated, and crepitates 
less than normal lung-tissue. If death occurs during or after the reaction- 
ary fever, extensive oedema, hypostatic congestion and hemorrhagic infarc- 
tions may be found. Capillary bronchitis, lobular and lobar pneumonia, 
and emphysema are present in those cases where death occurs during con- 
valescence. Pulmonary gangrene is a rare lesion. The trachea and 
bronchi are engorged and covered with a muco-pus, while later a second- 
ary diphtheritic process may be established upon their mucous surface. 

The pericardium is dry, and its visceral layer is ecchymotic, while the 
parietal is coated with a sticky, pasty material. 
45 



706 



ACUTE GENERAL DISEASES. 



The heart is hard, dry and contracted, containing in its right cavity, 
which may be distended, soft clots, which sometimes extend into the 
pulmonary artery and into the veins. The left cavity is empty, or has 
only a few small black, loose coagula in it. 

The blood is darker and thicker than normal, there is an increase in 
its albumen and corpuscles, as well as in its specific gravity and in 
organic solids ; while there is a decrease in its saline elements and in its 
coagulating power. Urea is occasionally present. 

The spleen is small, wrinkled, flabby and shrunken, though when typhoid 
symptoms co-exist, or when it is the seat of blood extravasations it is en- 
larged and softened. 

The liver is usually pale, containing patches of commencing fatty de- 
generation, and the large veins are distended with blood. There is ex- 
foliation of the epithelium of the mucous surface of the gall-bladder, 
which causes plugging and distention of the ducts. 

The meningeal vessels of the brain and the sinuses are engorged, while 
the cerebro-spinal fluid is frequently absent. Medullary hyperemia is 
common. But when death has occurred late, the brain contains less blood 
and is often superficially cedematous. 

The sub-cutaneous connective-tissue is hard and dry. Parotid swellings, 
furuncles, purpuric and scorbutic spots, ulcerations of the cornea, and 
bed-sores are often present. 

Etiology. — Cholera is an acute, infectious, non-contagious disease. The 
comma bacillus, which is found in the intestinal canal of cholera patients, is 
almost universally recognized as the specific cause of the disease. It prevails 
epidemically and may be endemic. It first appeared in the East, and thence 
spread in all directions, following the routes of commerce without regard to 
climate. No country has been entirely exempt from its ravages. It has pre- 
vailed, however, chiefly in hot climates during wet seasons. In this country 
it prevails most in midsummer. It is more liable to occur in low lands 
than in mountain regions. Badly drained malarial districts favor its de- 
velopment, especially where a cup-shaped rock or clay substratum is cov- 
ered by a thin layer of permeable earth, favoring the decomposition of 
vegetable matter. Bad food, overcrowding, mental depression, excesses in 
venery and alcohol drinking, predispose to cholera. Epidemics of cholera 
occur most Avhen the atmosphere is moist and sultry, or when a sultry 
period follows a warm rainstorm, Districts where these conditions pre- 
vail are regarded as favoring the development of the cholera bacillus. 

As soon as the cholera discharges undergo decomposition, the bacillus is 
rapidly developed and may be conveyed from one locality to another by 
the wind, by waters, and in clothing. The specific poison of cholera is con- 
tained in the discharges from the mucous surface of the alimentary canal ; 
it is not infectious when fresh, but it acquires virulent infectious prop- 
erties in from two to four days, and is rendered innocuous by cold. There 
is no evidence that the bodies of cholera patients are infectious. The estab- 
lishment of these facts readily accounts for its sudden appearance in dif- 
ferent places remote from one another. An individual travelling rapidly 



EPIDEMIC CHOLERA. 



707 



from one place to another becomes the carrier of the germ, which is to 
develop the infection in those localities in which the conditions favor its 
reproduction. 

Symptoms. — The length of the stage of incubation of cholera is not de- 
termined, but it undoubtedly varies from a few hours to as many days. 
Its symptoms may be divided into four stages. These divisions are arbi- 
trary ; first, the stage of invasion, or premonitory stage ; second, the stage 
of painless diarrhoea ; third, the algid or collapse stage ; fourth, the stage 
of reaction. 

The prodromal symptoms are a feeling of weight in the precordium, 
rumbling of the bowels, general malaise, a peculiar pallid anxious counte- 
nance, and nervous phenomena, such as vertigo, tinnitus aurium, head- 
ache, and tremor. Sometimes there is apathy, again a condition of ex- 
hilaration. Not infrequently, for a couple of days, there are frequent and 
moderately fluid dejections, sometimes accompanied by exhaustion, rarely 
by griping. This is called the cholera diarrhoea. These premonitory 
symptoms continue from a few hours to a week ; usually, however, about 
two days. They may be, and frequently are, absent, the disease commenc- 
ing precipitately with a painless diarrhoea. Occasionally the prodromata 
assume the character of cholera morbus, but cramps are more prominent, 
and there is little or no fsecal odor to the discharge. 

The second stage is characterized by a profuse diarrhoea, generally com- 
mencing in the morning or in the middle of the night, and the patient 
describes the dejection as passing from him in a stream. These painless 
discharges sometimes, after the second evacuation, lose their faecal odor 
and color, and assume a light straw-colored or whey-like appearance. They 
vary in number from three to twenty a day, and are often accompanied 
by attacks of regurgitative vomiting with each evacuation. The average 
amount of fluid discharged in this stage by a cholera patient in twenty- 
four hours is about sixty ounces ; the patient becomes exhausted and as- 
sumes a peculiar apathetic condition; dizziness, headache, and vertigo some- 
times are present. Complete anorexia is present from the onset, and the 
thirst is tormenting and constant. Bile pigment disappears from the 
stools, and the rice-water appearance is assumed ; there may be a pinkish 
tint on account of the admixture of blood. The rice-water discharges 
often have a whey-like appearance consisting of the watery elements of 
the blood; their specific gravity varies from 1.005 to 1.012, and they con- 
tain a small proportion of albumen and an excess of sodium chloride. On 
standing, the rice-water fluid deposits a sediment holding fine granular 
cells, amorphous granular matter, shreds of tissue, minute nucleated cells, 
epithelium and blood globules. Occasionally the blood globules are so 
numerous that the vomited matters are red. Vibriones, bacteria, urea, 
triple phosphates and a few leucocytes are also not infrequent ingredients. 
The vomited matter, after the contents of the stomach and bilious matters 
have been ejected, is a clear, watery fluid containing urea and carbonate of 
ammonia ; it is ejected in a stream, without nausea or effort, and is char- 



708 



ACUTE GENERAL DISEASES. 



acteristic of cholera. Everything introduced into the stomach causes vom- 
iting. 

The tongue is dry and covered with a thick white coating ; the coun- 
tenance becomes pinched and of a leaden hue, the expression is staring 
and dull ; as the exhaustion verges on collapse, the pulse becomes imper- 
ceptible at the wrist. Often there is distressing hiccough, and more or 
less dyspnoea. In rare instances the abdomen is tense, hard and sensitive 
to pressure ; it may be retracted. Suppression of the urine is not of infre- 
quent occurrence at this stage. 

The algid stage commences with a well-marked fall of temperature ; first 
in the hands, feet, and face, but soon over the entire body. The axillary 
temperature may fall as low as 72° F., or even lower, while the rectal tem- 
perature registers 101° or 102° R The accompanying sweat makes the sur- 
face feel colder than it really is ; the patient himself rarely complains of be- 
ing cold. The skin is in distinct, hard folds (" washerwoman's skin ") and 
of a bluish or livid color. The features and extremities are pinched, the 
eyes are deeply sunken, and have purplish rings about them. The patient 
is in a state of apathy or stupor ; and is roused therefrom only by the 
severe cramps, which cause him to shriek and throw himself about the 
bed. These cramps chiefly affect the muscles of the calf of the leg. 

In the last portion of this stage (called the asphyxial) the condition of 
the patient is apparently hopeless ; the deadly coldness is so marked in the 
tongue and mouth that the thermometer may show a temperature of only 
79° F. The lividity and cyanosis, the imperceptible heart sounds, the ab- 
sence of the radial pulse, the "cholera face, "and the hoarse sepulchral 
"cholera whisper," the agonizing cramps that now recur oftener than at 
first, complete the desperate picture of the disease. The vomiting and di- 
arrhoea now markedly diminish and the discharges are less fluid when they 
do occur. The stools are passed involuntarily or heedlessly. 

The urine is either completely suppressed, or a few highly albuminous 
drops are passed. The respirations are shallow and hurried, often being 
40 per minute, and alternate very often with paroxysms of intense dysp- 
noea. There is a loss in weight during this period, and so drained is the 
blood that there is an absorption of pathological fluid accumulations as in 
pleurisy and synovitis. The saliva and all secretions are suppressed. Late 
in this stage of cholera the stools, from being odorless, change, and assume 
a smell something like decayed fish. The state of collapse may last forty- 
eight hours, and yet recovery take place ; or death may occur in two or 
three hours from the onset of this algid condition. 

The mind is clear throughout, and consciousness is retained till the last ; 
it is even recorded that insane patients have, in "cholera collapse," re- 
gained (temporarily) their sanity. 

The " reactive stage," when reached, is often marked by as speedy a re- 
turn of favorable signs as was the algid stage by unfavorable ones. The 
pulse appears in the carotids and at the wrists, and the heart-sounds be- 
come distinct and regular. The temperature rises, the skin becomes warm, 



EPIDEMIC CHOLERA. 



709 



the face loses its " deathly " look, the cramps cease, and the diarrhoea con- 
tinues ; the stools soon acquire a faecal odor and a brown color ; although 
in cases where the algid stage is prolonged, foul-smelling, greenish, fluid 
discharges continue for some time. The urine next appears, although its 
return may be delayed from ten to thirty hours ; at first it is scanty, high- 
colored and albuminous, containing casts, and turning pinkish with nitric 
acid. Soon it becomes copious and normal in character. The duration of 
this period varies from one to ten days. This is a history of a typical case 
of cholera. I shall now briefly consider some of the more common varia- 
tions. 

Cholera typhoid is perhaps the commonest sequela of the collapse stage. 
After a few days, in some cases a week, of well-marked reactive symptoms, 
when the secretions are fully established and excretion is being normally 
performed, a quickening of the pulse is noticed, usually toward evening, 
and soon a febrile movement is established, which recurs with regular 
paroxysms. These are accompanied by adynamic symptoms, such as low, 
muttering delirium, a dry tongue, injected conjunctivae, coma, and often 
bed-sores and purpuric spots. The patient sinks into a state of extreme ex- 
haustion, and gradually the coma deepens, the bowels and bladder are in- 
voluntarily evacuated and death occurs. If patients recover from cholera 
typhoid, the convalescence is very protracted and uncertain. 

Urcemia is a frequent condition ; following the stage of collapse no urine 
is secreted in the reactive stage ; and in about thirty-six or forty-eight 
hours the pulse becomes abnormally slow, the face slightly flushed, and the 
eyes darkly injected. The urine is entirely suppressed or very scanty, and 
will be found to contain albumen and casts in abundance. There is con- 
stant headache, rarely a mild delirium. The patient becomes drowsy and 
listless, vomiting a spinach-green material. Epileptiform convulsions are 
followed by coma and death. The bowels are constipated, and the febrile 
symptoms are negative. 

A " cholera eruption" so-called, sometimes makes its appearance either 
in the typhoid variety, or in the stage of reaction. This eruption varies in 
character : it may be an erythema, or resemble urticaria or roseola. It ap- 
pears first on the hands and feet, then spreads to the trunk, the face being 
very slightly affected. Macular, papular and vesicular eruptions sometimes 
occur ; in all cases the appearance of a cholera eruption is a favorable 
symptom. The eruption lasts about two days, and is often accompanied by 
a "burning" sensation. Although in children the disease runs the same 
general course, collapse supervenes much more rapidly, and death often oc- 
curs after a few choleraic discharges. 

Cholerine is a mild form of cholera occurring during a cholera epidemic, 
and attended by all the characteristic symptoms of the disease, except that 
there is no algid stage. There is often a slight coolness of the extremities 
and cramps in the calves of the legs. Recovery is usually rapid. It may 
be followed by a severe and well-marked attack of cholera. 

Differential Diagnosis. — During an epidemic, cholera is not likely to be 



710 



ACUTE GENERAL DISEASES. 



mistaken for any other disease ; but when it occurs in isolated cases, it may 
be confounded with acute poisoning, as from arsenic or antimony, and with 
the g astro-enteric variety of pernicious feyer. 

In cases of poisoning there will be the evidences of the action of the 
poison on the mouth and pharynx which are absent in cholera. The 
vomiting in cholera is regurgitative and painless, whereas in cases of 
poisoning it is distressing, and is preceded by an intense burning pain 
in the oesophagus and stomach. Diarrhoea, if it occurs in poisoning, 
is never of a "rice-water" character, but mucous and blood-stained. A 
chemical analysis of the ejected matters will detect the presence of a 
poison. 

In the gastroenteric variety of pernicious fever the first two or three 
discharges from the bowels are bloody ; while in cholera they are never 
bloody at first, and soon assume the "rice-water" appearance. In gastro- 
enteric pernicious fever vomiting is rare, but if present, is painful and 
retching in character; while in cholera it is regurgitative. The temperature 
in pernicious fever is high, often reaching 106° or J 07° F., while febrile 
movement in cholera is slight. There is free pigment in the blood in per- 
nicious gastro-enteric fever, which is never found in the blood of a cholera 
patient. 

Prognosis. — The mortality-rate varies in different epidemics from 20 to 80 
per cent. ; generally one-half recover. The more dense the population in 
any locality and the nearer the sea-coast the higher the mortality-rate. 
The mortality-rate is always less toward the end than at the commence- 
ment of an epidemic ; it is greatest in those under one or over fifty years of 
age. Habits of life and hygienic surroundings influence very greatly the 
prognosis. The duration of an attack varies from a few hours to two weeks. 
Fatal cases usually terminate within two or three days, while the aver- 
age duration of those that recover is nine days. Each epidemic in this 
country has been milder than the preceding. 

The symptoms which indicate recovery are a general improvement in the 
appearance of the patient ; he becomes less restless, his breathing slower 
and more natural, the radial pulse returns, the lividity of the surface dis- 
appears, the shrunken tissues expand, the temperature rises to normal, the 
urinary secretions are re-established, the discharges from the bowels are 
again stained with bile, and the patient falls into a quiet sleep. The un- 
favorable symptoms are involuntary pinkish discharges from the bowels, 
absence of the radial pulse and the second sound of the heart, extreme cy- 
anosis, a complete suppression of urine, coma, persistency of the vomiting 
and diarrhoea, and the occurrence of complications. 

Cholera may be complicated by capillary bronchitis, lobular pneumonia, 
oedema and congestion of the lungs, pericarditis, peritonitis, and pleurisy. 
The sequelae are uraemia, membranous enteritis, cerebral oedema and 
hypersemia, gangrenous or purpuric patches, ulcerated corneaa, furuncles, 
bed-sores, and gangrene of the lungs. Death may result from the direct 
effects of the cholera poison without the occurrence of the diarrhoea, from 



EPIDEMIC CHOLERA. 



711 



the exhaustion produced by the diarrhoea, from heart-failure, and from any 
of its complications or sequelae. 

Treatment. — Prophylactic and hygienic measures may limit the duration, 
extent, and the mortality-rate of a cholera epidemic. When a cholera 
epidemic is prevailing quarantine regulations must be vigorously enforced, 
and those attacked by the disease should be isolated. All cess-pools, 
privies, and bodies of stagnant water in the neighborhood should be drained 
or disinfected, and each member of the community should be placed under 
the best hygienic conditions, and his diet carefully regulated. All excesses 
in food and drink, and all sources of intestinal irritation should be avoided. 
A diarrhoea occurring during a cholera epidemic should be immediately 
checked. 

Cholera stools should be immediately disinfected and buried in trenches, 
as in typhoid fever. The linen and all utensils used in the sick room 
must also be thoroughly disinfected. Instead of sulphate of iron and hydro- 
chloric acid mingled with the faeces, carbolic acid may be used ; indeed, 
many regard it as superior to any other disinfectant for the purpose. All 
persons, who are able, should be immediately removed from the infected 
district. 

The first great object of medicinal treatment is to control the prodro- 
mal diarrlma. For the accomplishment of this, opium is the most reliable 
drug ; it may be combined with nitrate of silver, sulphuric acid, small 
doses of calomel, or with vegetable astringents. Brown-Sequard states that 
morphine hypodermically in sufficient doses at the onset will prevent 
cholera. The patient is to be at once placed in bed, kept absolutely quiet, 
and the abdomen swathed in flannel bandages. If there are slight signs of ex- 
haustion early, stimulants may be given carefully. Turpentine stupes over 
the stomach and bowels in the early stage, when the symptoms are urgent, 
are often serviceable. Nausea in the premonitory stage is often allayed by 
carbonic-acid water, cracked ice, or effervescing draughts. 

When the disease is fully established, as indicated by the projectile vomit 
and rice-water stools, the treatment becomes " symptomatic " or •'ex- 
pectant." To relieve the agonizing thirst patients may take freely of 
cracked ice, very cold seltzer water, or carbonic-acid water combined with 
lime water. If the pulse becomes imperceptible at the wrist, indicating- 
heart insufficiency, stimulants are indicated, but they must be carefully 
administered. English physicians in India give opium, calomel, and acetate 
of lead (or tannin) during the stage of painless diarrhoea. If the cramps 
are not severe, they may be relieved by friction. But when they become 
severe, hypodermics of morphia combined with chloral are indicated. If 
the extremities become cold they should be wrapped in hot cloths, or hot 
water bags may be placed around them, or they may be rubbed with stim- 
ulating liniments or capsicum preparations. In the stage of collapse iced 
brandy or champagne given repeatedly and in small doses is the best stimu- 
lant ; musk and ammonia are also recommended. The inhalation of amyj 
nitrite has been tried, and found very efficient in combination with alcohol, 



712 



ACUTE GENERAL DISEASES. 



in the advanced stage of collapse. When death is impending, whiskey 
may be injected hypodermically, or milk may be administered intravenously. 
In the use of stimulants one must be guided by the pulse, and the effects 
of the stimulation. The India cholera pills, given in the collapse, are 
made of camphor, asafcetida, pepper, and the essential oils or ether. 

As the reactionary fever comes on, and the temperature begins to rise, 
nourishment must be given with the greatest care ; the rule being to post- 
pone a solid diet as long as consistent with maintenance of strength $ 
milk, beef-juice, and very light broths are the only articles of diet admis- 
sible for some time. When the stomach is weak and irritable, and there 
is a tendency to vomiting, bismuth and cherry-laurel water can be given 
with advantage. Cerebral symptoms must be promptly treated by ice-bags 
about the head, heat to the feet, and bromide of potassium internally. 
The surroundings of the patient, the maintenance of cheerfulness and 
calm, and even temperature — these are important points to be observed. 



EPIDEMIC CEREBKO- SPINAL MENINGITIS. 

Epidemic cerebro-spinal meningitis, or cerebro- spinal fever, historically 
belongs exclusively to the nineteenth century, although it unquestionably 
prevailed prior to this period. French writers were the first to accu- 
rately describe it. It is a continued fever belonging to the class of mias- 
matic-contagious diseases, which generally prevails in quite limited areas. 
It has received various names ; as spotted, petechial and congestive fever ; 
malignant purpuric fever ; cerebro-spinal and syncopal typhus. 

Morbid Anatomy. — Pathologically as well as etiologically there are two 
forms of cerebro-spinal meningitis ; the first is simply an acute inflam- 
mation involving the meninges of the brain, spinal cord and medulla. 

Its local symptoms predominate over the constitutional, and it occurs 
exclusively as a sporadic disease ; the second, — epidemic cerebro-spinal 
meningitis, — is accompanied by all the signs of an infectious disease, and, 
at the autopsy, are found, in addition to lesions that are the counterpart of 
those occurring in simple cerebro-spinal meningitis, those grave visceral 
and sanguineous changes, which are present in other acute infectious diseases. 

On examining the brain of one who has died of epidemic cerebro-spinal 
meningitis, the convexity and base will be found most extensively involved. 
Its dura mater is tense, shining, and studded with numerous punctate spots 
of extravasation. The cerebral convolutions are flattened and the sulci 
deepened. The pia mater of the brain and spinal cord is thickened. The 
vessels of the pia mater are always more or less intensely injected and the 
surface of the membrane roughened. In some cases extreme hyperemia 
may be the only discoverable lesion. The exudation is the characteristic 
lesion of this disease. A more or less abundant sero-fibrinous or sero- 
purulent exudation takes place into the meshes of the pia mater. Clear 
serum is first effused, then it becomes milky and clouded, then yellowish, 



EPIDEMIC CEREBROSPINAL MENINGITIS. 



713 



and finally a thick, viscid, greenish-yellow mass, consisting of granular 
fibrin, pus-cells and red blood globules, which gives to the surface a " leek- 
green " color. In the severest cases the fibrin and pus form a continuous 
sheet in the sub-arachnoidean space, always thickened above the sulci. The 
vessels are inclosed in the exudation, looking like red threads in a gelatin- 
ous filmy mass. When the layer is removed, the subjacent gray substance 
is dotted with red points. In rare cases the exudation is deeply stained 
with blood ; at other times it is a thin, colorless fluid. The sinuses are 
full of dark, soft coagula, or thin fluid blood. Hard thrombi are occa- 
sionally found in them. 1 

The brain substance is frequently softened, especially near the largest 
patches of exudations. This is the " mechanical softening" of French 
authors. 

On section there is more or less congestion and punctate extravasation 
in the brain substance, and the ventricles are usually full of serum ; more 
rarely of pus ; and this pus enters the ventricles by means of the velum in- 
terpositum, or along the cerebellar or choroid plexuses. 2 All the local changes 
have their primary starting point in the pia mater. Finally, if absorption 
occur, the pia mater often remains thickened. In prolonged cases cheesy 
metamorphosis occurs in various spots in the thickened pia mater. 

The changes in the spinal canal are similar to those within the cranium. 
The dura mater is injected, and extravasations of blood are often found 
upon its parietal surface ; it is tense and shining. The meshes of the 
spinal pia mater are occupied by the exudation, which occurs either as 
stringy, interlacing bands forming a network, or in the form of a thick 
sheet completely enveloping the cord's substance. The color and char- 
acter of the exudation are the same as that in the cranial cavity. The largest 
collections of pus are about the second and last dorsal and the lumbar ver- 
tebras. The posterior portion of the cord is the part most iuvolved ; the 
anterior portion suffering only in those cases where the whole cerebro- 
spinal tract is involved. The pia mater itself is hyperaemic ; it may be 
thicker than normal, shaggy and adherent to the cord. In some instances 
the exudation occurs in the form of lozenge-shaped, irregular masses whose 
ends are connected to one another by bands of fibrino-pus. In the severest 
cases suppuration is so rapid that a complete sheath of pus is formed about 
the whole cord in a few hours after the onset of the malady. The gray 
substance of the cord is of a pinkish color, and may be infiltrated with 
serum. It is sometimes reduced to a mere pultaceous mass. 

In addition to these local changes there are blood and visceral changes. 
The fibrin-factors of the blood are diminished, and hence there is a loss in 
its coagulating power. The number of white corpuscles is increased, and 
the red ones are shrivelled, serrated and partly disorganized. The blood 
is darker than normal, fluid, and rapidly decomposes when taken from the 
body. 3 

1 Merkel states that he has found " a nuclear proliferation in the vessels, extending from the cerebral 
meninges to the spinal cord." 
a Virchow's Arch. Be. 34, Heft 31, 866. 

8 The ventricular fluid contains chloride of sodium, phosphate of soda and ammonia and oxalate of irea. 
—Meschede. 



714 



ACUTE GENERAL DISEASES. 



The heart and the voluntary muscles undergo the same degeneration and 
present the same appearances as in typhoid fever. 

The lungs are frequently the seat of oedema, and hypostatic congestion 
is present when the disease is prolonged. Passive hyperemia, lobular, 
and, less frequently, lobar pneumonia, are often found at the post-mortem. 

The liver is congested. The liver-cells are often cloudy and granular — 
i.e., there is albuminoid or fatty degeneration. 

The spleen is enlarged and softened ; the lymphatics are usually hyper- 
aemic, having a fleshy look. 

The intestinal mucous membrane is hyperaemic and the follicles are con- 
gested. The projecting agminated glands are sometimes ulcerated. There 
is more or less congestion of the kidneys ; the microscopical changes are 
those of the first stage of acute Bright's. Abscesses (as in typhoid) often 
form in the subcutaneous connective tissue. Bed-sores are not rare in those 
parts subjected to pressure, and gangrene is sometimes present. 

The integument is often the seat of petechial spots, and large, irregular, 
discolored patches are sometimes seen over the body. Herpetic spots are 
frequently seen on the surface of the body, on the face, and about the lips 
especially. Rigor mortis is marked and very much prolonged. Finally 
the serous membranes are frequently all covered with petechial spots and 
small extravasations. 

Etiology. — I have included cerebro-spinal meningitis in the list of mias- 
matic contagious diseases, as it has more in common with this class than 
with any other. It has prevailed as an epidemic and as an endemic dis- 
ease, and occasionally sporadic cases have occurred in localities where it has 
been epidemic. Epidemics have occurred at all seasons ; by far the greater 
number, however, occur in cold weather. All classes and ages are subject 
to it, but it is most likely to attack those between ten and eighteen years of 
age. Young troops on the march are especially liable to it. 1 Its strongest 
predisposing causes are over-crowding, bad ventilation, insufficient or im- 
proper food, dampness, and all other bad hygienic surroundings. Mental 
excitement, excessive brain-work or bodily fatigue, exposure to excessive 
cold or heat, are also predisposing causes. Cerebro-spinal meningitis is in 
no sense a contagious disease. It is more closely allied etiologically to lobar 
pneumonia than to any other disease, although some have regarded it as a 
variety of typhus fever ; others of malarial fever. Its specific microbe 
has not been discovered. 

Symptoms. — Cerebro-spinal fever follows no regular order, either in its 
prodromata or in its subjective symptoms. Arbitrary classifications and 
many subdivisions have been made, such as the typhoid, the paralytic, the 
adynamic, the intermittent, the petechial, etc. Such classifications are 
useless and confusing, for cases differ in the same epidemic. If the gene- 
ral phenomena of the disease be known, the accidental circumstances that 
are the basis of this complex nomenclature will be of very little impor- 
tance. 

The premonitory symptoms of cerebro-spinal meningitis vary in differ- 
ent epidemics. In some the invasion is abrupt ; the patient, apparently in 



1 Out of forty-seven French epidemics, Hirsch attributes forty-six to the military population. 



EPIDEMIC CEREBROSPINAL MENINGITIS. 



715 



perfect health, is suddenly seized with a chill, loss of consciousness, becomes 
comatose and dies in a few hours. In others a feeling of lassitude, dull 
headache, pains in the joints and muscles, and sometimes nausea and 
vomiting precede its development. Again, patients complain of pains in 
the back of the head and neck — they have no chills, but after twenty-four 
hours a febrile movement is developed and they pass rapidly into the 
active symptoms of the disease. The prodromata may last from a few 
hours to three or four days. In sporadic or endemic cases there is 
generally a period preceding its invasion during which patients suffer 
from a feeling of general indisposition. 

When its onset is sudden its advent is marked by a distinct chill, in- 
tense headache, pain in the back and upper part of the spine, nausea, 
vomiting, a rise in temperature and an acceleration of pulse. The chill 
may last an hour or more, but is usually of short duration. The skin ia 
abnormally cool and dry in its early stage. 

Headache in most cases is a prominent, agonizing and persistent symp- 
tom, and the pain, even in a condition of coma, causes the patient to groan. 
In rare instances the headache intermits, and frequently it remits. Ver- 
tigo almost always is an attendant, and the patient may suddenly stagger 
and fall during the period of the headache. 

Pain in the back and upper part of the spine is a characteristic symp- 
tom of the disease ; attempts to flex the head on the chest increase the 
pain during the first twenty-four hours of the disease, and pressure up 
under the ligamentum nucha), against the cord, often induces excruciating 
agony. Soon the muscles at the back of the neck become stiff, then 
rigid, the neck becoming fixed, and the head extremely extended— opistho- 
tonos. So intense may be the opisthotonos that attempts to swallow are 
so painful that the sufferer soon ceases to make the effort. The signs of 
prostration are present early. 

The temperature, as a rule, is low ; although 107°, 109° and 110° F., 
are recorded by trustworthy observers. It may rise rapidly to 104° or 105° 
F., and then suddenly fall to 102° or 103° F., there to remain, with un- 
important and irregular variations until a gradual return to normal marks 
the beginning of convalescence. Often, before death — and an almost sure 
indication of it — a low temperature will suddenly give place to a high one, 
and death will occur during the time of the highest temperature. In 
children the febrile movement is less marked than in adults. 

The pulse at first is slightly accelerated, beating from 90 to 100 per 
minute ; but in twenty-four hours after the commencement of the attack 
it may range between 120 and 150. It bears no relation to the range of 
temperature, often varying 40 or 50 beats in a few hours. It is feeble, 
rapid and compressible in those cases where there are early symptoms of 
exhaustion. In many cases it is small and wiry in character ; sometimes it 
is dicrotic. In children the pulse is more accelerated and much more ex- 
citable than in adults. In a few cases the pulse is slow at the onset of the 
attack, but soon becomes accelerated, irregular and intermittent. Pho- 
tophobia, contracted pupils, great and increasing restlessness, nausea 



716 



ACUTE GENEKAL DISEASES. 



and urgent vomiting, and abdominal neuralgia, are among the early 
symptoms. 

The pupils are often unequal in size, and usually respond slowly to light. 
The face is pale and anxious, and the features have a fixed, rigid expres- 
sion ; in some the countenance has a dusky hue like that of one who is 
under the influence of narcotic poison ; indeed, in some instances, the 
patient believes, from the severity and suddenness of the attack, that he is 
the victim of wilful poisoning. About the second or third day of the 
disease, if the headache has been very severe, delirium comes on ; it may 
be mild and muttering, wild and uncontrollable, or " maudlin," like that 
of a drunken man. In women the delirium may be attended by, or merge 
into, a form of hysteria. The most fanciful hallucinations often visit the 
minds of such patients, and if left to themselves they are constantly getting 
out of bed. These patients are frequently roused from their wanderings by 
excruciating pains in the head and extremities. Muscular contraction is 
rarely absent even in the mildest cases. 

By the third or fourth day a tetanic and contracted state of the muscles 
of the extremities begins, and then the arms become flexed on the chest, 
the forearm on the arm, the thumb on the palm, the knee on the abdomen, 
and the leg on the thigh. When these excito-motor spasms of a tonic 
character are marked in the groups of muscles in the back of the neck and 
in the back, trismus may occur, and then the case is hopeless. Twitching 
of groups of muscles often causes the patient to start from a state of semi- 
stupor. General convulsions are absent in adults, but are frequent in 
children. Pains in the extremities and in the abdominal region are always 
more or less severe. They are shooting and lancinating in character. 
Pains when located over the abdominal region cause vomiting, and dyspnoea 
when in the thoracic region. The skin may be hyper- or anaesthetic, and is 
early the seat of an eruption. In the majority of cases the surface is so 
sensitive that palpation and percussion arc exceedingly painful ; the patient 
cries out and starts at every attempt, and will usually say that it is that 
particular spot which is the "sorest." Voluntary movements cause pain. 
Cutaneous anaesthesia rarely exists throughout the course of the disease, 
but follows the hyper-sensitiveness. 

The eruption is usually limited to the face, neck, and lips ; it is herpetic 
in character. It may appear on the trunk and limbs. Vesicles appear 
earliest on and about the lips, and may be confined to them. Sometimes 
the eruption is mottled like that of typhus, and covers the body ; it may 
have a distinctly petechial character. E^chymotic spots are often scattered 
irregularly over the body, especially on those parts that are subjected to 
pressure. Purpuric maculae, erythema and urticaria are sometimes present 
(indeed, there are many varieties of the eruption), but herpetic and pete- 
chial spots are the most common. As there is no definite time for the 
appearance of these eruptions, so their duration varies ; sometimes they last 
only for a day — at other times they are visible throughout the whole 
course of the disease. Epidemics in which eruptions are marked have 
given ris^ to the name of spotted fever. 



EPIDEMIC CEREBROSPINAL MENINGITIS. 



717 



With the photophobia the eye is subject to many disturbances. Paralysis 
of the orbicularis palpebrarum may result in keratitis ; there may be more 
or less intense conjunctivitis ; or a neuro-retinitis or choroiditis, the result 
of an implication of the optic nerve, may occur. Ptosis is present in 
nearly every case. Temporary or permanent blindness, squint, double 
vision, and nystagmus are not infrequent optical lesions. Atrophy of the 
eyeball and cataract are occasional sequelae. 

Taste is perverted or entirely lost ; yet the patient will often take with avid- 
ity any article of food which may be placed in his mouth. Thirst is often 
a constant and tormenting symptom. Deafness is even more frequent than 
loss of, or disturbances in sight. There is always intolerance to noise, and 
tinnitus aurium exists from the very commencement. Otorrhcea may be 
extensive enough to result in tympanic perforation ; and the internal ear 
may become the seat of an inflammatory process which sometimes ends in 
suppuration. The semicircular canals would seem to be involved here, for 
in many recorded cases " an uncertain gait " is mentioned as accompany- 
ing the deafness. The respiratory tract, as a rule, is involved, the respira- 
tions generally being accelerated out of proportion to the frequency of the 
pulse, but when the exudation presses on the medulla and respiratory 
centre, dyspnoea and slowed respiration occur, and in some few cases the 
Cheyne-Stokes' breathing is noticed. Usually the violent headache and 
the "wandering" are attended by great restlessness, tossing and jactita- 
tion that frequently demand restraint. Insomnia is a common symptom. 
There is often great tremulousness and subsultus tendinum ; in the ad- 
vanced stage of the disease the pupils are dilated, the respiration markedly 
sighing, deglutition difficult, the sphincters relaxed, or there is retention 
of urine and faeces, the removal of which, by means of the catheter or 
copious enemata, causes a slight return of consciousness. 

The tongue, at first, is moist and covered with a whitish coating ; soon 
it becomes dry and brown ; the parotids may enlarge, and even suppurate ; 
the abdomen is flattened. Bigidity, contraction and opisthotonus give way 
to palsies. The skin becomes cyanotic as in the asphyxia stage of cholera. 
In other cases tetanic spasms are the most prominent signs, the rigidity 
and contraction of the muscles -of the back and neck are excessive, and 
the sufferer dies with the grin of lock-jaw upon his face. In protracted 
cases the patient becomes emaciated and loses strength in a degree out of 
proportion to the duration of the disease. 

The joints are usually tender, and often inflamed ; suppurative arthritis 
occurs in a few instances. 

The urine is but slightly altered. There is an increase in the urates 
and phosphates, and albuminuria not infrequently occurs, especially late in 
the disease. Polyuria is often present in children. 

The towels are constipated ; exceptions to this rule are seen only in 
children. If the disease is prolonged, the symptoms assume a typhoid 
character; and so "typhoid cerebro-spinal fever" is one of the many 
varieties. The term intermittent cerebro-spinal meningitis has been ap- 
plied to those cases where all the symptoms remit on the second or third 



718 



ACUTE GENERAL DISEASES. 



day from the onset of the attack, and soon reappear or exacerbate and the 
patient rapidly passes into stupor and coma. As an epidemic advances the 
cases grow milder, so that toward its end the patients may hardly be ill 
enough to be confined to their beds. 

In the form called "meningitis foudroyante " the patient is struck 
down in full health, and death may occur within twenty-four hours from 
the first symptom. The initial chill and headache are severe, there is 
stasis in the capillary circulation of the surface, purpuric maculae soon 
appear over the body, and active delirium is followed by profound coma 
and death. The course is often so rapid that there are no tetanic exhibi- 
tions. Exhaustion, paralysis, and anaesthesia are complete before the fatal 
issue ; albuminuria is rarely absent in such cases. In fact all the prominent 
severe symptoms of the disease are crowded into a few hours, and the pa- 
tient rapidly passes into a state of collapse. 

When recovery is to occur, the restlessness, jactitation, insomnia and 
headache remit and finally disappear, or the patient emerges from a condi- 
tion of coma into consciousness. The muscular paralysis continues, how- 
ever, as well as the pains in the head and back of the neck, and in all 
cases the convalescence is tedious. Stiffness of the muscles of the nape 
of the neck is a persistent symptom during convalescence. Mental- 
psychical disturbances are also common attendants of the convalescence. 
Sometimes when the disease has pursued a mild course for a week or ten 
days and convalescence seems about to be established, the patient gradu- 
ally gets worse, and after weeks of suffering, death will occur from inani- 
tion and general marasmus, the respirations becoming more and more 
irregular, and deglutition often becoming impossible. 

Differential Diagnosis. — Cerebro-spinal fever may, in children, be con- 
founded with pneumonia, since convulsions and opisthotonus may occur 
in either. It may be mistaken (at any age) for typhus, small-pox, tuber- 
cular meningitis, the cerebral form of pernicious malarial fever, and acute 
myelitis. 

When, from the ushering-in symptoms, doubt arises as to whether a child 
has thoracic or cerebral disease, a careful physical examination of the chest 
will at once remove the doubt. 

The differential diagnosis between cerebro-spinal fever and typhus and 
pernicious malarial fever will be considered in the history of those fevers. 

In smallpox the pain in the head is confined to the frontal region, while 
in cerebro-spinal meningitis it has its seat in the occipital region. In men- 
ingitis there is early stiffness and rigidity of the muscles at the back of the 
neck. In small-pox this is a later symptom if it occurs at all. In small- 
pox, on the fourth day of the fever, the characteristic eruption appears about 
the roots of the hair, while in cerebro-spinal meningitis there is no peculiar 
eruption, and no regularity in the date of its appearance. The tempera- 
ture in small-pox is much higher than in cerebro-spinal meningitis. On 
the second day of small-pox there are redness, swelling, and soreness of the 
throat ; in spinal fever these are absent. Coma may occur early in cerebro- 
spinal meningitis, but is a late symptom in small-pox. After the initial 



EPIDEMIC CEREBRO-SPIHAL MEXIKGETIS. 



719 



pains in the back and limbs, pain is not a prominent symptom of small- 
pox ; while the severe and excruciating pains in the head, limbs, and 
trunk increase in severity with the advance of cerebro-spinal meningitis. 

The diagnosis between tubercular and cerebro-spinal meningitis is always 
difficult and often impossible. A careful study of the previous history, 
the insidious and characteristic slow advent of tubercular meningitis, the 
slowed pulse at the beginning, the "hydrocephalic cry, " the absence of 
eruptions, the very mild delirium, and the late appearance of muscular 
rigidity, are the points on which we may differentiate the otherwise analo- 
gous diseases. 

The ushering-in symptoms of acute myelitis are very similar to those of 
cerebro-spinal meningitis ; but when the myelitis is fully established there 
are the peculiar "girdling" pains — the feeling as if an iron band were 
around the waist — with paralysis of the lower limbs, which rapidly extends 
upward. The temperature of the paralyzed limbs is first elevated, but 
subsequently falls beloiv the normal ; there is almost complete anaesthesia 
of the surface, and impaired muscular contractibility ; later there is atrophy 
of the muscles of the paralyzed parts ; — all of these symptoms are in strong 
contrast with the symptoms of cerebro-spinal fever. Again, pressure on 
the spine in myelitis causes severe pain which is not increased by motion ; 
while in meningitis motion rather than pressure causes pain. The rectal 
and vesical sphincters are involved in myelitis, so that ammonasmia, pye- 
litis, cystitis, and various urinary complications are early attendants on the 
disease ; these are rarely present in cerebro-spinal fever. Trophic nerve de- 
rangement is shown, in myelitis, by the extensive formation of acute bed- 
sores, while this is a comparatively rare, and always a late, occurrence in 
cerebro-spinal meningitis. Keflex power is diminished or wholly absent in 
myelitis, while it is exaggerated in spinal meningitis. 

Prognosis. — Cerebro-spinal meningitis is always a grave form of disease, 
and a guarded prognosis should be given. The death rate in severe epi- 
demics is 80 per cent., and about 30 in mild ones. Toward the close of all 
epidemics the death rate markedly diminishes. Hence, the period as well 
as the severity of an epidemic will influence the prognosis. Its average 
duration is about fourteen days, but cases are recorded where death has oc- 
curred in five, twelve, fifteen, twenty-four, and thirty hours after the first 
symptoms. In the majority of cases which prove fatal, patients die during 
the second week ; if recovery takes place the disease is apt to last two or 
three weeks. In quite mild cases the disease lasts about two weeks ; and 
in the intermittent form, when the so-called relapses occur, the disease may 
be protracted seven or eight weeks. 

Age influences the prognosis. Statistics show that under fifteen, the 
mortality-rate is much greater than between fifteen and thirty-five ; and 
that after thirty-five, each year diminishes the chances of recovery. Every 
day that is passed after the seventh renders recovery more and more proba- 
ble ; the symptoms that tend to render the prognosis unfavorable are a 
rapid, and especially an irregular or intermitting pulse, an abundant erup- 
tion, excessive hyperesthesia and nervous excitement, absolute insensibility 



720 



ACUTE GEtfEKAL DISEASES. 



of the pupils, as well as symptoms of great mental depression and prostra=> 
tion early in the disease. Convulsions, a low temperature with attendant 
collapse, paralysis of the muscles of deglutition, continued vomiting, shal- 
low and irregular respirations and the occurrence of any of the complica- 
tions, all render the prognosis unfavorable. 

The complications of cerebro- spinal fever are bronchitis, broncho-pneu- 
monia, croupous pneumonia, pulmonary oedema, pulmonary atelectasis aris- 
ing from obstruction in one or more bronchi, and pleurisy. Endocarditis 
or pericarditis and nephritis are frequent complications ; the lesions of the 
eye, ear, joints, and subcutaneous areolar tissue can be regarded as belong- 
ing to, and complicating the ordinary course of the disease. 

The sequela? of cerebro-spinal fever are numerous : even in the most 
favorable cases basilar headaches and attacks of dizziness are liable to occur 
for years after recovery. Deafness or blindness may result, and in chil- 
dren deaf-mutism is a not uncommon sequence, especially if the disease 
occur before the child has learned to talk. The eye lesions, already men- 
tioned, may become permanent. The psychical disturbances may vary 
from complete idiocy to stupidity, impaired memory, and marked diminu- 
tion in intelligence. General motor weakness is rather unusual ; but 
paralysis of various muscles or groups of muscles is a frequent sequel. 
Single nerves are sometimes paralyzed. Death may result from the pul- 
monary complications, from paralysis of the muscles of deglutition and of 
the thoracic groups, from heart failure, and consequent oedema of the 
lungs, from intensity of poisoning at the onset, from asthenia, and from 
coma. 

Treatment. — The prophylactic measures to be observed during an epi- 
demic of cerebro-spinal meningitis may be summed up in careful attention 
to the surroundings : — remove all anti-hygienic influences, and when possi- 
ble isolate the sick. Indeed the general principles of prophylaxis are the 
same as in all miasmatic-contagious diseases. 

A patient with cerebro-spinal meningitis should be immediately put to 
bed, in a dark, cool, well- ventilated room, removed from noise and con- 
fusion. During the entire course of the disease the diet should be of 
the most nutritious kind, easy of digestion ; milk is to be preferred. The 
exhaustion and emaciation that render convalescence so tedious must be 
combated from the onset by a nutritious and generous diet. The thirst 
which is so tormenting may be relieved by allowing the patient to drink as 
much ice or seltzer water as he desires. If constipation exist it must be 
overcome by promptly acting cathartics, — a calomel purge is to be pre- 
ferred. It is well to administer a turpentine enema to aid the action of 
the calomel. A free catharsis must be early obtained. The condition of 
the bladder must be carefully attended to throughout the disease. If the 
patient does not evacuate it at the proper intervals, recourse must be had 
to the catheter. Sometimes cystitis has resulted from neglect of this. 

As with all severe forms of disease, various plans of treatment have 
been adopted. The plan of general blood-letting and depletion has no 
doubt raised the death rate. In no case is blood-letting indicated or al- 



EPIDEMIC CEBEBROSPINAL MENINGITIS. 



721 



lowable in this disease any more than in typhoid fever or diphtheria. The 
internal and external use of calomel in its treatment, although it has been 
extensively employed, is not sustained by the result of experience. Nor has 
iodide of potassium the reputation which it once had for promoting the 
absorption of inflammatory products. Quinine, if useful at all, is only so 
at the very onset, and if used then it should be administered in large doses. 
It has no antipyretic power in this disease. 

The medicinal agents which are generally accepted as most useful in 
the treatment of this disease are the narcotics : among these opium stands 
first in the list; administered hypodermically, it not only promptly re- 
lieves the pain in the head, the restlessness, jactitation, insomnia, delirium 
and convulsions, but it likewise increases the arterial tension. This drug 
should be given until the desired effect is produced, namely, complete re- 
lief ; there must be no hesitation in the administration of large doses if 
required, for there is a remarkable tolerance of the drug in this disease. 
It may be combined with atropia. Bromide of potassium is regarded by 
some as especially indicated in this disease, and it has been given quite ex- 
tensively with apparent benefit, especially in children. 

When cerebral symptoms are violent, cannabis indica 1 may be cau- 
tiously administered. Chloral hydrate is contra-indicated, and ether and 
chloroform inhalations should not be resorted to unless neurotics have 
failed to relieve convulsions or pain. Ergot is recommended by many on 
the ground that by its action on the vasomotor system it produces cere- 
bral and spinal anaemia. It is proposed to give the ergot until dizziness is 
produced. Experience, however, does not sustain the theory. 

When symptoms of great exhaustion are present, stimulants are de- 
manded ; decreasing restlessness and a continued fall of temperature are 
some of the signs that indicate that stimulants are acting remedially. 
The rules and methods of stimulation are the same as in typhoid fever. When 
cerebro-spinal fever is long continued and there is reason to believe that 
there is an abundant serous effusion, iodide of potassium in large doses 
may be of service. 

Cold applications to the head and spine, by means of evaporating lotions, 
sprays, or ice-bags, are regarded by some as a most important adjuvant to 
its treatment. In all cases their use demands great caution, and in this 
country the profession favors the application of heat rather than cold to 
the spine, in the form of hot- water douches or hot-water bags. Many are 
in favor of first blistering the region over the spine from occiput to loins, 
and then covering the parts with a poultice. Blisters at the nape of the 
neck are of service in most cases after the acute stage is passed. In sthenic 
cases leeches may be applied over the temples and mastoid processes ; 
they diminish the headache at the beginning of the disease. The extremis 
ties must never be allowed to get cold, and warm flannel is to be continu- 
ally wrapped about the legs and body. Mustard foot-baths, stimulating 
enemata, and the external use of turpentine, are indicated when the simple 
means fail to accomplish the desired result. Cold baths do harm. As 



46 



Mannkopf, 



ACUTE GENERAL DISEASES. 



soon as convalescence shall have been established, a tonic plan is to be 
adopted. The vegetable bitters, arsenic, and iron are to be used. In some 
cases electricity may be employed with benefit. 

SEPTICAEMIA. 

Septicaemia is a constitutional disease due to the absorption into the 
blood of a septic material which is developed in decomposing animal mat- 
ter by the action of putrefactive bacteria. The disease is closely allied to 
" surgical " or " traumatic fever " 

Morbid Anatomy. — The changes in the blood in septicaemia are similar to 
those which occur in fevers. It is darker than normal, coagulates less read- 
ily, and tends to rapid decomposition. This loss of coagulating power has 
been supposed to be due to the destruction, by the septic poison, of the 
white blood corpuscles, which contain the main factors for producing a 
clot. Bacteria and micrococci are present in the blood in septicaemia. 

The spleen is enlarged and often softened. The heart, kidney, and liver 
exhibit more or less cloudy swelling. The mucous membrane of the stom- 
ach and intestines is congested and oedematous, and the agminated and sol- 
itary glands are prominent. Enteritis is not infrequent. In severe cases 
ecchymotic spots are found in the intestinal tract. 

The serous membranes may be inflamed, but generally they are only 
ecchymotic. There is always more or less lymphangitis present. It seems 
evident that the septic material enters the circulation chiefly through the 
lymphatic vessels. 

Etiology. — The nature of the septic poison that is the product of the 
decomposing animal tissues is still a matter of dispute. Some claim that 
it is a chemical substance, formed in a wounded part, which acts as a fer- 
ment in the blood, and produces the septic symptoms. Others regard the 
bacteria which are present as themselves the sole cause of the septic infec- 
tion. Several pathologists have attempted to find the true poisonous prin- 
ciple, and have isolated — from decomposing fluids — " sepsin " and other 
ptomaines. It has been observed that the blood of an animal with septi- 
caemia produces greater disturbances and graver results, when injected into 
a healthy animal, than decomposing fluids. 

Dr. Sanderson, who says "that the agency of bacteria is essential to 
the production of the septic poison," also says that "they are incapable 
of producing the poison in a healthy organism." After considering the 
various theories which have been advanced, it seems most jorobable that 
there is no one body which causes the septic infection, but a combination 
of a number of poisonous substances which produce changes analogous to 
those caused by fermentation, and that the poison is absorbed by the 
blood-vessels only in exceptional cases, when their walls have undergone 
degenerative changes. 

Decomposing tissues which cause septicaemia may be in the body, on 
the surface of the body, or outside of the body. 

I. Thus, a decomposing placenta in utero, sloughing ulcers in typhoid 



SEPTICEMIA. 



723 



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98 



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me. 



fever, necrotic processes in chronic phthisis, diphtheritic sloughs, ulcera- 
tive endocarditis, abscess and gangrene of the lung, — these are some of the 
internal conditions which may induce septicaemia. 

II. Wounds, gangrene, decomposing membranes, or the suppuration and 
necrosis in small-pox, any ill-conditioned wound, especially if lacerated and 
contused, may cause septicaemia. 

III. Dissecting wounds and post-mortem manipulation of those who 
have died of infection, even without a surface abrasion, may induce sep- 
ticaemia. The respiratory and the gastro-intestinal tracts are sometimes 
the mode of entrance of the infection. 

Symptoms. — The symptoms of septicaemia will vary with the amount of 
the septic material introduced into the system and the length of the in- 
fection ; a slight infection will produce fewer and less grave symptoms 
than one more extensive ; hence the symptoms will vary : — sometimes 
urgent, sometimes so mild 
as to be overlooked. In 
a well-marked case, after a 
rigor, or feeling of chilli- 
ness, but rarely a distinct 
chill, there is a rapid rise 
in temperature ; 105° or 
107° F. may be reached 
within the first twenty- 
four hours. There is no 
typical range to the tem- 
perature. The pulse is 
rapid (120 to 140), feeble 
and thread-like. The 
mouth, tongue, and sur- 
face of the body become 
hot and dry. If sweats 
occur they are very slight, 
and only present during 
the initial stage, and can 
hardly be confounded with the profuse 
is not infrequent. The nervous symptoms 



I 



i 



Pig. 158. 

Temperature Kecord in a case of Septicaemia, following an 
Amputation. 

the profuse sweats of pyaemia. Vomiting 
are always well marked. 
The expression of countenance is dull and apathetic, the patient lying in a 
listless condition, generally free from pain. There is restlessness and low^ 
muttering delirium. The respirations are feeble, labored, and hurried. 
The skin may be slightly jaundiced. Diarrhoea is present in about 50 per 
cent, of all cases, and in nearly all severe cases. The urine is scanty, high 
colored, of high specific gravity, and contains urates and often albumen. 

In mild cases the symptoms may remit, and complete recovery be 
established within a couple of days. This happens when the septic cause 
is discovered and removed. In severe cases death may occur within 
twenty-four or seventy-two hours, the patient dying in complete collapse. 
Typhoid symptoms, a dry tongue, rise in temperature, diarrhoea, and mut- 



724 



ACUTE GENERAL DISEASES. 



tering delirium, following an abortion or child-birth, should always excite 
suspicion. Septicaemia often gives rise to pyaemia, or is combined with 
it, which is shown by the initial chill being severe or often repeated, and 
by the occurrence of profuse sweatings. 

Differential Diagnosis. — Septicaemia may be confounded with pyamiia, 
typhoid and typhus fever. 

Pycemia is ushered in by a distinct chill ; septicaemia by slight shivering 
or mild rigors only. In pyaemia the chills recur ; in septicaemia there is 
but one — the initiatory — chill. In pyaemia there are profuse sweats which 
recur ; in septicaemia there are slight, if any, sweatings, and they are 
never recurrent. In pyaemia the temperature gradually rises to 102° to 
104° F.; in septicaemia it is high at the onset, i. e., 105° to 107° F. The 
skin is of a dark, leaden yellow, jaundiced hue in pyaemia, while the dis- 
coloration of the skin is never so marked in septicaemia. There is a sweet 
" sickish " odor to the breath in pyaemia, absent in septicaemia. Pyaemia 
develops slowly, septicaemia rapidly. In pyaemia the heart impulse is less 
forceful than in septicaemia. Finally, infarctions, thrombi and multiple 
abscesses develop in pyaemia and are its distinguishing objective evidence, 
while they never occur in simple septicaemia. 

Prognosis. — This, in most instances, depends upon the extent of the 
poisoning, " when the symptoms of the disease are well marked the prog- 
nosis is bad." The possibility of the removal of the source of the infection, 
and the length of time that the decomposing mass has been in contact with 
the living tissues, influence the prognosis. Its duration is from two days 
to two months. Death occurs from asthenia, exhaustion, or rapidly from 
overwhelming of the system with the materies morbi. Collapse is nearly 
always the precursor of dissolution. 

Treatment. — The first thing to be accomplished in the treatment of this 
condition is the discovery and, when possible, the removal of the cause. 
Antiseptics should always be used at the seat of the infection. The bowels 
must be freely acted upon by salines throughout the whole course of the 
disease. The tonic, stimulant and antipyretic plan laid down for the treat- 
ment of pyaemia should be employed here. Quinine, salicylic acid, and 
brandy are the three drugs on which we place our reliance. Tanner 
recommends quinine and nitric acid. The diet must be as nourishing as 
possible. 

Billroth's treatment is cooling drinks, a fever diet, morphine at night 
to secure sleep, from six to ten grains of quinine during the afternoon ; 
the induction of profuse perspiration when the skin is dry, by warm baths, 
afterward wrapping the patient in blankets. 



PYEMIA, 



725 



PYAEMIA. 

Pyaemia is an infections disease, and under certain conditions is conta- 
gious. It is attended by the formation of infarctions, metastatic abscesses, 
and diffuse local inflammation. Many authors make no distinction between 
septicaemia and pyaemia. The bacteria found in the blood are the same as 
are present in ordinary suppuration. 

Morbid Anatomy. — The blood in pyaemia is characterized by a tendency 
to coagulate spontaneously wherever there is slowing of the blood-current. 
Colonies of micrococci are very frequently found in the blood and on the 
walls of the vessels ; 1 venous thrombosis and embolism are essential feat- 
ures of this disease. The thrombi are usually near the seat of the pus ab- 
sorption ; these emboli have a specific action on certain organs, stamped as 
they are with the peculiar pyaemic infection. When these emboli become 
lodged in the small arteries of different organs they lead to the development 
of infarctions which terminate in the formation of abscesses. 

" Metastatic abscesses," the result of suppuration of a pyaemic in- 
farction, caused by venous thrombosis and embolism, may form in the 
lungs, liver, kidneys, spleen, muscles, heart and brain. 2 In the lungs 
there is usually more or less 
pneumonic inflammation about 
the abscesses. Even patches of 
gangrene may be found near 
them. In the kidney the tu- 
bules and vessels are found 
crowded with micrococci. 

The spleen is swollen and 
shows more or less parenchyma- 
tous degeneration, according to 
the amount of fever. Gener- 
ally will be found, scattered 
through the organ, a few firm 
wedge-shaped nodules with, 
their apices inward, or their 
interior partly broken down 
into pus. Metastatic abscesses 
vary in size from a pea to a 
large walnut. When multiple 
abscesses are found scattered 
through the various viscera, 
softened puriform and decom- 
posing thrombi are rarely found 
in the veins ; but when the abscesses are few the reverse is the case. The 

1 Weigert states that small thrombi are often formed solely of bacteria. 

3 Recklinghausen says that these abscesses depend on " extra-vascular accretion of fungi." 




Fig. 159. 
Pyaemia. 

Metastatic Pyaemic Abscesses of the Lung. 



726 



ACUTE GENERAL DISEASES. 



joints, the serous membranes of the body, and the connective-tissue ol 
various parts are often involved. 

Pleurisy, pericarditis, and peritonitis of pyaemic origin are frequent and 
always fibrino-purulent in character. I have known the pleural cavity to 
fill with pus twenty-four hours after the first evidences of pyemic suppu- 
rative pleurisy. Suppurative arthritis is a rare complication. Lymphangi- 
tis is usually established in the neighborhood of the injury or source of in- 
fection. 

Ulcerative endocarditis with the presence of large quantities of bacteria is 
not infrequent. Pyaemic pan-ophthalmia with sloughing of the cornea is of 
rare occurrence. In some cases nearly all the tissues and serous and mucous 
membranes exhibit deep post-mortem staining; the gastric and intestinal 
mucous membrane being swollen and congested, the solitary glands and 
Peyer's patches prominent. Ulcers may form at points along the intestine. 
The skin always shows more or less jaundice. Suppurative cellulitis often 
occurs. Occasionally there are cases of pyaemia, or conditions closely re- 
sembling pyaemia, where there are no recognizable pathological lesions. 

Etiology. — Eecent observations and experiments seem to show— first, 
that pus with micrococci causes suppurative pyaemic inflammation; sec- 
ond, that the micrococci alone can establish a similar inflammation ; and 
third, that without micrococci pus is inert. Many regard the pyaemic and 
septicaemic poison as identical, and pyaemia as nothing but a metastatic 
septicaemia, claiming that pyaemia is invariably associated with more or 
less septicaemia, and therefore have advised the use of the term septico 
pyaemia. 1 

Inflammation of bone is a very frequent cause of a phlebitis which leads 
to pyaemic infection. Thus a blow on the head of one saturated with 
alcohol is followed by a phlebitis in some of the diploic veins ; as a result, 
thrombi are formed, which break up into emboli and thus lead to pyaemic 
infarction and abscess. Suppuration of the eye or middle ear has led to 
the same results. 

Cellulitis, carbuncle, erysipelas, "malignant pustule," and dissecting 
wounds are often complicated by pyaemia. Endometritis or lacerations 
about the genital tract are fruitful sources of pyaemia in the puerperal 
state. The question of pyaemic contagion is still unsettled. From a 
surgical standpoint it seems evident that certain atmospheric conditions 
and surroundings and want of cleanliness predispose to the development 
of the pyaemic bacteria, but it has never been shown that pyaemia can be 
contracted as small-pox or scarlatina can. 

Symptoms. — Pyaemia is ushered in by well-marked symptoms. First, 
there is a chill or decided rigor, followed by a gradual rise of temperature 
to 101° or 104° F., the rise of temperature being proportional to the phe- 
nomena of the chill. The chills of pyaemia occur irregularly, rarely at 

1 Holmes' 1 Sys. Surg., Vol. v. Sanderson claims that "pyaemic poison multiplies in the organism." 
Whether the poison becomes more infective or virulent as time elapses or as it is developed from new 
foci, is a mooted question. Panum claimed that " there is, in putrefying fluids, a specific chemical sub- 
stance soluble in water and which, when introduced into the blood, causes the symptoms of putrid or 
septic infection.'" Others claim that pyaemia is due to a peculiar miasm which Ins a specific action 
similar to the exanthemata, and which may be introduced through the lungs, mucous membranes, and 
through abraded surfaces. 



PYiEMIA. 



727 



night, and are followed, after the first two or three, by profuse and exhaust- 
ing sweats, which only afford marked relief for a time, the skin soon be- 
coming hot and dry. An irritability of the nervous system has been 
noticed as preceding the occurrence of these chills. During the chill the 
temperature will be higher than in the sweating stage, the thermometer 
often showing a temperature of 103° or 105° 
F., or 108° F., which often suddenly falls 
below the normal, soon to rise again. 1 The 
heart power is notably and early diminished. 
The pulse is frequent, 120 to 140, small and 
often intermittent ; it does not vary with 
the range of temperature. The conjunc- 
tivae and skin assume a sallow tinge ; later 
they may become markedly jaundiced. The 
breath has a peculiarly sweet, sickish odor. 
The tongue is at first covered with a white 
fur; later it becomes glazed, dry, brown, 
and fissured. Sordes collect on the teeth. 
Anorexia is marked from the onset. The 
patient complains of great thirst. The 
bowels are usually relaxed. The copious 
diarrhoeal discharges, with the attendant 
nausea and vomiting, soon bring about a 
condition of asthenia. The mind remains 

Clear Up to the time Of great exhaustion Temperature Record in a "case cf Pysemia. 

and the appearance of multiple abscesses in 

some central organ or organs ; then the patient becomes dull, apathetic, 
and often slightly delirious. The respirations are hurried and shallow, 
and are always more accelerated just before a chill or sweat. As death ap- 
proaches, delirium occurs, the pulse becoming more feeble and intermittent, 
reaching at times 150 or 170, or 200 ; the face has a yellowish, leaden hue, 
and finally the patient passes into a comatose state and dies. 

When the internal organs are involved the local signs of multiple abscesses 
will be present. The physical signs of pyemic pulmonic infarctions are at 
first obscure, for the foci are so small and so scattered through the lung 
that percussion fails to detect them. Usually the evidences of a severe 
bronchial catarrh accompanied by a cough, with frothy, blood-stained, 
watery expectoration, are followed by the physical signs of lobular pneu- 
monia. 

The kidney changes are marked by albuminuria and haematuria, together 
with the. presence of epithelial and gelatinous casts. The amount of urea 
is always increased. The changes in the liver and spleen cause abdominal 
tenderness, accompanied by a marked increase in these organs as shown by 
percussion. In pyaemia there is generally more or less jaundice. The signs 

ir rhis intermittent type of fever is peculiar to this disease. Billroth says statistics favor the idea that 
recurrent chills depend on new inflammations, having their chief source in repeated purulent infections 
about the wound. 



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728 



ACUTE GENERAL DISEASES. 



of arthritis, pleuritis, peritonitis and cellulitis can be early recognized, and 
should be looked for in severe cases after the second or third day. 

Chronic pyaemia is met with among the robust, in whom the infection is 
moderate, and not often repeated. The abscesses are confined to the cellu- 
lar tissue and followed by suppuration in the joints, marked debility and 
muscular weakness. Weeks, or even months, may elapse before death or 
recovery takes place in this class of cases. 

Differential Diagnosis. — The diagnostic points of pyaemia are, irregularly 
recurring chills and sweats, great variations in temperature, with the signs 
of multiple abscess in the internal organs. It may be mistaken for septi- 
caemia, intermittent (malarial) fever, acute yellow atrophy of the liver, acute 
articular rheumatism, typhus and typhoid fever. The diagnosis between 
pyaemia and septicaemia has already been considered under septicaemia. 

The paroxysms in intermittent fever are regular in their development 
and time of occurrence ; they are not so in pyaemia. The temperature in 
intermittent fever ranges higher than in pyaemia. There is slight, if any, 
jaundice in malarial fever, while deep hematogenous jaundice is common 
in pyaemia. The history of the case, together with the presence or absence 
of small points of local infection, helps to differentiate between the two dis- 
eases. The sweet, nauseating breath, marked muscular prostration, and 
dull expression of the face, are noted in pyaemia and not in intermittent 
fever. 

The points of differential diagnosis between pyaemia, yellow atrophy of 
the liver, rheumatism, and typhoid fever are found in the history of these 
affections. 

Prognosis. — In pyaemia the prognosis is always unfavorable. Some deny 
the possibility of recovery in a well-marked case ; still recovery is possible 
in cases that are mild at the onset and slow in their development, in which 
the chills are not often repeated, the intermissions between the exacerba- 
tions of fever are long, loss of strength is not rapid, and the tongue re- 
mains moist. Thus we see that the prognosis depends entirely on the course 
of the disease. The duration of pyaemia varies : it is usually acute, lasting 
from two to ten days, often subacute, lasting from two to four weeks, and 
rarely chronic, when it may run on for months. The duration of puer- 
peral pyaemia is usually about one week. If death occurs in four or eight 
days, it is due to the intensity of the pyaemic poison. If later, it depends 
upon the exhaustion incident to the formation of abscesses and the occur- 
rence of complications. The earlier the symptoms of multiple abscesses 
appear the more hopeless the case. 

It must be remembered that pyaemic patients differ in their power of 
eliminating poison ; hence in some cases the system will be at once over- 
whelmed, while in others the shock will be recovered from. Every day 
after the eighth that the patient survives increase j his chance of recov- 
ery. 

Treatment. — The treatment of pyaemia may be divided into the prophy- 
laxis, and the treatment of the developed disease. Its prophylactic treat- 



DIPHTHEEIA. 



729 



ment is by far the most important : it consists in avoiding everything 
that mav favor the development of the disease, the details of which are 
included under the general management of surgical operations and the 
treatment of wounds. The history of these antiseptic methods comes 
within the domain of surgery rather than medicine. Obstetricians cannot 
be too careful in these matters. 1 Cleanliness, good ventilation, sunlight 
and quiet are important prophylactic measures. There are undoubtedly 
certain atmospheric conditions which influence the development of pyaemic 
marasmus, and are always to be considered. 

Pyaemic poison, if eliminated at all, is eliminated by the intestinal 
tract and not by the skin or kidneys, and treatment should be directed to 
aid this elimination. 2 With the idea of neutralizing the pyemic poison 
after it has gained access into the body, or counteracting its effects, nearly 
all the antiseptics have been employed. The sulphites and hyposulphites 
of sodium, calcium, and magnesium ; carbolic and salicylic acids ; the oil 
of turpentine, and many like agents, — are still under trial. Quinine is the 
drug which is most extensively employed for its antiseptic and also for its 
stimulant and antipyretic powers. 

The most important thing in the treatment of pyaemia is to support the 
patient ; and, with this end in view, the largest possible amount of nour- 
ishment and stimulants should be administered. There is no disease in 
which so large an amount of stimulants can be administered with benefit 
as in pyaemia. The indications for their administration are the same as 
in the essential fevers. If life can be prolonged, in mild cases, until the 
violence of the infection is passed, recovery is possible. 



DIPHTHERIA. 

Diphtheria is a specific constitutional disease, characterized by a granu- 
lar, fibrinous exudation upon the surface and into the substance of mucous 
membranes, and upon abraded surfaces. Various countries of Europe 
were visited by epidemics of diphtheria in the sixteenth and seventeenth 
centuries. In the middle of the last century it reached England, and in 
the early part of the present century it prevailed at different points in the 
New England States. 

Dr. Samuel Bard, of New York, gave the first accurate description of 
the disease in this country, and brought clearly before the profession its 
specific contagious character ; his clear accounts tally perfectly with the 
experience of the present day. B The labors and investigations of Louis, 



1 An interesting proof of this is shown in the case related by Dr. Teale : Three gentlemen who aided 
him in dissecting a en >ject who died of hernia attended the same day five midwifery cases in all. 
Four of these cases died of puerperal fever, while no other cases of it occurred in their extensive prac- 
tice. t 

2 Billroth says diarrhoea is a severe complication which quickly induces collapse. 
8 He published his pamphlet in 1812. 



730 



ACUTE GENERAL DISEASES. 



Trousseau, Rilliet, G-raefe, and Virchow have done more than those of any 
other investigators to perfect our knowledge of diphtheria. 

Morbid Anatomy. — The characteristic pathological lesion of diphtheria 
consists in a membranous infiltration of some mucous surface. Of the 
mucous surfaces, those of the pharynx, tonsils, uvula, and nasal passages 
are its most usual seats ; beginning on the tonsil and anterior wall of the 
pharynx, the diphtheritic process may extend upward into the posterior 
nares, forward into the anterior nares, or pass down the larynx, larger 
bronchi, bronchioles, and even enter the air-cells. From the pharnyx 
it may pass down into the oesophagus, the larynx often escaping ; or it 
may first appear in the larynx and extend upward into the pharynx : this 
latter is rare. Occasionally the mucous membranes of the mouth, stomach, 
vagina, rectum, and biliary passages are the seat of the diphtheritic pro- 
cess. If the skin is abraded it may become covered with diphtheritic 
exudation. 

The first change in the part that is to be the seat of this exudation is a 
passive hyperemia ; the capillary vessels are gorged, and the mucous mem- 
brane is of a dark, purplish-red color ; somewhat swollen at the point 
where the membrane is to develop. The hyperaamia is not active, the color 
is not the bright red of active inflammation, but dark, livid, and " angry." 
The amount of serous infiltration of the sub-adjacent tissues determines, 
in each case, the amount of tumefaction. On the surface of the affected 
part there is an abnormal secretion of mucus, and the epithelial cells cov- 
ering it become enlarged and cloudy, from exudation into them. Little 
by little they lose their nuclei and become transformed into a homogene- 
ous mass, presenting numerous ramifications — in other words, the meta- 
morphosed epithelium-cells form a reticulated membrane. 

The first and most superficial diphtheritic exudation is into the epithe- 
lium. The cells of the deeper structures may be simultaneously or sec- 
ondarily involved. The surface exudation becomes thicker and of a grayish 
color as the sub-epithelial mucous and sub-mucous coats become succes- 
sively involved. In mild cases the membrane first resembles a gauzy film, 
then it assumes a light yellow color, or occurs as white patches of varying 
size. Tn severe cases a leathery, gray exudation from one-eighth to one- 
fourth of an inch in thickness will form in five or six hours, which can 
be removed, and when removed leaves a raw bleeding surface which will 
immediately be covered by a new exudation. The membranous exudation 
may become infiltrated with blood, and assume a black color ; this is not a 
condition of gangrene, but gives evidence of great blood changes. Ab- 
sorption of the exudation is only possible when the epithelial layer is alone 
involved ; when the mucous and sub-mucous tissue is involved, the mem- 
branous exudation can only be removed by a suppurative or gangrenous 
process. 

As the exudation is taking place into the epithelium, micrococci or 
spherical bacteria will be found ; as the diphtheritic process involves the 
deeper tissues, the bacteria greatly increase in number. Some regard the 
bacteria originating within the epithelial cells as the result of the path- 



DIPHTHERIA. 



731 



ological processes; others as the cause of the pathological changes. 1 It 
seems reasonable to regard the diphtheritic exudation as a granular fibrin of 
low vitality, which possesses no power of organization. 

The arrest of the diphtheritic process may be first by suppuration. Un- 
derneath the diphtheritic exudation, there may be a suppurative process 
established which separates the layer of exudation from the tissues which 
it involves. In such a case the membranous exudation becomes more 
sharply defined at its boundary, the tumefaction of the surrounding mucous 
membrane subsides, the inflammatory zone draws closer and closer to the 
margin of the patch, whose edges curl up, and finally the mass is removed 
from its base, and is thrown off spontaneously. The duration of this exfo- 
liative process varies from two to five days. In some cases the diphtheritic 
process is so mild that while the exudation occupying the epithelium is 
thrown off, that in the subjacent structures is absorbed, no suppurative 
process occurring. In this, the mildest form, there is absorption accom- 
panied by a simple epithelial desquamation. 

Another termination of the local diphtheritic process is in gangrene. 
The nutrition of the tissues is so extensively and rapidly interfered with 
by the abundant exudation that the blood supply is cut off and death of the 
parts is the result. Some observers claim that gangrene is caused by the ob- 
struction of the lymphatics with bacteria. With the gangrenous process 
large numbers of putrefactive bacteria develop in the membrane and in the 
tissues underneath, which break down into a semi-fluid, dark mass, which 
has the peculiar odor of gangrene. Sometimes the sloughs are quite 
firmly attached to the adjacent tissues. The so-called septic variety is 
characterized by the formation of an extensive necrotic membrane, the 
color of which is a dark gray, or brown with streaks of capillary hemor- 
rhages throughout its entire extent. Larger colonies of micrococci are 
found in its deeper layers, and pressing against the fibrinous bands they 
form alveoli, in which myriads of the bacteria lie. The exudation in this 
variety occurs most frequently in the nasal cavities, where in and beneath 
the Schneiderian mucous membrane is an extremely rich plexus of lym- 
phatic and blood-vessels. This variety may involve tissues other than the 
mucous and submucous layers ; cases are recorded where the vomer was 
eroded, and little depressions in it were filled with nests of micrococci. 

A piece of membrane on examination will be found soft and friable, 
breaking down into an ichorous, semi-fluid, dirty brown pulp. If a por- 
tion of "septic" diphtheritic membrane is removed, ulcers are found in 
the tissue beneath, which may be shallow or deep. When shallow, they 
bleed very readily ; when deep, they are covered by dirty gray sloughs. 
The variety of the epithelium, and the number of mucous glands in the 
mucous membrane involved in the diphtheritic process, modify the patho- 

iZatm thinks he can distinguish three varieties of diphtheritic membrane : (1) one that is the result of 
morbid processes situate in the pavement epithelium ; (2) one that arises from solidification of a nmco- 
fibrinous exudation : (3) and one that is the result of solidification of a fibrino-puruloid exudation. This 
careful histolo-pathologist states fur; her that an}- or all forms of the bacteria may be found in each of his 
varieties, that they may also be absent, and that they are not an essential factor in diphtheria. 



732 



ACUTE GENERAL DISEASES. 



logical course of the exudation. When diphtheria invades the bronchioles 
and alveoli, the characteristic microscopical appearances of the exudation 
are discovered, and some air cells are filled with micrococci. 

The heart is pale, flabby, and friable, presenting changes similar to those 
in typhoid fever. The right heart is often filled with clots ; and the peri- 
cardium may be the seat of numerous ecchymotic spots, rarely of large 
size. Endocarditis is not an infrequent complication, and when present it 
is in many cases ulcerative, particularly if the disease has been severe and 
there are extensive blood changes. 

The blood sometimes is but slightly altered ; in the severer forms it is 
thick, of a dirty brown color, slightly coagulable, and after death contains 
micrococci. The arteries and veins are equally filled. A transient increase 
in the number of the white blood corpuscles is very common. 

The spleen is usually enlarged, the capsule is tense, shining, and covered 
with numerous points of capillary hemorrhage. The splenic parenchyma is 
congested, softened, and friable, darker than normal, and often the seat 
of multiple infarctions. 

The lymphatic glands become swollen and inflamed on account of their 
free communication with the infected parts. The hyperplasia occurring 
within the gland causes a swelling which may be tense and hard or doughy. 
This doughy feel results from oedema of the peri-glandular and subcutaneous 
connective-tissue, in which vegetable parasites are frequently found. The 
lymph vessels are often clogged with micrococci. Suppuration in the 
lymphatics is of very rare occurrence. 

The kidneys are congested or the seat, in severe cases, of parenchymatous 
nephritis, differing in no respect from that occurring in scarlatina, which 
has received the name of scarlatinal nephritis. Those who favor the para- 
sitic origin of diphtheria regard the micrococci as the starting-point of the 
morbid nephritic processes ; yet they state that if a child die rapidly from 
.suffocation, only a cloudy swelling of the epithelium exists; but if the disease 
shall have progressed for several days, attended by severe symptoms of in- 
tense blood poisoning, then the micrococci are discovered. Thus the 
morbid processes, by their own statements, are shown to be primary and 
not secondary to bacterian developments or migration. 

The Brain and Cord. — In severe cases there are numerous small spots of 
capillary hemorrhage scattered throughout the meninges of both brain and 
cord. These extravasations may sometimes be large enough to form clots, 
and then softening of the brain in localized spots will occur. Cells and 
nuclei swell the spinal nerves at the point where their roots join, so that 
their thickness may be twice the normal ; blood may be extravasated at 
this point, and then the swelling will be distinctly red. Punctate hemor- 
rhages into nerve centres where white matter is predominant are said to be 
the cause of diphtheritic paralysis, and after degenerative processes have 
occurred in these hemorrhagic spots the paralysis gradually disappears. 1 

Etiology. — Diphtheria is a contagious disease, often prevailing epi- 



1 Einiges iiber Diphtherie. L. Buhl, Zeit. f iir Berl., iii. 4. 1867. 



DIPHTHERIA. 



733 



demically. It is undoubtedly of microbic origin, although its specific 
microbe has not as yet been universally accepted. Many of its etiologi- 
cal conditions are identical with those of typhoid fever : filth, bad sewer- 
age, overcrowding, etc. I have met with diphtheria in houses where 
the water and sewerage pipes were defective, and where no other causa- 
tive factor could be found ; nevertheless I have a belief that the miasm 
of diphtherias^ be present with the other etiological conditions before 
diphtheria will be developed. Trousseau claims that the infectious ele- 
ment is confined to the exudation, but many clinical facts indicate that 
it is present in the exhalations and in the excretions, as well as in the 
exudation itself. Diphtheritic contagion clings to the objects that have 
been in contact with the diseased individual, and may thus be carried a 
long distance. 

Another vexed question in its etiology : Is it first local, and then consti- 
tutional, or vice versa? From a clinical standpoint it seems that the 
disease starts locally ; that some particle, for instance, of the exudation, 
too small to be detected with the unaided eye, is received upon the mucous 
membrane of the pharynx, nose, mouth, larynx, trachea, vagina, or upon 
a cut or abraded surface, and thence contaminates the whole system. 
The point of infection cannot be determined until after constitutional 
infection has taken place. It seems to be well established that when the 
local signs of diphtheria are present, there is already a constitutional infec- 
tion. The experiments of Oertel 1 and others show that the point of inocu- 
lation is the point from whence radiates the disease. 

The stage of incubation usually varies from one to eight days ; it may 
last one month ; when the disease is directly communicated, as in some 
recorded instances when a piece of diphtheritic membrane is dislodged 
and coughed into the mouth, nose, or eye of the physician or attendant, 
the disease has developed within twenty-four hours. But the question 
arises : May not the one thus attacked have been under the influence of 
the diphtheritic poison for some time, and thus prepared for the rapid 
reception of the local poison ? During epidemics the period of incubation 
is shorter, and there is reason to believe that the more virulent the poison 
the less time elapses between the exposure and the initial symptoms. As 
a rule, the latent period of diphtheria rarely exceeds five days. 

Diphtheria may prevail as an epidemic, or be endemic. It also occurs 
sporadically. Sporadic cases occur most frequently in those localities 
where the disease has prevailed as an epidemic. Climatic influences have 
little to do with its development, but autumn and spring are the seasons 
when the disease is most fatal. Age is a powerful predisposing cause ; 
from the second to the fifth year is the period of greatest susceptibility ; 
but no age is exempt. Previous attacks afford no immunity against sub- 
sequent ones ; certain individuals seem to be perfectly proof against the 
diphtheritic infection. Filth, bad sewerage and drainage, overcrowding 



1 Expemmentalle Vntersiichungen uber Diphtherie, M. J. Oertel, Deutsch. Arch, fur klin. Med., viiL 
1871. 



734 ACUTE GENERAL DISEASES. 

and a general bad hygienic condition favor the development and spread of 
diphtheria. Exposure to cold and wet, and sudden chilling of the body, 
may bring on, or hasten an attack of diphtheria during an epidemic. In a 
region where the soil is porous, the spread of the disease is much less ex- 
tensive than in clay soil. 

Symptoms. — The symptoms of diphtheria are local and constitutional. 
The constitutional may precede the local ; or both may appear at the same 
time. In some cases the local are the primary, and for a time the only 
signs of the disease. The ushering-in symptoms vary not only in different 
epidemics, but in different cases during the same epidemic. It is a dis- 
ease which has no typical course. 

The local symptoms begin with a sensation of dryness and prickling in 
the throat, with, perhaps, slight pain independent of attempts to swallow. 
There is more or less stiffness along the angle of the jaw. Deglutition be- 
comes more and more painful; solids do not cause as much dysphagia as 
fluids. There may be marked and painful swelling of the glands at the 
angle of the jaw — in the bifurcation of the common carotid artery — but 
many severe and fatal cases are accompanied by only slight glandular en- 
largement, and occasionally the disease runs its entire course without any 
glandular swellings. In some epidemics most of the cases will be attended 
by extensive glandular swellings, while others, of equal severity, only 
exhibit this symptom in a slight degree. However the disease may com- 
mence, when fully established there will be noticed upon the anterior pil- 
lars of the soft palate, the velum, and tonsils, sometimes also upon the 
posterior pharyngeal wall, whitish patches, surrounded by a livid, tumefied 
and congested mucous membrane. At this early stage the exudation can 
be removed without causing even punctate hemorrhage ; and under the 
microscope the epithelial cells will exhibit the appearances that have 
already been described. The sub-epithelial tissue becomes cedematous, and 
later, both tonsils, the uvula, and the anterior part of the soft palate will 
become ©edematous. At this period the membrane may be easily removed, 
but soon after its removal it will reappear in the same situation, and 
have the same extent. As a rule the more extensive the exudation, the 
thicker will be the membrane and the firmer its attachment. 

When the posterior nares are involved it is usually the 'result of the ex- 
tension of the diphtheritic process upward : the tonsils, uvula, and pos- 
terior pharyngeal wall having been the primary seat of the exudation. A 
coryza is soon developed, and the sanious, ichorous discharge irritates, red- 
dens, and excoriates the surfaces over which it flows. At the same time 
rapid swelling of the cervical, lymphatic, and sub-maxillary glands occurs ; 
and there is undoubtedly a special connection between enlargement of the 
glands at the angle of the jaw, and diphtheria of the nares and posterior 
wall of the pharynx. The nostrils are soon clogged, often completely so, 
and repeated attacks of epistaxis may mark the later stages of nasal diph- 
theria. When the disease extends upward the parotid is not infrequently 
swollen and tender. Nasal diphtheria is in a few instances primary. The 



DIPHTHERIA. 



735 



nose, in cases of invasion of the posterior nares, is often swollen and red, or 
shining and (edematous ; the parts excoriated by the now from the nostrils 
are soon covered with ulcers, and the latter are often covered with the gray 
diphtheritic exudation. 

When the Eustachian titles are involved, there will be tinnitus aurium, 
darting pains on attempts to swallow, marked loss of hearing, and perhaps 
otitis ; perforation of the tympanum, and caries of the adjacent bones may 
result. The external ear has in rare cases been the seat of secondary and 
also of primary diphtheria. The middle ear has also sometimes been im- 
plicated. The eye may be invaded in diphtheria when the nasal duct is 
the seat of the exudation ; or a piece of membranous exudation being 
coughed into the eye of the examiner may excite a diphtheritic conjunc- 
tivitis. If the diphtheritic process passes downward it may enter either 
the digestive or the respiratory tract. 

If the oesophagus is involved there will be a marked dysphagia, and fluids 
will be regurgitated ; accompanying paralysis of the muscles of deglutition 
in many instances increases the dysphagia. If no special signs of pharyn- 
geal exudation are present in a suspected case of oesophageal diphtheria, 
portions of the exudation may appear in the vomited matters, for vomiting 
is an important sign of oesophageal diphtheria. Portions of membrane in 
the feecal discharges point to the existence of the oesophageal diphtheria 
when there are evidences of tonsillar and pharyngeal exudation. 

When the vagina, rectum, or labia are involved there will be more or 
less swelling of the inguinal glands in the immediate neighborhood. 

The diphtheritic process may extend from the pharynx into the larynx 
and trachea. Sometimes laryngeal diphtheria is developed when the pri- 
mary seat of the diphtheria is in the nasal passages, or in the mouth. 
Laryngeal diphtheria occurs most frequently in children ; the younger the 
child the greater the liability to laryngeal complication ; when adults are 
attacked, it is the wea*k and feeble and the aged. The epiglottis becomes 
hyperaemic, livid, and swollen, its edges are harder than the remainder of 
its substance, and the diphtheritic patches are developed irregularly upon 
its surface. 

The first symptom indicative of laryngeal diphtheria is a change in the 
voice, which loses its volume, becomes hoarse, rough and indistinct, 
then falls to an inarticulate whisper. The respirations become noisy and 
whistling, and dyspnoea becomes more and more urgent as the exudation 
advances. The cough is first dry and stridulous — "brassy," — but soon 
changes, losing the brassy tone, and, indeed, it has no distinct tone what- 
ever, and is so peculiar as to be almost diagnostic of laryngeal diphtheria. 
In children the invasion of the larynx is often sudden. In a short time 
there is complete aphonia ; a cough is developed that is " barking" or 
" croupy " in character, but (as in adults) it soon becomes abortive. The 
dyspnoea is extreme ; all the auxiliary muscles of respiration are called 
into play. The attacks of difficult breathing assume a paroxysmal form, 
and in one of the paroxysms death may occur. If the upper part of the 



736 



ACUTE GENERAL DISEASES. 



larynx only is involved there is difficulty of inspiration, but when the 
whole larynx is involved expiration is also affected. There is falling in of 
the supra- and infra-clavicular spaces during inspiration, showing that im- 
perfect inflation of the lungs results from the mechanical obstruction to 
the entrance of the air into them. Cyanosis becomes marked, and there 
is either stupor, or restlessness and jactitation. When the child dies it is 
with all the symptoms of croup (q. v.). Death is not from the action of 
the poison but from local obstruction which has mechanically forestalled 
its constitutional effects. 

A laryngoscopic examination shows epiglottis, vocal cords, and the in- 
terior of larynx to be the seat of a diphtheritic exudation, the ventricle being 
usually wholly obliterated. 

Auscultation reveals abnormal laryngeal sounds, together with rales of 
various kinds, and a loss of vesicular respiration. In some instances the 
diphtheritic process may have its primary seat in the larynx, and then ex- 
tend upward, the same processes occurring upon the tonsils, uvula, and soft 
palate, as when they are the primary seat of the disease. In such cases 
laryngeal symptoms are present from the onset of the disease. 

Constitutional Symptoms. — There are no regular stages in the develop- 
ment of diphtheria, therefore no typical clinical sketch can be given which 
shall include all cases. The division of diphtheria into the catarrhal, 
croupous, gangrenous and septic forms can only be made at the expense of 
facts, for they may rapidly merge into each other, and are only stages of 
one and the same diseased process. Diphtheria may begin with well- 
marked, active symptoms, as a chill, fever, pain in the head and back, 
nausea, vomiting, and even convulsions. „ Or it may come on insidiously, 
the patient complaining only of the throat symptoms. It may run so mild 
a course that the patient at no time feels sick ; the throat symptoms are 
not marked ; and there is a small patch of exudation upon the tonsils, but 
it does not extend. 

There is little or no febrile movement, and at the end of a week the 
patient is fully convalescent. In those cases where well-marked symptoms 
usher in the disease, the temperature ranges higher than in any other form 
of the disease ; in rare cases it may reach 105° F. by the end of the second 
day. Insidious cases are marked by a gradual rise in temperature, 102° 
or 103° F. being the highest point reached during the whole course of the 
disease. Mild and severe cases often occur in the same household during 
the same epidemic. 

In whatever manner diphtheria is established, the constitutional and local 
symptoms do not always progress with the same severity. In some cases 
while the exudation is rapidly extending the temperature falls to normal, 
the pulse diminishes in frequency, the patient seemingly having decidedly 
improved in every respect — in fact, the constitutional symptoms remit if 
they do not intermit. The pulse, however, will show the influence of the 
poison on the nervous system, either in irregularity or abnormal frequency, 
or both. But during all this time the membranous exudation is spreading. 



DIPHTHERIA. 



737 



After a time the temperature rises to 103° or 104° F., the pulse to 120 or 130, 
and all the severe constitutional symptoms reappear. Death often occurs 
early in such cases. In another class of cases the constitutional symptoms 
are severe from the onset, while the local manifestations of the disease are 
but slight and not progressive. In some cases the nervous system may be 
overwhelmed by the intensity of the diphtheritic poison at the onset of the 
disease, and death result before any local manifestations of the disease have 
had time to make their appearance. 

In the more common forms of diphtheria the first symptom will usually 
be the soreness of the throat, which will be found congested ; and either 
upon a tonsil or at some point in the pharynx, a small white patch of ex- 
udation will be seen. Slight febrile movement may accompany the throat 
symptom, or it may not come on for forty-eight hours. The exudation 
gradually extends until a large surface is covered with a thick layer of 
membrane, which assumes a gray or brown color. The sub-maxillary glands 
become more or less swollen. There is always some obstruction in the 
throat and difficulty in swallowing. As the disease becomes fully developed, 
patients are unable to sit up. There is nausea and often vomiting. The 
urine is usually albuminous. The pulse becomes frequent and feeble ; the 
temperature ranges from 101° to 103° F. The membranous exudation 
continues to extend, involving more and more of the throat. The patient's 
general condition becomes worse each day until about the end of a week ; 
when the membrane is thrown off, the pulse becomes less frequent and the 
patient slowly recovers. Or, as happens in some instances, as the exuda- 
tion disappears from the tonsils it extends into the larynx : then are de- 
veloped all the symptoms of laryngeal obstruction, the breathing becomes 
difficult, cerebral symptoms are prominent, and patients die in a few days 
after the laryngeal symptoms appear. Occasionally after the local mani- 
festations of diphtheria have disappeared, patients experience a degree of 
prostration and feebleness that is met with in no other disease. The pulse 
becomes feeble, frequent and intermitting : and the heart-sounds are 
muffled and indistinct. Death occurs in such cases as if a poison — such 
as prussic acid for instance — had been taken. 

Symptoms which indicate danger. — Diarrhoea, although not often present 
in diphtheria, may be so profuse as to cause exhaustion which will hasten the 
fatal termination. Nausea and vomiting coming on late are most unfavor- 
able symptoms. Albuminuria occurs in mild as well as in severe cases, 
rarely lasting longer than a week, except in those severe cases where oedema 
is present, and where epithelial, granular, small hyaline and exudative 
casts are found in the urine. It is stated by some that the amount of 
albumen in the urine is in direct proportion to the intensity of the diph- 
theritic infection. In a few rare instances diphtheritic nephritis has been 
so intense that death has resulted from it, before either the constitutional 
or local symptoms of the disease were present. Albuminuria generally 
comes on toward the end of the first week of the disease. Coma may occur 
as the result of the nephritis. An erythematous eruption sometimes makes 
47 



738 



ACUTE GENERAL DISEASES. 



its appearance in diphtheria between the first and third days. Its usual seat 
is the upper part of the chest and back. 

The pulse is peculiar and varies greatly in different cases. There are 
three distinct varieties : 

I. In a large number of cases the pulse from the very commencement is 
feeble, small, and rapid, ranging from 120 to 160, or, in young children, 
even to 170 in the minute. 

II. There is a class of cases where the pulse rises to 120 or 130 early in 
the disease, but falls to 60 or even 40 within twenty-four or forty-eight 
hours from its onset. 

III. There is a class of cases in which the pulse is irregular and inter- 
mittent throughout the entire course of the disease. The prognosis in the 
latter variety is always bad. 

If the temperature falls to normal, or below, and the exudation shows 
no signs of exfoliating, no matter how trifling its amount, or how 
slight the glandular swelling, the case is grave and death is not usually 
long delayed. Convulsions occurring late in diphtheria are always un- 
favorable symptoms, while as ushering-in symptoms they have no special 
significance. Swelling of the lymphatic glands, although not present in 
all cases, is so frequently present that it must be regarded as one of the 
symptoms of the disease. If it is extensive so as to interfere with degluti- 
tion and respiration, the prognosis is unfavorable. 

After the exudation disappears and convalescence is apparently estab- 
lished, sequelae may develop, which may continue for months and even 
years. The commonest is paralysis of some of the voluntary muscles ; the 
muscles most frequently affected are those of the soft palate and pharynx. 
Usually the first thing indicating the occurrence of this paralysis will be 
difficulty in swallowing — first fluid and then solid food— with an inability 
to articulate clearly. When paralysis is unilateral the velum is drawn to 
the healthy side ; when both sides are involved the velum hangs pendulous 
and motionless ; there is also a loss of sensation as well as of motion, for 
pricking it causes no pain. The voice is altered, and children cry as with 
a cleft-palate, Avhile adults have a sort of nasal twang. These changes come 
from paralysis of the velum, anterior pillars of soft palate, and pharyngeal 
wall. Fluids are only partially swallowed, the greater portion being re- 
gurgitated through the nose, especially if the individual is standing or 
leaning forward while drinking. This variety of paralysis sometimes comes 
on while the exudation is yet visible in the fauces, just as it is disappear- 
ing, or in a week or ten days after it has entirely disappeared. With the 
dysphagia there is sometimes difficulty in expectorating ; the patient will 
choke, cough and strangle in vain endeavors to get rid of mucus that has 
collected in the pharynx. 

As the pharyngeal paralysis is disappearing, — or from two to ten days 
after, — the muscles of some other part of the body will be involved — the 
lower extremities being much more frequently affected than the upper. 
Though usually beginning in the feet, diphtheritic paralysis follows no 



DIPHTHERIA. 



739 



regular order ; a hand may first be affected, then a leg, and subsequently 
the other hand, arm and leg. Before the occurrence of the paralysis there 
will be a sensation of coldness, pricking, crawling (formication) and 
numbness in the part about to be affected. The patient cannot determine 
precisely where he has placed his foot— on the floor or some object higher 
than the floor ; movements are ungainly and hesitatingly made, the gait 
becomes tottering, and finally he cannot stand, the paralysis becoming com- 
plete. Sensation is likewise more or less impaired. The hand loses its 
usual dexterity ; the patient being unable to button his coat, or even write 
his name. When the muscles of the neck are involved the head 
" wobbles," or is held upright with the greatest difficulty. The neck is 
usually the last part to be attacked. The power of ocular accommodation 
is often seriously interfered with on account of the paralysis of sorne of the 
ocular muscles. The ciliary and recti suffer oftenest. First, sight is 
diminished or lost for objects close at hand ; and later, distant objects be- 
come invisible. There is always diminished refraction, and there may be 
strabismus and double vision. 

When diphtheritic paralysis is general the laryngeal muscles will usually 
be wholly or partially involved. The voice is hoarse, non-resonant, and 
often there is complete aphonia. There is no loss of sensation until the 
superior laryngeal branch of the pneumogastric is involved ; this is attended 
with danger, for particles of food may pass into the bronchi, and suffocative 
dyspnoea may result in death. In nearly all forms of laryngeal paralysis 
there is more or less dyspnoea, greatly increased by exercise. If the paraly- 
sis involves the sphincters there will be involuntary discharges from the 
bladder and rectum. The genital organs may be paralyzed, and all sexual 
desire and power may be lost for months. Paralysis of the muscles of the 
thorax, trunk and diaphragm gives rise to grave symptoms, pulmonary 
oedema and death usually resulting. Finally, paralysis of the heart may 
occur. 

Diphtheritic paralysis is always entirely recovered from. In mild cases 
its duration is two or three weeks, while in others it has continued one 
or two years. Another sequel of diphtheria is parenchymatous nephritis. 
When developed during the exudative stage it usually ends in complete re- 
covery. Barely does it directly cause death. When so developed it may 
be regarded as part of the active history of the disease. But when it 
occurs during convalescence it may lead to chronic Bright's disease. In- 
flammation of a serous membrane may complicate- or be a sequel of diphr 
theria ; the most frequent serous inflammation is endocarditis. 

Pleurisy, peritonitis and pericarditis are of rare occurrence. Chronic 
pharyngitis is a sequela only in those cases where there has been paralysis 
of the pharyngeal muscles. 

rifferential Diagnosis. — The diagnosis of diphtheria rests on the presence 
of a membranous exudation. When it prevails as an epidemic, a form of 
"sore throat," a pharyngeal catarrh usually prevails at the same time, 
sometimes called "diphtheritic sore throat." 



740 



ACUTE GEISTEKAL DISEASES. 



This sore throat is ushered in by a chill, followed by a more or less in- 
tense febrile movement. There is a sense of fulness in the throat with 
swelling of the sub-maxillary glands, and more or less dysphagia. The 
mucous membrane over the tonsils is intensely congested, the uvula is 
cedernatous, and a few points of whitish exudation stud the mucous 
membrane. If these little dots are examined closely they are found to 
be mucus, exuded from the enlarged follicles. The process is purely 
catarrhal, and not membranous. This is called by some "catarrhal diph- 
theria," but is nothing more than a catarrhal pharyngitis. It is never 
contagious, but is due to atmospheric influence, and has none of the char- 
acteristic local or constitutional features of diphtheria. 

The points of differential diagnosis between diphtheria and croupous 
laryngitis are the following : croupous laryngitis, or membranous croup, is 
a local affection, while diphtheria is a constitutional disease. Croup is 
not contagious or inoculable ; while diphtheria is markedly so. In croup 
the exudation is on the surface of the mucous membrane ; in diphtheria it 
is in its substance as well as on its surface. Laryngeal symptoms are 
primary in croup, while in diphtheria they usually follow severe con- 
stitutional symptoms, and in the majority of cases also follow the ap- 
pearance of the exudation upon the nasal or pharyngeal membranes. 
Croup rarely attacks those who have passed the age of puberty ; diph- 
theria attacks all ages. Croup is sporadic ; diphtheria is often epidemic. 
The sub-maxillary glands may be, and often are, enlarged in diphtheria, 
but never in croup. 1 From a clinical standpoint they must be regarded as 
distinct diseases. 

Diphtheria may be distinguished from scarlatinal sore throat by the 
following points : — in scarlatina there is a diffuse redness of the mouth 
and pharynx ; in diphtheria tne redness is local and of a darker color. In 
scarlatina the exudation is mucus, and on the surface of the tonsils soft 
palate and pharynx ; in diphtheria it commences at one point, and spreads, 
is adherent and tough, and has a grayish or brown color. When an erup- 
tion occurs in diphtheria it will have the characteristics already referred 
to, will last but a few days, and will appear on the trunk only. In scarlet 
fever the characteristic eruption rapidly spreads over the whole surface, 
lasts three to four days and is followed by desquamation. In diphtheria 
there is no characteristic eruption, only occasionally transient roseola. The 
temperature is far higher in scarlet fever than in diphtheria, the ushering- 
in symptoms more severe, and there is the peculiar strawberry tongue in 
scarlatina which is not present in diphtheria. 

Typhoid or typhus fever may be suspected when intestinal diphtheria 
•exists. The only means of diagnosis is to watch the passages for the mem- 
brane, and take the temperature carefully ; in typhoid there will be the 
typical range, and in typhus the rise will be sudden and higher. Finally 
idiopathic erysipelas of the throat is very difficult to distinguish from diph- 

! The sides of the neck are to be examined for enlarged glands; those at the anterior border of the 
stemo-mastoid arc always palpable, but it is important to note that the glands at the angle of the jaw are 
not enlarged. 



DIPHTHERIA. 



741 



theria. In erysipelas the tongue is blackish brown, dry, and fissured ; and 
there is more puffy swelling of the parts than in diphtheria. The glands 
are not enlarged and the process is limited in its extent in erysipelas. 

Prognosis.— The prognosis in diphtheria varies with different epidemics, 
and with the type of the disease. The prognosis is more unfavorable the 
younger the subject, since extension into the larynx is more frequent in 
the young child. The death rate varies in different epidemics from twenty 
to fifty per cent. A peculiar fact, and one to be remembered, is that a 
mild case— one where all things are progressing favorably— is liable to as- 
sume, in a few hours, a most malignant type. The system may be over- 
whelmed with the poison even when the exudation shall have disappeared ; 
and, again, in convalescence heart-paralysis may suddenly occur ; all of 
these points make a very guarded prognosis not only safest but necessary. 
Its duration varies from three to twelve or fourteen days, but death may 
occur within thirty-six hours ; and again the disease may continue three or 
four weeks. 

The symptoms which may be regarded as unfavorable are extreme gland- 
ular swellings, huskiness of the voice, a dark-colored extensive exudation, 
and, above all, laryngeal implication ; when diphtheria extends into the 
larynx, about 95 per cent, of the cases end fatally. Repeated convulsions 
are unfavorable ; and a pulse that is irregular and intermittent, or one that 
drops to 60 after having been rapid at the onset, indicates danger. When 
at the same time that the exudation is extensive, it has a dark gray, green, 
or black color, and when it emits a gangrenous or sickly, sweet odor, the 
prognosis is unfavorable. Nausea, vomiting, diarrhoea and epistaxis, when 
they occur late in the disease are very serious symptoms. Coma, ac- 
companied by casts and albumen in the urine, or by entire suppres- 
sion of urine, is a most dangerous occurrence. If pharyngeal paralysis 
occurs before the exudation has disappeared, the case is a very serious 
one ; the future course will be troublesome, owing to intense involve- 
ment of the nervous system, and these cases are often fatal. The 
temperature is not a reliable element in prognosis : in the most malig- 
nant types of the disease it may range low, between 101° and 102° F. A 
sudden rise or a sudden fall, especially to sub-normal limits, is exceedingly 
unfavorable. Primary diphtheria of a wound, in which the throat shows 
no manifestations of the disease, generally runs a favorable course. Pri- 
mary infection of a wound with diphtheria, in which the throat becomes 
secondarily involved, is always unfavorable. Secondary wound infection, 
during the course of a pharyngeal diphtheria, shows an intense degree of 
poisoning, and is a bad prognostic omen. 

All complications render the prognosis unfavorable. Among the com- 
plications are meningitis, endocarditis (usually ulcerative), pleurisy, peri- 
tonitis, pericarditis, pneumonia, bronchitis, tracheitis, laryngitis, pulmon- 
ary oedema and congestion, oedema glottidis, acute Bright's disease, and a 
septic fever that ordinarily complicates the malignant form. Septicaemia 
and pyaemia may occur, and intestinal hemorrhage, purpura, and jaundice 



742 



ACUTE GENERAL DISEASES. 



are occasional and very grave complications. Death may occur from any 
of these complications, from paralysis of the herrt, from inanition, espe- 
cially in children where deglutition is interfered with, or from asthenia. 
The nervous system may be overwhelmed with the poison at the onset. The 
exhaustion from vomiting, diarrhoea or hemorrhage may sometimes be so 
great as to cause death. The patient may be asphyxiated from intercostal 
and diaphragmatic paralysis or from getting a bit of solid food in the 
larynx or trachea. 

Treatment. — The treatment of diphtheria will be considered under four 
heads : I. Hygienic ; II. External local ; III. Internal local ; IV. Inter- 
nal constitutional treatment. 

Hygienic— A patient sick with diphtheria should be kept in bed from 
the advent of its first symptom until convalescence is fully established, 
and the pulse is normal in frequency and regular in its rhythm and force. 
The membranous disappearance is not the guide ; it is the exhausted and 
anaemic condition which demands absolute rest in bed. Only attendants 
that are agreeable to, and can manage the child well should be admitted 
into the sick room, which must be large, well ventilated, and have a tem- 
perature of 70° to 75° F. Perhaps one of the most important indications is 
cleanliness ; the patient should be kept scrupulously clean, — eyes, nose, 
ears and mouth, as well as the face and limbs. All utensils of whatever 
kind, all clothing and linen, must be frequently cleansed and disinfected. 
The disinfection may be accomplished as in typhoid (q. v.). The patient 
must be strictly quarantined, the attendants must mingle as little as possi- 
ble with the rest of the household, and must avoid taking the breath of, 
and unnecessary manipulation of, the patient. The rule is, not to disturb 
a diphtheritic patient except so far as it is necessary for cleanliness. The 
physician should be careful not to make unnecessary examinations of the 
throat. The instruments used in the examination should be thoroughly 
cleansed after each examination. Freshly slacked lime mixed with pow- 
dered charcoal may be placed about the room as disinfectants. Fresh 
air and sunlight are important, and should be so admitted into the sick 
room so as to avoid draughts. A grate fire in cold weather is the best 
method to attain ventilation. 

External Local Treatment. — This treatment may be considered under 
four heads : — 1. Hood-letting by means of leeches at the angle of the jaw ; 
2. cold applications — ice-bags — to the throat ; 3. counter -irritation — 
blisters, etc. — over the neck and enlarged glands ; and 4. hot poultices or 
other hot applications to the throat. 

Blood-letting, local or general, while it does not arrest the exudative 
process, diminishes the resisting power of the patient ; clinical experience 
teaches us that all antiphlogistic remedies are contraindicated in the 
treatment of this disease. 

Ice to the throat is with some a favorite plan of local treatment. It is 
to be remembered that the exudation is a local manifestation of a consti- 
tutional disease, and that its extension is arrested and its removal accom- 



DIPHTHEEIA. 



743 



plisbed by tbe establishment of a suppurative process ; and for this reason 
the local application of cold is contraindicated. It may relieve pain, but 
it does not arrest the diphtheritic process. 

Counter-irritation is also powerless to check the membranous exuda,- 
tion ; besides, whenever a surface becomes abraded, the diphtheritic process 
is liable to be established upon it. 

If the diphtheritic exudation is arrested and removed by a suppurative 
process, the external application of heat is indicated, and may be of service. 
Hot fomentations must be regarded as the safest and best means of hasten- 
ing the removal of the membrane, and they afford the greatest relief to the 
patient. 

Internal Local Treatment may be considered under three heads : — 1. Me- 
chanical means employed for removing the membrane. 2. Escharotics 
employed for its destruction. 3. Astringents to prevent an extension of 
the exudation by their action on the unaffected mucous membrane. 

It is not difficult to pull off a patch of diphtheritic exudation by median- 
ical means ; but the membrane will reappear as soon as the removal is 
effected ; and the second membrane has a deeper intimacy with the tis- 
sues than the primary. For this reason no attempt should be made to re- 
move a diphtheritic exudation unless it hangs loosely detached, and then 
the dependent portion may be carefully snipped off. Any irritation pro- 
duced by instruments favors the extension of the diphtheritic process. It 
is to be remembered that, however pleasant it may be for parents and 
friends to see patches of the membrane removed, after each removal the 
diphtheritic process is increased both in depth and extent. 

The powerful escharotics which have been used for the destruction of 
the diphtheritic exudation are hydrochloric and nitric acids, nitrate of 
silver, bromine, chromic acid, etc. It is claimed by partisans of this plan 
that, when seen very early, and when the diphtheritic patches are small, 
extension of the exudation may be arrested by the destruction of its local 
manifestations. There seems no more reason for the use of escharotics 
than for the mechanical removal of the exudation ; for each one of the 
escharotic sloughs leaves an ulcer, which is a favorite spot for the develop- 
ment of a new membrane in the deeper tissues. 

Astringents, by constringing the mucous membrane about a diphtheritic 
patch, thus prevent the spread of the exudation. But as the primary 
action of all astringents is to cause irritation of the mucous surface, and 
as the irritation favors the development of the diphtheritic membrane, 
their use is contraindicated. 

The thing to be accomplished by local internal treatment is to hasten 
the suppurative process ; the local means which will aid the process of 
suppuration is the inhalation of the vapor of hot water. The external and 
internal local treatment of diphtheria resolves itself into the application 
of poultices externally and vapor inhalations internally. The vapor in- 
halations should be commenced as soon as the exudation is detected, and 
continued until all signs of it have disappeared. As the steam inhalation 



744 



ACUTE GENERAL DISEASES. 



increases mucous secretion, it favors the removal of the membrane, and 
furnishes another reason for its use. To prevent or limit septic poisoning, 
antiseptics are to be used, and those that are non-irritating are to be pre- 
ferred. The diphtheritic surfaces should be frequently sprayed with chlo- 
rine water, or with weak solutions of permanganate of potash, carbolic 
and salicylic acid, boric acid, benzoate of soda, or muriated tincture of 
iron. Lime water, glycerine, and lactic acid have been used with benefit ; 
and when an atomizer is not at hand, disinfectant gargles and washes 
may be substituted. It is especially important that disinfectants should be 
employed in nasal diphtheria, after thoroughly cleansing the nasal cavities. 

The constitutional treatment of diphtheria consists essentially in sup- 
porting the vital powers of the patient. There are no specifics for its 
treatment, any more than for scarlet fever or smallpox. All-depressing 
remedies are contraindicated. The alcoholic treatment is a favorite plan 
with a large number of practitioners ; under this plan alcohol is given, not 
merely to sustain the patient, but for its constitutional effects. With this 
end in view, it is given in large quantities ; one-half an ounce of brandy 
may be given to an adult every half hour ; to a child two years old from 
one-half to one drachm every hour. The amount to be given must be de- 
termined only by its effects. The object is to get the physiological effects 
of the alcohol as quickly as possible. The beneficial effect of the stimulants 
will be indicated by the pulse becoming slower after its use, by a diminu- 
tion in its tremulousness, by an increased desire for food, and by a manifest 
feeling of general amelioration. The stimulating plan should be carried 
out more strictly in diphtheria than in any other infectious disease. An 
intermittent and irregular pulse demands freer stimulation than a rapid 
and feeble, but regular, pulse. An increasing apathy, a feeble pulse, ir- 
regular at times, a dry tongue, a dark and offensive-smelling exudation, 
often indicate a crisis that may be tided over by crowding stimulants. 

The diet should be milk and yolk of eggs ; when there is great dysphagia, 
food may be administered per rectum. Ether, musk, and camphor are re- 
garded by some as valuable adjuncts to the alcoholic plan of treatment. When 
the temperature ranges high, quinine and cold sponging may be enrployed. 
I do not consider it safe to administer large doses of antipyretics in diph- 
theria on account of the danger of heart failure. Quinine is by far the 
most desirable one in this disease. The tincture of the chloride of iron 
and chlorate of potassa are favorite internal remedies in the treatment of 
diphtheria. From five to twenty drops of the tincture of iron are given 
in glycerine or water every hour ; and from two to twenty grains of the 
chlorate of potassa every two hours. The use of these drugs, given either 
alternately or in connection, is at the present time a ruling practice in the 
profession. The internal use of the benzoate of soda, and solution of the 
bromides, to neutralize the diphtheritic poison, although strongly advocated 
by some, is not sustained by the experience of the profession generally. 

If nutrition be kept at a high standard, and if the use of tonics be per- 
sistently kept up, the paralyses that are the chief sequelae of diphtheria 
will usually soon be recovered from. Porter is one of the best tonics in 



ERYSIPELAS. 



745 



the treatment of the sequelae of diphtheria, especially the paralyses. When 
pharyngeal paralysis occurs, the food is to be given through an oesophageal 
tube. 

When the nose is the seat of diphtheritic exudation, the nasal chambers 
must be thoroughly cleansed. Lime water or dilate carbolic acid are the 
best washes to accomplish this ; the washings must be frequently and care- 
fully employed. 

When the larynx is invaded, exudations may be mechanically removed, if 
suffocation is imminent. Inhalation of alkalies, lactic acid, etc., are bene- 
ficial only in theory. Tracheotomy, if performed at all, should be per- 
formed early, as soon as suffocative symptoms or signs of asphyxia begin to 
show themselves. The hyperaesthesia, which is often so troublesome, is best 
relieved by large doses of bromide of potassium, and if restlessness and jac- 
titation are marked, moderate opium narcosis may be beneficial. 

To sum up : — a diphtheritic patient should be quarantined in a large, 
well-ventilated apartment, attended by a well-trained nurse ; poultices 
should be applied externally to the throat ; steam inhalation should be 
constant from the onset of the disease until the exudation has disap- 
peared ; iron and brandy should be given freely ; the diet should be fluid, 
— milk preferably, — and the patient kept in bed until the convalescence is 
complete. 

ERYSIPELAS. 

Erysipelas is an acute contagious disease with local manifestations, which 
are first developed in most cases about wounds, but may appear primarily 
in previously healthy parts. 

The streptococcus erysipelatis is regarded as its specific cause. They 
appear as very fine cocci in chains. 

Morbid Anatomy. — The changes in internal organs and the blood are in 
no way characteristic. Early in the disease the fibrin and white cells are 
increased, but the blood rapidly assumes the condition found in other acute 
febrile diseases, and becomes thin and fluid, or dark and pitchy, does not 
coagulate readily, and stains the heart and vessels. The local manifesta- 
tions may affect any surface, as the mucous and serous membranes or 
lining membrane of the blood-vessels and lymphatics, but are most charac- 
teristically displayed in the skin. 

They are essentially inflammatory. Early there is hyperaemia, followed 
by exudation of lymph and cells, which gives the part a bright red color, 
and causes some swelling and induration. This inflammation is peculiar 
in its tendency to become diffuse, and in its antagonism to reparative pro- 
cesses. When it attacks a wound already partly united, the adhesions are 
speedily resolved and the wound is reopened. On the unbroken skin, it is 
not limited by inflammatory products, but extends by continuity, and may, 
from a small primary focus, involve the head, an entire limb, or the whole 
body. The intensity of the inflammation is very inconstant. 

In most cases it involves only the skin, and is hardly more than a simple 
erythema. In some, and generally where the skin is lax, there is well- 



746 



ACUTE GENERAL DISEASES. 



marked and more or less extensive oedema. In more severe eases there is 
often suppuration, which is generally a diffuse infiltration, but may be cir- 
cumscribed. 

The inflammation may terminate in resolution, vesication, abscess, or 
gangrene. The former is the usual ending. The hypersemia subsides, the 
• infiltration is absorbed, and the process terminates in desquamation. 
When vesication occurs previous to resolution, the cuticle is raised by 
serous effusion, and when thrown off leaves healthy skin or superficial 
ulceration. Abscess and gangrene present the same pathological changes 
as under other conditions. 

Erysipelas is not always limited to the skin, but often involves deeper 
parts. It is somewhat doubtful, however, whether the inflammations of 
the pleura, pericardium, and peritoneum, which often complicate severe 
attacks of the disease, are the result of direct extension of inflammation or 
are due to the systemic poison. 

When meningitis complicates erysipelas of the scalp, or laryngitis and 
oedema glottidis accompany the inflammation of the neck, the relation is 
probably one of continuity, but the peri- and endo-carditis which are occa- 
sionally present in a similar erysipelatous condition, together with the 
implication of the veins and evidences of nephritic complications, point to 
a more general etiological basis for such conditions. 

The lymphatics are implicated, and their course can be traced by red lines 
running from the inflamed area to the adjacent glands, which are enlarged 
and indurated. The specific cocci of the disease are found most abundantly 
in the lymph spaces. If the veins are involved, a phlebitis may result in 
infarction, or, more rarely, in pyaemia. 

Following an attack of erysipelas there remains some thickening and indu- 
ration of the skin, which may become permanent after repeated attacks. 1 

Etiology. — All the causes of general debility — as, indulgence in drink, 
and anti-hygienic conditions — predispose to erysipelas. In a large propor- 
tion of cases it is preceded by some abrasion of the surface or a distinct 
wound, and is then considered traumatic. 

Some individuals show a constitutional predisposition to the disease, and 
certain unknown atmospheric conditions favor its dissemination. 

It is fully determined not only that erysipelas, once developed, is highly 
contagious, and spreads rapidly among surgical patients and puerperal 
women, but that the disease is the result of a specific contagion which 
may render buildings, clothing, and the persons of attendants infectious 
centres. 

Inoculation of the bacteria which fill the inflamed tissues produces ery- 
sipelatous inflammation. Its contagiousness, period of incubation, and 
evidences of constitutional disturbance preceding the local inflammation, 
and the fact that it can be propagated by inoculation, establish its conta- 
gious character. 

Symptoms. — The symptoms of erysipelas are constitutional and local. 



1 Virchow. 



ERYSIPELAS. 



747 



Both traumatic and idiopathic erysipelas have a period of latency of from 
two days to a week or more, during which there will be some fever, pos- 
sibly of a remitting type, with slight chills, headache, and malaise. As the 
local symptoms appear, the fever increases, and is marked by decided even- 
ing exacerbations. It seldom passes 106° F., and the morning remission 
mav be two or three degrees, and be attended by sweating. The fever is • 
accompanied by a rapid pulse, coated tongue, nausea, anorexia, and dis- 
ordered bowels. In some sthenic cases the attack is sudden, and attended 
by severe chills and a rapid rise of temperature. The duration of the fever 
is very varied. 



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Fig. 161. 

Temperature Record in a case of Facial Erysipelas. 



When the inflammation is localized and recovery occurs, generally from 
the fifth to the tenth day there is a rapid decline in the fever and dis- 
appearance of all unfavorable symptoms. The temperature may even be- 
come subnormal and continue so during early convalescence. When the 
local condition is progressive, however, the fever continues at 104° or 105° 
F. for two, three, or more weeks. 1 In these cases the fall in temperature 
is commonly more gradual and convalescence more prolonged. 

In children and nervous patients a mild delirium may be present with- 
out any meningeal complications, or in sthenic cases it may become con- 
tinuous and violent. 

When the course of the disease is unfavorable it assumes a typhoid char- 
acter, the temperature rises rapidly, the pulse is frequent and feeble or 
irregular, the delirium becomes low and muttering, and passes into coma 
which ends in death. Sudden extension of the inflammation, or relapses 
when convalescence is apparently established, are frequent and are marked 

1 In a case where the imflammation involved by degrees the entire surface from a wound on the head to 
the toes, the temperature was between 102°-104° for over four weeks. 



748 



ACUTE GENERAL DISEASES. 



by a rapid rise of temperature, corresponding with the extent of new tis- 
sue involved. Final recovery may thus be delayed for weeks, during which 
there will be periods of normal or subnormal temperature. 

The urine is always scanty and high-colored. It contains an excess of 
urea and often a small amount of albumen. 

This course of the fever is often greatly modified by complications. 

The local symptoms are equally variable. Traumatic erysipelas begins 
as a diffuse rose or bright red blush about the point of injury, in which a 
white line follows the finger as it is lightly drawn across the surface. 
This is generally preceded for a day or two by some enlargement and ten- 
derness of the adjacent lymphatic glands. In uncomplicated cases there 
are no further changes, but the inflammation subsides and is followed by 
flaky desquamation. 

Idiopathic erysipelas is most commonly facial, starting from either the 
nose, eyelid or ear. It may begin either in the skin or areolar tissue, and 
is attended by more or less oedema. The part is first swollen and second- 
arily the characteristic blush appears. The part becomes enlarged, hot 
and painful, and the swelling may extend so as to close the eyes and involve 
the whole head and neck to such an extent as to greatly disfigure the 
patient. In from six to twelve days the color becomes darker, the swell- 
ing recedes and the cuticle peeling off leaves a slightly reddened surface 
which slowly regains its normal color. 

When the disease is " erratic " it extends more or less rapidly from its 
primary seat, where the inflammation slowly ceases as it advances else- 
where, so that it may be present in all stages from the first faint blush to 
desquamation. 

When the disease assumes a phlegmonous or suppurative form, the pus, 
if diffuse, gives a peculiar boggy sensation on palpation, but if circum- 
scribed it has the usual appearance of an abscess. 

Approaching gangrene is indicated by an intense burning pain, and the 
parts become livid and finally black and crackling. 

Erysipelas may be complicated by meningitis, which will be indicated by 
its usual symptoms somewhat modified by the preexisting fever. Peri- 
carditis and pleurisy are at times recognized by dyspnoea, or often only by 
their physical signs. 

Differential Diagnosis. — When erysipelas attacks a joint it may be mis- 
taken for a short time for acute articular rheumatism, but the peculiar 
deep rose color and the rapidity with which the inflammation extends will 
speedily distinguish it. Similar symptoms with the oedema will also dif- 
ferentiate the disease from simple erythema. High febrile movement 
lasting twenty-four to forty- eight hours, and attended by pain, swelling and 
tenderness of the lymphatics, has been considered diagnostic of develop- 
ing erysipelas. 

Other questions of differential diagnosis belong entirely to surgery. 

Prognosis. — Traumatic erysipelas is a very unfortunate complication in 
surgical injuries. It arrests all reparative action an^ adds largely to the 
gravity of the previous condition. 



ACUTE MILIARY TUBERCULOSIS. 



749 



Idiopathic erysipelas, when it attacks the face and head, is a dangerous 
and uncertain disease under any circumstances, and is especially so in 
aged people. Many patients sutler from a simple erysipelas of the face 
at almost regular intervals without serious discomfort, but there is always 
danger that the meninges will become involved and the disease at once 
assume a most serious asj^ect. 

Death may result from the overpowering effects of the poison, from the 
complications, or from exhaustion clue to suppuration, gangrene, or a pro- 
longed course of the disease. (Edema of the glottis from extension of 
inflammation may cause sudden death. The disease is especially fatal in 
chronic alcoholism, B right's disease and gout, and in patients over sixty. 
Recurrent attacks indicate a debilitated condition and are apt to be of 
increasing severity. 

Treatment. — In common with other contagious diseases, great care should 
be taken to avoid extension of the disease, and as we are unable to control 
the poisonous emanations, complete isolation of such patients affords the 
only sure means of prophylaxis. 

In mild cases local treatment is unnecessary, and it is doubtful if it ever 
restricts the inflammation. Cold dressings with mildly astringent and 
anodyne lotions are the most grateful to the patient and as efficacious as 
any. More powerful astringents and distinct caustics — as iodine and a 
saturated solution of nitrate of silver, or even the actual cautery— have been 
employed with a view to cut short the inflammation or to prevent its 
spreading. 

Erysipelatous inflammation often improves in five or six days under such 
treatment, or halts at a line where iodine or silver has been employed ; 
but it quite as frequently, when extending, is not perceptibly restricted 
by such boundaries. A saturated solution of nitrate of silver may be 
applied, however, two or three times in twenty-four hours. Subcutane 
ous injections of carbolic acid in surgical erysipelas have seemed to give 
more appreciable and better results than any other local treatment. If 
oedematous swellings are excessive, minute punctures will afford marked 
relief. Hot applications and poultices are to be used only when suppura- 
tion or gangrene is present. We have no means of neutralizing the poison 
of erysipelas, and internal treatment is confined to general tonic measures. 
Concentrated nutriment should be administered frequently in small quan- 
tities, and stimulants employed as in other acute febrile conditions. The 
bowels and kidneys should be kept active by cathartics and simple diu- 
retics. Various remedies have been employed, but the tinctura ferri chloridi 
seems to be generally accepted as the most useful drug, and is even con- 
sidered to have specific effects in erysipelas. 

Quinine and other tonics may be employed with advantage. 

The bromides and chloral are preferable to opium or hyoscyamus for 
producing sleep. 

ACUTE MILIARY TUBERCULOSIS. 

Although acute miliary tuberculosis is etiologically an acute contagious 



750 



ACUTE GENERAL DISEASES. 



disease, clinically the dangers of contagion are comparatively slight. In 
the majority of instances it is secondary to, and a part of, a more chronic 
tuberculous process, the symptoms of which, in some cases, are so obscure 
as to escape notice, while the manifestations of the more acute process 
alone attract attention. More frequently the preceding chronic condition 
and the acute disease appear as a part of a general tuberculosis. It is only 
when it occurs without any recognizable previous tubercular infection that 
it can be considered a distinct disease. 

Morbid Anatomy. — While acute miliary tuberculosis is not a local affec- 
tion and is to be carefully distinguished from acute phthisis, its pathologi- 
cal changes are more abundant and far more frequently found in the lungs 
than in any other organ. They are also generally present and may be 
principally located in the pia mater (acute hydrocephalus), intestines, 
lymph glands, serous membranes, and, rarely, liver, spleen, and brain. The 
characteristic lesion of acute miliary tuberculosis consists of an irruption 
of delicate, gray, translucent, miliary granules, varying in size from a pin's 
head to a poppy-seed. They are quite evenly distributed throughout the 
affected organs and show little tendency to coalesce. 

In the early stages, affected lungs show little change from the normal, 
aside from the presence of the tubercle granules. Later they become 
slightly hyperaemic and (edematous, with some infiltration, about the 
granules, of an amorphous matter. Although the air cells may become 
partially filled with epithelium, pus-cells, and fibrin, hepatization is of 
rare occurrence. The pleura is studded with similar tubercular granula- 
tions, and they are also present more or less abundantly in the peritoneum 
and the various glands and organs throughout the body. They can be 
recognized in some cases in the choroid. In the pia mater they occupy 
the perivascular lymph spaces. 

All tubercle manifests a strong tendency to undergo caseous degenera- 
tion, but in acute miliary tuberculosis the patient usually succumbs to the 
disease before any such change occurs. 

Etiology. — The predisposing causes are very prominent in the etiology 
of acute miliary tuberculosis, and it is very doubtful if it ever occurs 
when they are not present. 

The specific cause of acute miliary tuberculosis, and the manner in which 
the general infection occurs, has been definitely stated under the heads of 
tuberculosis and acute phthisis. 

Symptoms. — When acute miliary tuberculosis complicates the last stage 
of phthisis, its symptoms are so modified that it is not easily recognized. 
In such a case a sudden and decided increase in the fever, and marked 
aggravation of the dyspnoea, will be the most characteristic symptoms, and, 
occurring in connection with unchanged physical signs, may lead to a cor- 
responding diagnosis. When the disease attacks an individual in apparent 
health, the symptoms are well marked. 

It is generally ushered in by repeated chills, a rather rapid rise in tem- 
perature and pulse rate, and the other symptoms of an acute general 
disease, accompanied by rapid respiration and a short, dry cough. The 
temperature ranges from 103° to 106° or 107° F., with irregular but marked 



ACUTE MILIARY TUBERCULOSIS. 



751 



remissions, and is more frequently high in the morning and low in the even- 
ing than in any other acute affection. The pulse is soft, small, and com- 
pressible, varying from 120 to 150 per minute, but in no constant or definite 
ratio to the temperature. The respirations are from 50 to 60 per minute, 
and later the dyspnoea becomes inteuse. The persistent sharp, hard cough 
is rarely accompanied by expectoration ; when present, the expectoration 
consists of viscid mucus, occasionally blood-streaked. The skin is pale and 
cyanotic ; there is anorexia, rapid emaciation, and diarrhoea, as a rule; the 
lips and tongue become dry and covered with brown crusts ; the patient is 
dull and semi-comatose, and at night delirious, presenting all the symp- 
toms of the typhoid state. The spleen is generally slightly enlarged. 




Fig. 162. 

Temperature Record in a Case of Acute Miliary Tuberculosis. 



The patient may survive for five or six weeks, but more frequently suc- 
cumbs within two or three. As death approaches, the pulse rapidly grows 
weaker and more frequent, the cough ceases, the temperature falls, or, if 
already low, suddenly rises, the cyanosis deepens, and death occurs from 
pulmonary oedema and asphyxia. 

Physical Signs. — In most cases the physical signs are entirely negative. 
Percussion may show points of slight dulness, surrounded by extra reso- 
nant areas, and auscultation occasionally reveals moderate bronchial 
catarrh, with fine moist rales, but they are not characteristic. A soft fric- 
tion sound may be produced by a roughened nodular pleura. 

Differential Diagnosis. — The symptoms of aeute miliary tuberculosis are 
often so similar to those of typhoid fever that a diagnosis is exceedingly 
difficult. The points have been given under typhoid fever. 

Pneumonia and acute diffuse bronchitis in their early stages may simu- 
late acute miliary tuberculosis, but the rapidly developing physical signs 
and the absence of the constitutional symptoms of an acute wasting dis- 
ease render an early diagnosis possible. 



752 



ACUTE GENERAL DISEASES. 



Prognosis. — The prognosis is unfavorable. The duration of the disease 
is from a few days to six or seven weeks, with an average of three weeks. 
The more general the infection, the more violent the fever and the nervous 
symptoms, the sooner is a fatal termination to be expected. When com- 
plicating phthisis, its course is very rapid. Asphyxia from pulmonary 
oedema, asthenia, cerebral anaemia and collapse, are the principal causes of 
death, but in about one-third of the cases it occurs from implication of the 
meninges. 

Treatment. — The only indications for treatment which afford any hope 
of attaining favorable results are in the way of prophylaxis, and are largely 
included in the treatment of the predisposing diathesis. In treating scrofu- 
lous patients, acute miliary tuberculosis should be remembered as among 
the impending dangers. Caseous matter, wherever situated, should be 
removed when the attending danger is not great. 

When the general tuberculosis has once occurred, treatment is confined 
to the reduction of temperature and supporting the patient. For the first, 
quinine is of little avail. It is sometimes used as long as recurring chills 
are present, but is of doubtful value. Cold will be found more useful in 
reducing temperature, and may be used in baths, packs, or by sponging. 
Stimulants and highly nutritious food fulfil the second indication, and 
must be used as in other wasting diseases. Morphia must be used for the 
relief of the cough and dyspnoea. 

TYPHUS FEVEK. 

Typhus fever is a contagious disease, which usually prevails epidem- 
ically. Although it has many phenomena in common with miasmatic-con- 
tagious fevers, and was at one time classed with typhoid fever, to-day it is 
regarded as a distinct type of fever, dependent upon a specific poison with 
certain pathological and etiological phenomena, which distinguish it from 
all other forms of disease. It has received a great variety of names, such 
as ship fever, hospital fever, jail fever, camp fever, petechial fever, putrid 
fever, Irish ague, brain fever, spotted fever, continued fever, typhus fever, 
petechial and exanthematous typnus. 1 

Morbid Anatomy. — Those pathological lesions which are common to ty- 
phus and typhoid fever will be first considered, and as the line of distinc- 
tion between them is drawn it will be noticed that, in many respects, the 
difference is one of degree, rather than of kind. 

The changes in the blood are as follows : it is darker in color than nor- 
mal, and when drawn from the body during life coagulates imperfectly or 
not at all ; if a clot is formed it is of the consistency of putty. The fibrin- 
factors are diminished, or the blood loses its coagulating power to a greater 
or less extent. At first the red globules are increased in number, but as 
the disease progresses they diminish ; the salts of the blood are also changed, 
and urea and ammonia are present in excess ; by some the latter is sup- 



1 The Germans describe an abdominal and cerebral typhus. Their abdominal typhus corresponds to 
our typhoid fever and their cerebral typhus is our typhus fever. 



TYPHUS FEYEK. 



753 



posed to be produced by the decomposition of the former. The blood of a 
typhus fever patient, when drawn from the body, rapidly undergoes am- 
moniacal decomposition. When the blood is examined microscopically, 
many of the red globules will be seen to have lost their normal outline, 
and their edges to have become serrated and irregular. In some instances 
they will be found to have undergone degeneration ; their coloring matter 
will then pass through the walls of the blood-vessels and stain more or less 
deeply the tissues and effusions which may have taken place in the serous 
cavities. These blood-changes are very similar to those which take place 
in the miasmatic-contagious fevers — they differ in degree only. 

Parenchymatous Degenerations. — There is the same tendency to par- 
enchymatous degenerations of the different organs and tissues of the body 
in typhus as in typhoid. Usually the body is not very much emaciated ; 
it undergoes decomposition rapidly after death. In severe cases decom- 
position apparently commences before death. The muscles are usually of 
a brownish color, dry, presenting an infiltration of fine granules in the 
primitive fibres ; sometimes hemorrhages take place into them. The 
liver and spleen undergo degenerative changes similar to those described 
as occurring in typhoid, but they are not so extensive nor are they so con- 
stant. One may make very many autopsies on persons dying of typhus 
fever, without finding any softening, or only a very moderate softening, and 
enlargement of the spleen, while blood extravasations are not uncommon. 
In severe cases the cortical portion of the kidneys is swollen, opaque and 
more or less fatty, according to the duration and severity of the disease. 
The primary enlargement of the kidneys is mainly due to a cloudy swelling 
of the epithelium of the renal tubes. 

This tendency to cloudy swelling and granular fatty degeneration, the 
so-called (e vitreous degeneration of Zenker,*' which occurs in the vol- 
untary muscles and the kidneys, also occurs in the muscular tissue of 
the heart. If the fever is protracted, the cardiac walls become flaccid, of 
a brownish color, and parenchymatous changes are found similar to those 
which occur in typhoid fever, though less marked. There is often a con- 
siderable amount of serum in the pericardium. Pultaceous clots are found 
in the heart cavities, and thrombi are found firmly adherent to the walls 
of the larger veins. There is the same tendency to ulceration of the 
mucous membrane of the mouth and larynx as in typhoid fever. In ty- 
phus fever the ulcers are deeper, involving more extensively the submucous 
tissue. Splenization of the lungs also occurs in typhus as in typhoid 
fever. Hypostatic congestion of the lungs and pulmonary oedema are as 
common as in typhoid ; some claim that they are found much oftener. 
Thus far I have noticed only these lesions which occur both in typhus 
and in typhoid fever. I now come to those which are found only in 
typhus. 

Brain. — Although there is nothing in the appearance of the brain which 
is characteristic of this fever, yet it is very unlike that met with in ty- 
phoid fever. In the latter disease it usually presents an anaemic appear- 
ance. In all cases of tvphus the cerebral vessels will be found more or less 
48 



754 



ACUTE GEKERAL DISEASES. 



congested. In some epidemics all the sinuses and blood-vessels of the brain 
will be found engorged with dark blood, so that when the calvarium is re- 
moved the vessels will stand out upon its surface. In other epidemics, in- 
stead of finding intense congestion, there will be more or less extensive se- 
rous effusion into the meshes of the pia mater : the quantity of the effusion 
varies from one to eight or ten ounces, and it is most abundant upon the con- 
vexity, although it takes place to a limited extent into the ventricles. When' 
ever there is a large amount of fluid effusion there will be little cerebral 
congestion. The fluid effusion is usually clear ; if it is turbid one may 
be certain that the fever is complicated by meningitis. The arachnoid 
loses its natural glistening appearance, and in many instances one will find 
the membrane dotted over with yellow or yellowish-white spots. The 
brain undergoes little or no change unless the fluid effusion is abundant, 
when by its pressure the sulci are deepened and the convolutions are 
sharpened. 

Abdominal Lesions. — In typhus and typhoid fever, the lesions found in 
the abdominal cavity widely differ. The real pathological distinction is 
in the presence or absence of intestinal changes. These are present in ty- 
phoid and absent in typhus. In typhus fever there are no changes which 
show a tendency to ulceration of the intestinal glands, except those which 
are produced by congestion, such as are frequently seen in scarlet fever and 
measles, where the Peyerian patches present the shaven-beard appearance ; 
while in typhoid fever, either ulceration of the intestinal glands will be pres- 
ent, or the glands will present the appearance which just precedes ulceration. 
At the post-mortem examination, if ulceration of the agminated and sol- 
itary glands is found, one may be certain the patient died of typhoid fever. 
The presence or absence of intestinal changes settles the question as to 
whether the fever is typhus or typhoid. 1 

Complications. — Although the complications which occur in the course 
of typhus fever are in no way peculiar to it, yet they are of such frequent 
occurrence, and are developed during its active progress, and modify its 
phenomena to such a degree, that it is necessary that they should be taken 
into account in the study of its pathological lesions. These complications 
will vary according to the peculiar type of the epidemic which is prevail- 
ing. In one epidemic the complications will be pulmonary, in an- 
other they will be almost exclusively cerebral and spinal, in another nearly 
all will be glandular in character. The pulmonary complications are bron- 
chitis, pneumonia, pleurisy, pulmonary congestion, and oedema. In most 
cases these pulmonary complications are developed during the primary 
fever, before convalescence commences. Their advent is always insidious. 
An extensive capillary bronchitis may develop with very few of the rational 
symptoms of bronchitis until within a short time previous to the death of 
the patient ; in fact, the bronchitis might pass unrecognized but for the 
presence of its physical signs. All the rational symptoms of pneumonia 
may also be absent and still a physical examination of the chest may reveal 



1 Lebert states that rarely, in epidemics, small ulcers of Peyer's patches and of solitary glands and 
swelling of the mesenteric glands have been seen. (Ziemssen's Encyc.) 



1 



TYPHUS FEVER. 755 

a whole lung in a state of pneumonic consolidation. The pneumonia which 
complicates typhus is usually hypostatic. It sometimes leads to pulmonary 
gangrene. At most of the autopsies there will be found pulmonary con- 
gestion and oedema. In many cases when these are associated with capil- 
lary bronchitis or pneumonia they are the immediate cause of death. Lar- 
yngitis is often associated with more extensive bronchitis which occurs 
during the active part of the fever. 

The only cerebro-spinal complication which is met with in typhus fever 
is meningeal inflammation. As has been stated, in a large majority of 
autopsies of typhus fever serum is found in the meshes of the pia mater, 
but that is not a certain sign that meningeal inflammation has existed prior 
to death. In addition to the subarachnoid effusion, there must be an ex- 
udation of plastic material into the meshes of the pia mater, causing it 
to become thicker than normal. When such appearances are found it shows 
that the case has been complicated by meningitis. 

Glandular Enlargements. — The glandular enlargements and inflam- 
mations which occur in the course of typhus fever are peculiar in their 
character, and are rarely met with in typhoid, and then are not extensive ; 
but in typhus fever the superficial glands — especially those about the neck, 
the parotid and sublingual — often become so much enlarged and inflamed 
as to interfere with deglutition, and not infrequently these glandular en- 
largements are apparently the immediate cause of death. 1 The inguinal 
glands sometimes become so enlarged as to interfere with the return circu- 
lation, and, as the consequence of this interference, swelling of the lower 
extremities may be developed. The bronchial glands are nearly always en- 
larged and softened. There is a swelling of the lower extremities which 
depends upon a different cause. It may occur at the beginning of con- 
valescence ; then the limbs will present very nearly the same appearance 
as that noticeable in the condition called phlegmasia dolens. Under such 
circumstances phlebitis might be suspected. 

It has been stated that the voluntary muscles undergo a peculiar waxy or 
vitreous degeneration, and that the same kind of degeneration occurs in 
the muscular tissue of the heart. When this does occur the walls of the 
heart become very flabby, and when this change has reached a certain point 
there is developed a tendency to the formation of clots in the heart cavities, 
and a slowing of the general circulation. The result of such retarding or 
obstruction of the return circulation is the formation of thrombi in the 
superficial veins, which interfere with the venous circulation, and a swell- 
ing of the lower extremities follows ; this closely resembles that which is 
seen in phlegmasia dolens. With this swelling of the lower extremities, 
suppuration and cellular inflammation may occur, which often result in 
the formation of quite extensive abscesses. 2 

1 Lebert regards enlargement and suppuration of the parotid as a very dangerous complication. 

3 It is an established fact that whenever the return circulation is slowed from any cause in any disease 
where there is great feebleness of heart power, thrombi are liable to form in the veins of the lower 
extremities. This is often well illustrated in the later stages of phthisis, when swelling of one or both 
lower extremities occurs as the result of the formation of venous thrombi in the superficial veins. 



iff 

756 ACUTE GEITEKAL DISEASES* 

Diseases of the organs of special sense, which so frequently complicate 
typhoid, rarely occur in typhus fever, and there are no serious or constant 
complications of the digestive organs ; the gastric mucous membrane is 
sometimes softened, reddened, and mammilated. 

Etiology. — At the present day this fever is regarded as depending upon a 
specific poison, of whose exact nature we are ignorant. From the manner 
of its development and its contagious properties it must be regarded as 
due to a specific microbe. All observers agree that in the majority if not 
in all instances it is the product of contagion, and that the contagion only 
emanates from the bodies of those who are affected with the fever. Care- 
ful clinical observation has established the fact beyond a doubt that there 
exists a specific typhus poison which can be communicated from the sick 
to the healthy. It is possible to develop a fever from overcrowding, im- 
perfect ventilation, filth, and a combination of causes belonging to this 
category, but such a fever is not typhus. 

The results of my investigation of the origin of the epidemic of typhus 
fever which prevailed in New York, from July, 1861 to 1864, have led me 
to the belief that typhus poison is of endemic origin — in other words, that 
there are certain endemic centres ; that Ireland, Italy, and Russia are the 
great centres, and that, whenever it occurs in other localities, it has been 
conveyed from these endemic centres to those localities. 1 The histories of 
those cases which were developed within the limits of the hospital, showed 
that a residence in an atmosphere necessarily more or less tainted with 
typhus poison, is not sufficient to develop the disease, but that it is neces- 
sary for the subject of the contagion to have been brought in contact with 
an infected person, or within the atmosphere immediately impregnated 
with his exhalations. The fact that no employee in the hospital who was 
only brought in contact with the clothing of fever patients contracted the 
disease, as well as the absence of any evidence that the disease was propa- 
gated by such clothing, goes far to show that typhus is not readily propa- 
gated by fomites alone, 2 although most authorities claim that it can be 

1 In the month of July, 1861, fourteen cases of typhus fever were admitted in one day to the fever wards 
of Bellcvue Hospital, of which wards I had the charge. Previous to this lime, for several years (I think 
for more than ten years), there had been no case of typhus fever in the wards of the hospital. Iimme- 
mediately commenced investigations in order to ascertain the origin of the fever in these cases. I found 
that it had its origin in the upper story of a rear tenement-house in Mulberry Street, in the most filthy por- 
tion of the city. The first case was that of a little girl, who had been brought into the house, ten days be- 
fore she sickened, from a ship which had come from Ireland, and which had cases of typhus fever on 
board. Two weeks after her illness commenced, her aunt, the only other occupant of the apartments (con- 
sisting of a room and dark bed-room), sickened of fever and died. In gradual succession, nearly every 
family residing in the building took the fever. Becoming frightened, some of these families moved into 
other streets, formed the nucleus for the development of the disease in the different localities to which 
they removed, and it soon became a wide-spread epidemic. There were two hundred typhus fever patients 
at one time in the hospital. These families were as well nourished and lived in as well ventilated apart- 
ments as thousands of their class in other parts of the city. The only difference was that typhus poison 
was brought to them in the person of the little girl, and, on account of their badly ventilated apartments 
and their utter disregard of all hygienic laws, they furnished a fit soil for the reproduction and spread of 
that typhus poison, the constant and unrestrained intercourse between the healthy and the sick being the 
means by which the fever was spread. I found unmistakable evidence that persons living in healthy locali- 
ties, simply by visiting friends sick with the fever, contracted the disease. 

2 In Quain's Dictionary it is stated that it is "not carried by clothing or excreta, and free dilution with 
fresh air destroys its virulence." 



TYPHUS FEVER. 757 

thus propagated ; that it is thus that ships, barracks and jails become hot- 
beds of it ; that the poison may be latent and held in garments, especially 
those that are dark and woolen. The certainty with which every unpro- 
tected person who was brought in personal contact with fever patients con- 
tracted the disease, proves the contagious power of the poison. 

The distance that typhus poison can be transmitted through the atmos- 
phere (from the manner in which the disease was contracted by some of the 
house physicians), would seem to be limited. It has been proved by actual 
experiment that the contagious distance of small-pox, in the open air, does 
not exceed two and one-half feet, and it would seem that the contagious 
distance of . typhus fever is even less. 1 Typhus poison is undoubtedly 
present in the body exhalations and the expired air of typhus fever patients; 
but it requires a concentration of the poison to render it infectious. Slight 
exposure is not sufficient ; it requires a concentrated poison and a prolonged 
exposure. The more numerous the typhus fever patients are, the more power- 
ful does the contagion become ; yet a single exposure even to such an atmos- 
phere is rarely sufficient to develop the disease in an individual who is in 
good health at the time of the exposure. 

The length of the period of incubation varies. It usually requires about 
two weeks of exposure such as comes to one who is around those sick with 
the fever. Eepeatedly have I noticed this fact in my own case. I have 
never had typhus fever, and have never taken special care to avoid infec- 
tion. My immunity is probably due to some special constitutional idiosyn- 
crasy. I have noticed that whenever I enter upon a typhus fever service I 
do not experience any effects from the exposure to typhus poison until after 
about two weeks 2 have elapsed, then I begin to suffer from a peculiar form 
of headache which continues for about two weeks ; the period before the 
commencement of the headache corresponds to the period of incubation, 
and the period of headache to the average duration of the disease. 

The established belief is that typhus fever attacks an individual but 
once, and that those who have had typhoid fever are to a certain degree pro- 
tected from typhus. Of all the typhus fever patients treated in Bellevue 
Hospital, only three gave histories of having previously had the disease. 
From these facts one may reach the following conclusions : — 

First. — That typhus fever is due to a specific poison. 

Second. — That this poison is communicated from the sick to the 
healthy mainly by personal contagion — that is, the recipient of the poi- 

1 The qn^stion now arises : — can this poison be conveyed in the clothing ? During the epidemic to which 
I have referred, when typhus fever patients were brought into the hospital, their clothing was removed in 
the reception-room and afterward washed and packed away in a lower room of the building. Upon a most 
thorough investigation made at that time, I found that not a single person contracted the disease whose 
duty it was to wash or pack away the clothing; but every one whose duty it was to carry the fever patients 
from the reception-room to the hospital ward took the fever. Every physician and nurse who had the care 
of typhus fever patients contracted the disease ; those who were on the surgical service escaped. Every 
clergyman who came to administer spiritual consolation to the patients in the fever ward fell a victim to 
the disease. I have brought forward these facts to show that during this epidemic there was no evidence 
that the disease was either of spontaneous origin, or that it was transmitted from the sick to the healthy, 
except by direct personal contagion. 

a Lebert puts Ave to seven days, and Murchison says, " no longer than twelve days for the period of 
incubation ; one week is the average ; some patients have the fever one-half to two hours after first and 
second exposure {St. Thorn. Hos. Rep., vol. ii.). 



758 



ACUTE GEKEKAL DISEASES. 



son must be brought in contact with the exhalations of the infected 
person. 

Third. — That where there is free ventilation, contagion is confined to 
narrow limits. 

Fourth. — That the evidences of the spontaneous origin of typhus are not 
sonclusive, although there can be no question but that overcrowding and 
bad ventilation favor its spread and increase its severity. 

Fifth. — Typhus poison passes into the body mainly through the respired 
air. Whether it can be taken into the system in the food and drink is still 
an unsettled question. 

Sixth.— Immunity from a second attack is enjoyed after the first in a 
large majority of cases. 1 

Symptoms. — An outline of the phenomena which attend the development 
of typhus will first be given and afterward some of its more prominent 
symptoms will be considered in detail. 

Its advent is usually sudden ; there are no constant premonitory symp- 
toms. In some cases, for a few days, there may be a feeling of indisposi- 
tion, perhaps of headache, restlessness at night, nausea, loss of appetite, 
and vertigo ; but in a large majority of cases it is ushered in by a distinct 
chill. This differs from the chill of pneumonia or that of malarial fever, 
in that it is short, sharp, and sudden. It may amount to nothing more 
than a chilly sensation. There may be several chilly sensations on the day 
of attack with distinct intervals between them. Following the chill there 
is a severe and steadily increasing headache ; it is frontal and increases in 
intensity from hour to hour. This is accompanied by a more or less severe 
pain in the back and limbs, especially in the thighs. The headache of 
typhus is more constant and persistent than that which attends the devel- 
opment of any other fever ; usually, after a few days it diminishes in inten- 
sity. Headache is associated with dulness and confusion of mind, and in 
the case of children with vomiting. A sense of extreme prostration very 
soon follows the ushering-in chill. 

In some cases the patient is compelled, within twenty-four hours from 
the commencement of his sickness, to take to his bed from muscular weak 
ness. This loss of muscular power will sometimes show itself by the un 
steady, tottering gait of the patient, and is more marked in the early stage 
of typhus fever than it is in any other disease. At one time, while I was 
making my visit in the fever ward, my house physician, who w T as sicken- 
ing from typhus fever, staggered and fell by my side from loss of muscular 
power. He died on the eighth day of the disease. 

Within the first twenty-four hours after the chill the temperature may 
rise as high as 105° or 106° R, although at the same time the patient 
may complain of a chilly feeling, and will draw up to the fire or cover 
himself with blankets. It is a peculiarity of this fever that, during the 
first two or three days the patient experiences a sensation of coldness, 

1 Lebert says : "all agree that the disease is spread by a typhus germ. Some say it is microspheres, 
others that it is bacteria, spiral forms, fungus, etc. It must be either organic poison or organized 
germ. 1 ' 



TYPHUS FEVER. 



759 



while the thermometer shows the temperature to range at 105° F. or 
higher. During the first week of the disease the temperature remains at 
104° F. or 105° F. There will be morning and evening variations, most 
marked at noon and midnight ; but these variations follow no regular 
course, as in typhoid fever. From the eighth to the fourteenth day the 
temperature is liable to sudden depression. As a rule, the temperature 
falls between the eighth and fourteenth days. There is, without doubt, a 
day of crisis in this disease. Just before the critical fall in temperature 
there may be an abrupt temporary rise of 3° or even 4° F. In typical cases, 
before the fourteenth day there is a marked decline, and often a sudden fall 
in temperature. By the beginning of the second week the temperature 
ranges at its highest. If there is a sudden rise in temperature during the 
second week, it is almost certain evidence that some complication exists. 

At first the tongue is swollen and covered with a white coating. It pre- 
sents very much such an appearance as is seen in many nervous affections. 
As the disease progresses, after a day or two it assumes a yellowish-brown 
color, and the coating becomes thicker ; later it becomes dry, dark and fis- 
sured. Nausea is sometimes present, rarely vomiting. The abdomen is 
free from pain, except over the liver ; the bowels are constipated. Some 
enlargement of the spleen can usually be detected quite early. 

The pulse is accelerated from the very beginning of the fever, ranging 
from 100 in the morning to 110 or 130 in the evening ; the acceleration is 
greater in children than in adults. At the onset of the fever the pulse is 
full, but it soon becomes soft and compressible, and finally feeble. It is 
rarely dicrotic. It is only in the severest cases, just preceding death, that 
the pulse becomes irregular and intermitting. The face is flushed, the 
conjunctivas, injected, the expression of countenance is dull, heavy, and 
weary, and as the fever progresses, the cheeks assume a mahogany color. 
The sleep is disturbed, and when the patient is awake his mind is con- 
fused ; in very severe cases delirium is very early present, and the patient 
needs careful watching at night. 

Between the fifth and eighth, usually on the fifth, day of the disease, an 
eruption makes its appearance upon the surface. The skin is extremely 
hot, and there is no tendency to perspiration. It appears first upon the 
sides of the abdomen, and gradually extends over the whole anterior portion 
of the body, except the face and palms of the hands. In a few cases it first 
appears on the back of the hands and wrists. It is more marked upon the 
trunk than on the extremities. At first the eruption consists of dirty pink- 
colored spots, varying in size from a mere point to three or four lines in di- 
ameter. These spots are slightly elevated above the surface, and temporarily 
disappear on firm pressure. After a day or two the eruption becomes darker 
in color, and assumes a purplish hue. It is no longer elevated above the sur- 
face, does not entirely disappear on firm pressure, and the spots have no well- 
defined margin. This eruption is made up of irregular spots, varying from 
a point to two or three lines in diameter, either isolated or grouped to- 
gether in patches, presenting a very irregular outline ; in children it often 



760 



ACUTE GENERAL DISEASES. 



resembles the eruption of measles. When the eruption is abundant it im- 
parts to the skin a mottled aspect, which has given rise to the term " mul- 
berry rash " of typhus. Another distinctive peculiarity is, that each spot 
or patch remains visible from its first appearance until convalescence is 
established or death occurs, and it is often seen upon the bodies of those 
who have died of typhus fever. 

In some cases of typhus there are only a few spots of the eruption, while 
in other cases they are very abundant, and the surface of the body pre- 
sents a well-marked mottled appearance. In a certain proportion of 
cases, after the eruption which I have just described has been visible for a 
few days, there will appear, scattered over the surface, small dark spots, 
due to minute subcutaneous hemorrhagic extravasation ; these are called 
.petechias. On this account the disease has been called petechial typhus; 
but these petechias are by no means distinctive of typhus, for they are also 
met with in other diseases. The majority of cases of typhus which one 
meets will have no eruption except the " mulberry rash." When the 
petechial spots are present they indicate a severe form of the disease, 
and more extensive blood-changes than usual. This mottling or marbling 
of the skin begins as the mulberry rash fades ; it appears once for all — not 
in crops — and resembles slightly the rose-rash of typhoid fever. It is the 
subcutaneous eruption, so-called. 

In all severe cases, at the close of the first week the headache, which 
has been the most troublesome symptom, disappears, and delirium comes 
on. The delirium will vary in character and severity in different epidemics, 
being much more violent and active in some than in others. Sometimes 
at the very outset of the disease the delirium is very active, the patient 
shouts and talks more or less incoherently, and is more or less violent. If 
not restrained, he may throw himself out of the window. This period of 
intense nervous excitement may last two or three days, during which the 
countenance becomes livid, the conjunctivae injected, the hands tremulous, 
and suddenly the patient may pass into a state of apparent coma. It is 
not that of complete coma, for the patient can be easily aroused ; but he 
lies upon his back, with a tendency to slip down in bed, picking at the bed- 
clothes. The mental faculties, the special senses, are all blunted, and the 
patient is in a condition of stupor for three or four days preceding the 
delirious period, and sometimes, when the delirium is not active, this 
stupor lasts till the end of the disease. It is not a state of unconscious- 
ness, although one of apparent coma, for the mental processes are going 
on with great activity, and the imagination will conjure up a great variety 
of horrid fancies, and the visions which pass before the patient will be dis- 
tinctly remembered after recovery has taken place. 

This condition has been called "coma vigil " During this period the 
experience of years may be crowded into a day or an hour, and the patient 
may feel that he has lived a lifetime while in this state. Those who have 
the greatest mental power and possess the highest culture have the most 
distressing fancies during this somnolent period. If, in this condition, 
there is a tendency toward a fatal issue, the patient will pass into a more 



TYPHUS FEVER. 



761 



complete stupor and the coma will become more and more profound ; the 
respiration becomes less and less frequent ; the pulse, which has ranged 
about 120 per minute,, rises to 140 or 150, and finally becomes imperceptible 
at the wrist ; the tongue, rolled into a round mass, becomes brown and dry, 
so that the patient is unable to protrude it from the mouth ; or, if he pro- 
trude it, he does not withdraw it until asked to close his mouth ; sordes 
collect upon the teeth ; the conjunctivae are red, and the eyes, when open, 
present a leaden- appearance. The face has a dusky pallor. The patient 
has no longer power to move his body; he lies on his back with his head 
thrown back, perhaps is only able to make slight tremulous motions with 
his hands. There may now be some intestinal catarrh, with diarrhoea! dis- 
charges. The urine collects in the bladder, and, if not removed with a 
catheter, dribbles away. The extremities become cold, but the body tem- 
perature remains at 105° F., or it may rise as high as 107° or 108° F. In 
one case under my observation it rose to 110° F. just preceding death, while 
the extremities were cold. 

If the case is tending to a favorable termination, about the tenth to the 
fourteenth day of the fever there is an amelioration of all the symptoms. 
The patient falls into a quiet sleep, from which he awakes conscious and 
convalescing. The pulse and temperature fall, the tongue becomes clean 
and moist, the delirium subsides, and there is a desire for food. After two 
or three clays the pulse reaches its normal standard and strength gradually 
returns. Critical sweats, diarrhoea, and large flows of urine are not infre- 
quent occurrences. 

This is an outline of the progress of the disease in a severe case of typhus 
fever, terminating either in death or in recovery. In a mild case there will 
be no delirium. The temperature may not rise above 102° F. ; the tongue 
is neither brown nor dry. There is no great acceleration of the pulse, 
the rate never being over 120 per minute, and that only for a very short 
period. During the entire course of a severe or mild case, there is no 
gastric or intestinal disturbance, no diarrhoea, no distention of the abdo- 
men, no pain in the right iliac fossa, no gurgling — in a word, no abdomi- 
nal symptoms. In mild cases the erv;ntion is never very abundant, but 
it appears on the fifth day, and remains visible until convalescence is 
established. 

Those more important symptoms which determine the character of the 
fever will be considered in detail. As has been already stated, symptoms 
indicating disturbance of the nervous system are among the earliest and 
most prominent. Of these, headache is the most constant. For the first 
week or ten days it is severe and persistent, after which time it gradually 
abates and disappears towards the close of the second week ; it is confined 
to the forehead and temples, rarely to the occiput. 

Delirium comes on usually about the eighth day ; sometimes it is pres- 
ent at the onset of the disease. At whatever period it may be developed, 
it will continue until the termination of the disease. Delirium is preceded 
by a dull, apathetic state, w r hich follows the abatement of the headache. 
At first it shows itself at intervals during the night, or lasts all night to 



762 



ACUTE GENERAL DISEASES. 



disappear during the day. Its character varies from a low, muttering form 
to a very active and noisy delirium. Every possible variation is met with 
during an epidemic of typhus fever. 1 Acute delirium is more liable to be 
present with the intelligent and highly cultured, while the delirium is usu- 
ally low and muttering in character in the case of the aged or uncultured : 
other things being equal the intensity of the fever can be measured by the 
kind and amount of delirium. 

Stupor or somnolence in some degree is seldom absent. It may develop 
with or without previous delirium. Usually, as the case progresses toward 
a fatal termination stupor comes on ; this becomes more and more profound 
as the disease advances. The patient often lies for hours apparently un- 
conscious, with his eyes open as though awake, but he is absolutely indif- 
ferent to all that is going on around him. This is another condition to 
which the term " coma vigil " has been applied. It is almost invariably fol- 
lowed by a fatal termination. Sometimes coma comes on suddenly, without 
any antecedent somnolence ; under such circumstances the urine will be 
found loaded with albumen. 

Loss of muscular strength is an early and striking symptom. In the 
majority of cases it is present from the very first day of the fever. In many 
cases, as the fever progresses, the loss of muscular power is so great that 
the patient is unable to turn in bed ; the prostration always increases as 
the disease advances. In some cases there is little loss of strength during 
the first week, but the prostration comes on suddenly during the second 
week. 

In addition to the general loss of muscular power, in certain cases there 
is paralysis of some muscles, such as the sphincter ani and the muscles of 
the bladder, so that the urine and faeces are discharged involuntarily. Dys- 
phagia, partial or complete aphonia, and inability to protrude the tongue, 
are common symptoms. Muscular tremor is an indication of very great 
muscular prostration, and is usually met with in the aged and infirm and 
in those who have been addicted to the use of intoxicating drinks. Muscu- 
lar spasms and subsultus tendinum are present to a greater or less degree 
in all severe cases ; the tendons of the wrist are most frequently affected. 
One form of these spasmodic movements is manifested by the patient's pick- 
ing or fumbling the bed-clothes ; another by obstinate hiccough. Trismus, 
strabismus, and in rare cases ojusthotonos, have occurred. All these symp- 
toms must be regarded as grave. Emaciation is never a marked symptom. 
It is rarely present to any great degree before the third week of the fever. 2 

Temperature. — During the first week of typhus fever there are no such 
marked typical variations in temperature as are met with in typhoid — none 
that will enable one to make a diagnosis. Usually the temperature rises 
rapidly from the very onset of the fever, and in cases of average severity 

1 The incoherent, nonsensical muttering is beyond the control of the patient, who is himself aware of 
its disjointed and erratic character. 

2 The eyes at first are suffused ; later the conjunctiva becomes dry. The pupils are contracted and are 
insensible to light in many cases. Vertigo, dizziness, noises in the head, partial and even complete deaf- 
ness are observed. Coryza, epistaxis, slight hypersesthesia, and, finally, general anaesthesia, are infrequent 
?ymptoms. 



TYPHUS FEVER, 



703 



attains its maximum from the third to the sixth day. At this period the 
evening temperature will range 
between 103° F. and 106° F. In 
severe cases, the maximum tem- 
perature is not reached until the 
eighth or tenth day. Before the 
temporature reaches its maximum, 
the morning and evening varia- 
tions are slight, about 1° or 1£° F. 
After the temperature has reached 
its maximum for several days there 
will be little change, but at some 
time, usually between the seventh 
and tenth days, there will be a 
slight remission until the twelfth 

01' fourteenth day, when it rapidlv Temperature Record in a Case of Severe Typhus Fever, 
„ -i lu I ±. • ending in Recovery. 

falls, m typical cases that termi- 
nate in recovery, to its normal standard. Any sudden rise or fall (except 
in crisis) indicates a complication. Occasionally an elevation of two or 
more degrees precedes the fall. This sudden fall about the fourteenth day 
is peculiar to typhus. The fall may amount to 4° or 5° F. 

A very high range of temperature during the first week is an indica- 
tion that severe cerebral symptoms will be developed during the second 
week of the fever. A case of typhus fever may terminate fatally, in which 
the temperature at no time has exceeded 103° F. In all fatal cases, just 
preceding death there is usually a rise of from 2° to 5° in temperature. 
During the first week of convalescence the temperature often remains below 
the normal standard, especially in the morning. 

Pulse. — The pulse in this fever is usually frequent, soft, easily com- 
pressed, and often irregular. The heart may partake of the general muscular 
weakness, so that the first sound may become inaudible. There is a soft sys- 
tolic ("fever") murmur heard over the heart. In the severe cases, during 
the first week the pulse may reach 120 beats per minute, after which time 
it increases in frequency and feebleness with the severity of the general 
symptoms. By the third day it may reach 120 beats per minute ; usually in 
the milder case it does not exceed on that day 100 beats per minute. If 
during the first week it continues for three consecutive days so frequent as 
120 beats per minute, it indicates danger. The rate may be 106 in the 
morning and 120 in the evening. The higher the temperature, and the 
more frequent the pulse during the first week, the more severe will be the 
symptoms during the second week. If during the second week it becomes 
small, feeble and frequent, perhaps beating 140 or 150 per minute, the case 
may be regarded as unfavorable. Absence of pulsation in the radial artery 
for several days has been observed, and is explained on the ground of embolic 
obstruction of the medium-sized vessels. 

During the first week, if the pulse increases in frequency the temperature 
rises, and if the pulse diminishes in frequency the temperature falls ; but 




764 



ACUTE GENERAL DISEASES. 



during the second week the pulse may increase in frequency, and the 
temperature fall, or it may diminish in frequency and the temperature rise. 
The pulse is not an infallible guide as to the condition of the heart, for 
sometimes the pulse is full and distinct, while the heart power is yery feeble ; 
on the other hand, the cardiac pulse may appear strong and the sounds 
distinct, and yet the radial pulse may be imperceptible. In most fatal cases, 
after the first week the radial pulse becomes imperceptible for several days 
prior to death. Although in most severe cases there is a rapid pulse, yet a 
slow pulse does not necessarily indicate a mild attack. In some severe and 
fatal cases the pulse may never be over 100. 

Eruption. — The general character of the typhus eruption has already 
been described. Its appearance is preceded and accompanied by a bright 
redness of the whole surface, on which dark red spots are scattered, giving 
the skin a mottled appearance " sub-cuticular rash." These spots have 
an irregular outline, and vary in size from a point to three or four 
lines in diameter. Sometimes they are few in number, but more com- 
monly they are numerous ; the large spots are formed by the coalescence of 
the smaller ones. It is a macular, not a papular eruption. At first they 
have a dusky pink hue, partially or wholly disappearing on pressure, and 
as the finger passes over them they seem to be slightly elevated. After a 
day or two they assume somewhat of a brick-dust color, and are but slightly 
changed by pressure ; then the color of the spots becomes darker in hue, 
and finally they are not affected by firm pressure. Another peculiarity is 
that each patch or cluster remains visible from its first appearance until 
the termination of the disease. The eruption may appear upon any por- 
tion of the body. Usually, it first makes its appearance upon the trunk, soon 
spreading to the extremities ; very rarely is it seen on the face. When the 
eruption is scanty, it is limited to the chest and abdomen. In some pa- 
tients the eruption, though well developed, is not prominently marked; 
\he spots are pale and undefined ; and though grouped in patches are so 
irregular that they give to the entire surface a faint, dingy appearance. 
Blood-extravasations into the centre of the typhus spots may occur at the 
end of the second week. 

Respiration. — Usually, during the first week the respirations do not ex- 
ceed twenty or thirty per minute ; but during the second week they often 
run up to forty or fifty per minute. In cases where there is great prostra- 
tion accompanied by stupor, the respirations sometimes fall to eight or ten 
per minute. Under such circumstances they are often irregular and puffing 
in character. Hypostatic congestion of the lungs, if extensive, is attended 
by great frequency of respiration and evidences of cyanosis. The occur- 
rence of these changes in respiration ought always to lead to careful exam- 
ination of the chest. 

The digestive system is very little disturbed in typhus fever. Nausea and 
vomiting are rare, and an examination of the abdomen presents nothing 
abnormal. There is r#o tympanitis or tenderness on pressure. Spontane- 
ous diarrhoea is of exceedingly rare occurrence ; the bowels are generally 
constipated. Intestinal hemorrhage is of rare occurrence, and when it is 



TYPHUS FEVER. 



705 



present depends either upon congestion of the mucous membrane of 
the colon or on hemorrhoids, which accompany an engorged portal circu- 
lation. 

Urine. — The urine in typhus undergoes important changes. The quan- 
tity varies somewhat with the amount of fluid taken into the stomach ; 
usually, it is diminished during the first week to one-fourth or one-half the 
normal quantity. In the advanced stage of severe cases there is sometimes 
complete suppression of urine, but more frequently the quantity of urine 
increases during the later stages of the fever. The reaction is first acid, later 
neutral or alkaline. The quantity of urea excreted in twenty-four hours 
during the first few days of the feyer is increased, and the increase is in 
proportion to the intensity of the feyer. In the majority of cases it remains 
abnormally increased until the period of crisis is reached, when it gradu- 
ally, or in some instances rapidly falls below the normal standard. TJric 
acid is similarly increased. The chlorides grow less and less till the second 
week, when they disappear. In all severe cases, during the first week of the 
disease, a small amount of albumen is found in the urine ; when the quan- 
tity is large the case may be regarded as severe. In the severe cases the 
urine will also be found to contain vesical and renal epithelium, and when 
the quantity of albumen is large, epithelial and fatty casts of the urinifer- 
ous tubes will be present with blood. 

In this connection it is important to bear in mind the necessity of daily 
inquiry into the expulsive power of the bladder. When there is little cer- 
ebral disturbance, the urine is passed without difficulty ; but when stupor 
and a tendency to coma exist, there is often retention or an involuntary 
dribbling of urine, which might lead one to think that there was no ac- 
cumulation of urine in the bladder. It is safe to inquire at least o::ce a 
day as to the state of this organ, and if involuntary discharges of urine 
occur, the contents of the bladder should be evacuated by means of a 
catheter. Copious sediments form in the urine on the day of crisis. 

Differential Diagnosis. — Before the appearance of the eruption, the diag- 
nosis of typhus fever is always difficult, and sometimes impossible. The 
diseases with which it is most liable to be confounded are typhoid fever, 
relapsing fever, measles, pneumonia, acute Brighfs disease, meningitis, 
delirium tremens, and some of the other acute blood diseases, such as 
erysipelas, pymmia, septicaemia, etc. 

The early characteristic symptoms of typhus fever are chilliness, pain in 
the back and limbs, and headache. During the first week the headache 
increases in severity from hour to Lour, and is accompanied by a rapid rise 
in temperature. These symptoms occurring in one who has been exposed 
to typhus poison are always sufficient for a diagnosis. The appearance of 
the eruption settles the question. On account of the similarity in appear- 
ance of the eruption of typhus fever and that of measles in children, the 
one disease is sometimes mistaken for the other. In both diseases the erup- 
tion may appear on the fifth day, but the eruption of measles is of a brighter 
tint than that of typhus fever, and its appearance is preceded by a cough 
and coryza, which are not present in typhus fever. 



766 



ACUTE GEXERAL DISEASES. 



Meningitis. — The differential diagnosis between typhus feyer and cerebro- 
spinal meningitis is often difficult. Not infrequently, days may elapse be- 
fore one is able to decide whether a case is one of typhus fever or of cerebro- 
spinal meningitis. 1 The distinguishing points between the two diseases 
are as follows : — the headache of meningitis, at the outset of the disease, 
is much more distressing than that of typhus, and it alternates with delir- 
ium. When delirium comes on in typhus fever, the pain in the head ceases. 
Vomiting is prominent in meningitis, absent, as a rule, in typhus. Photo- 
phobia and contracted pupils are among the early symptoms of meningitis, 
and the patient is greatly disturbed by noise, while in typhus fever he seems 
indifferent to both. Dulling and blunting of all the senses are common 
in typhus. All the senses are abnormally acute at the onset of meningitis. 
Inequality of the pupils, strabismus, ptosis, and paralysis are common in 
meningitis and rare in typhus. In meningitis the countenance is pale and 
expressive of pain, wildness, and anxiety ; in typhus fever it is dusky, 
blank, and stupid. Convulsions are an early symptom in meningitis and 
rare in typhus. Again, in meningitis the pulse is hard and wiry, rapid 
and irregular, and at the last intermitting ; while in typhus fever it is 
rapid at the onset of the disease, easily compressed, full and bounding. 
Lastly, the eruption of typhus fever is characteristic. If an eruption is 
present in meningitis, it has no regularity in its development ; it may ap- 
pear within twenty-four hours after the development of the first symptom 
of the disease, or it may be postponed for several days. It does not appear 
on the fifth or sixth day of the disease with the uniform regularity of the 
typhus eruption. Petechias may be present in meningitis as well as in 
typhus fever, but they are not characteristic of either disease. The tem- 
perature rises rapidly in typhus, and reaches a higher range, e. g. , 104° to 
106° in twenty-four to forty-eight hours ; while in meningitis the average 
temperature on the second and third days — indeed, during its entire course — 
is 102°, often lower. Eigidity of the muscles of the neck is not always 
positive evidence of meningitis, for it sometimes occurs in typhus fever. 
The ataxia, muscular prostration, and character of the tongue in typhus 
are also points that greatly aid in distinguishing it from cerebro-spinal 
fever. 

Pneumonia. — Sometimes a latent pneumonia with typhoid symptoms is 
mistaken for typhus fever ; especially is this the case when the latter is pre- 
vailing. I frequently saw cases where such a mistake had been made, while 
in charge of the typhus fever patients on BlackwelPs Island, during the 
epidemic to which reference has been made. In these cases there will bs 
active typhoid symptoms, e. g., dry tonguo, delirium, high temperature, etc. 
The countenance in this pneumonia, although the cheeks may have a pur- 
plish hue, does not exhibit that dull, heavy expression so commonly seen 
in typhus. Although there may be delirium in both instances, the delirium 

1 To show how difficult is the diagnosis between these two affections, a circumstance may be men- 
tioned which occurred in Bellevue Hospital . A patient was brought into the hospital directly from a 
ship, and the diagnosis of cerebro-spinal meningitis was made by several of the attending staff ; but at 
the autopsy there were found none of the lesions of meningitis ; all the changes corresponded to those 
found at the autopsies of patients dying of typhus fever. 



TYPHUS FEVER. 



707 



in the former disease is of a milder type than the latter. The characteristic 
pneumonic expectoration is not usually present in these cases ; so that in 
making the differential diagnosis this symptom cannot be relied upon. 
The physical signs of pulmonic consolidation will lead one to diagnosticate 
pneumonia, and unless the typhus eruption is present, this will be sufficient 
for a diagnosis. If pulmonary consolidation is a complication of typhus 
fever, it will not be developed until after the sixth day of the fever, the 
time when the eruption should have appeared. If no eruption is present, 
the pneumonic consolidation may be regarded as the primary affection, and 
the symptoms which simulated those of typhus fever may be regarded as 
secondary. 

Delirium Tremens. — The delirium of alcoholism may sometimes so 
closely resemble that of typhus fever that the one may be mistaken for 
the other. Typhus fever patients have been placed in the cells under the 
supposition that they had delirium tremens. If the delirium tremens is 
uncomplicated by pneumonia, the temperature will suffice for the differen- 
tial diagnosis, for in delirium tremens the temperature is rarely above 100° 
F. There may be a rapid pulse in delirium tremens, and often the patient 
has a brown, dry tongue, and other typhoid symptoms ; but there is only 
a slight rise in temperature ; besides, there is no eruption. The attack is 
not ushered in by headache, but by an inability to sleep ; and the circum- 
stances which precede and give rise to such an attack will establish beyond 
a doubt the true nature of the attack. 

Acute Brightfs Disease. — It is not surprising that acute uraemia should 
be mistaken for typhus fever. The brown, dry tongue, the tendency to 
stupor, the contracted pupil, the low, muttering delirium, and all the phe- 
nomena of the typhoid state, as well as the albuminous urine, belong to both 
diseases ; but the temperature is not raised in uraemia as it is in typhus 
fever, and the oedema which is always present in acute uraemia is absent in 
typhus fever. 

Erysipelas, pyemia, septicemia, and all similar acute blood diseases are 
often attended by many of the symptoms which attend, the development of 
typhus fever. In pyaemia and septicaemia there are irregular chills, followed 
by fever and profuse sweats, with evidences of septic and pyaemic poison- 
ing; in erysipelas, there are evidences of a localized phlegmon. It should 
not be forgotten that erysipelas is sometimes ushered in by all the phe- 
nomena that attend the ushering-in of typhus fever ; this is before the local 
inflammation shows itself. In such cases it is impossible to make a differ- 
ential diagnosis until the local phenomena which characterize erysipelas 
show themselves, or until the typhus eruption appears. In many of the 
acute infectious diseases one is compelled to wait until the time for the ap- 
pearance of the eruption before typhus fever can be excluded. When ty- 
phus fever is prevailing and the physician is watchful for its appearance, 
there will usually be little difficulty in diagnosis. Sometimes typhoid, ty- 
phus and relapsing fever prevail at the same time in the same locality. 

The importance of early forming a correct differential diagnosis between 
typhus and typhoid fever cannot be over-estimated ; and to accomplish 



768 



ACUTE GENEKAL DISEASES. 



this, the prominent symptoms of each will be reviewed and compared. 
The first point to be considered in the differential diagnosis of these two 
diseases is, that typhus fever is sudden in its advent, while typhoid fever 
comes on insidiously, and is slowly developed. In the majority of cases of 
the former disease there is a chill at the commencement, and severe pain 
in the head, whereas in the latter there is only a chilliness, some aching in 
the limbs, and a slight headache. Muscular prostration and progressive 
muscular weakness appear earlier, and are much more marked in typhus 
than in typhoid. 

The ranges of temperature in the two forms of fever differ greatly. 
Typhoid fever commences, on the first day, with a slight rise of tem- 
perature, which continues, with morning remissions and evening exacer- 
bations, until the end of the first week, when it has reached its highest 
point ; during the second week it remains at about the same height, 
with only slight variations ; during the third week there are more marked 
morning remissions ; and by the end of the fourth week the temperature 
has reached its normal standard, by intermittent periods. In tyjDhus 
fever, the temperature rises rapidly, and before the end of the second day 
reaches 104° F. or ]05° F. Whatever degree is reached on the third 
day may be regarded as the maximum temperature ; after this time 
there are slight, irregular variations until the tenth or twelfth day, when 
the temperature begins to fall, and rapidly reaches the normal standard. 
In typhoid there is great emaciation ; in typhus it is slight, but the 
exhaustion and muscular prostration are far greater than in typhoid. The 
eruptions of these two forms of fever differ very markedly. In typhus it 
makes its appearance upon the fifth or sixth day ; while the eruption of 
typhoid fever makes its appearance between the seventh and ninth days. 
The eruption of typhus fever appears upon the arms and chest, and more 
or less over the entire body ; whereas the eruption of typhoid appears upon 
the chest and abdomen, very rarely upon the extremities ; sometimes it 
appears upon the loins when it cannot be found on any other part of the 
body. As a rule, the spots in typhus are numerous, while in typhoid they 
are not very abundant. In typhus fever, the spots at first are small, 
slightly elevated, of a dark pinkish hue, and disappear only on firm press- 
ure. As the disease advances they become darker, and finally are not 
affected by firm pressure, and remain visible from the time of their appear- 
ance until death occurs or convalescence is established. In typhoid fever 
each spot is rose-colored, slightly elevated, and disappears on slight press- 
ure. Each spot remains visible for three days and then disappears, to be 
followed by another crop. Usually the eruption is visible about two 
weeks, and when it disappears it leaves the skin unstained, whereas in ty- 
phus the eruption leaves a stain upon the surface. There is a mottling of 
the surface in typhus fever, the mulberry rash, which is not seen in 
typhoid. 

The brain symptoms in these two diseases also differ. In typhus 
fever they appear early, and the headache and delirium are more intense 
than in typhoid. Delirium in typhoid more commonly appears at the 



TYPHUS FEVEE. 



769 



end of the second or during the third week of the disease ; whereas in 
typhus it appears early, and before the end of the second week has disap- 
peared if recovery is to take place. As a rule, in typhus fever constipation 
is present, and a mild cathartic must be given to move the bowels ; whereas 
in typhoid fever the pea-soup diarrhoea is a prominent symptom. Tym- 
panitic distention of the abdomen, gurgling and tenderness in the right 
iliac fossa, and intestinal hemorrhage, are all phenomena of typhoid fever, 
but are never present in typhus fever. Epistaxis is frequent in typhoid 
and not in typhus fever. In typhus fever convalescence will usually be 
established before the end of the second week ; it may occur at any time 
between the eighth and fourteenth days. The average duration of typhus 
fever is fourteen days, whereas the average duration of typhoid fever is 
from twenty-one to thirty days. Typhus fever is contagious, typhoid fever 
is non-contagious. 1 Typhus fever is generally epidemic ; typhoid fever is 
always endemic. In regard to the protection which one attack of typhus 
fever furnishes against a second attack, it very markedly differs from ty- 
phoid fever. One may have typhoid fever whenever the system has been 
exposed to the typhoid poison ; but one attack of typhus is almost a cer- 
tain protection against a second attack. 

Prognosis. — The prognosis in this disease is always grave, and no opinion, 
as to its termination, can be given until every point in each case has 
been considered, such as the age of the patient, the character of the epi- 
demic, and the tendency to certain complications. In all epidemics the 
majority of cases will recover. The ratio of mortality, as given by differ- 
ent writers, varies from one death in five to one death in sixteen cases. 2 The 
surroundings of each patient should be carefully noted, also the hygienic 
influences which he is under, and his habits of life should be taken into 
account. With the intemperate the disease is likely to prove fatal. Some 
of the circumstances which increase the danger in any particular case are 
a debilitated condition of the patient from advanced age, intemperate hab- 
its, privation, and previous disease ; mental depression, presentiment of 
death, overcrowding and bad ventilation ; a gouty diathesis is always dan- 
gerous. 

Death may occur in typhus fever from three general causes : first, 
from coma, the result of overwhelming the system with typhus poison. 
The patient does not die from the effect of a prolonged high temperature, 
nor from any complication, but dies as patients die in acute uraemia, be- 
cause the system is overwhelmed by the typhus poison, and the functions 
of organic life are arrested by its action on the nerve-centres. 

1 When the pathological lesions are studied and the manner in which death occurs in these two forms 
of fever is considered, it can readily be seen how widely they differ. The characteristic pathological 
lesions of typhoid fever are the changes which take place in the intestinal glands, such as ulceration or 
tendency to ulceration. In all cases these characteristic lesions are present. Suppose a case of what has 
been called typhoid fever is followed to the dead-house, and ulceration or evidences of a tendency to ulcer- 
ation of Peyer's patches are not discovered, then it is certain a mistake in diagnosis has been made. If, 
on the other, hand, in a case of supposed typhus fever is found ulceration of Peyer's patches, it is equally 
certain that a mistake has been made, and that a case of typhoid, and not typhus fever has been treated. 
The parenchymatous changes which are common to both diseases have already been sufficiently con 
sidered. 

2 Griesinger and Murchison state "that in certain epidemics the mortality runs as high as 40 to 50 per 
cent." An average epidemic shows about 15 per cent, of deaths ; a mild one, about 6 to 8 per cent. 
49 



770 



ACUTE GENERAL DISEASES. 



Death may occur, secondly, from syncope, due to heart failure, whethei 
the heart failure is the result of the prolonged high temperature, or the 
direct action of the typhus poison. A continued temperature of 105° 
or 106° F. is very liable to be followed by fatal syncope from failure of 
heart power, although the evidences of parenchymatous degeneration of 
the heart may not be present. Death may occur, thirdly, from complica- 
tions. Although they do not properly belong to the primary disease, yet 
they so modify it that they enter very largely into its history. In a large 
number of cases which terminate fatally, death is due to some one of 
these complications. In some epidemics they are all pulmonary ; in others 
they are all cerebral. The advent of pulmonary complications is always 
insidious; the cough and expectoration which usually attend pulmonary 
diseases are either absent, or so slight as not to attract the attention of 
the physician. Eapid breathing and lividity of the face are often the first 
obvious indications of extensive disease of the lungs. When these symp- 
toms are present, a careful physical examination of the chest should be 
made. 

Bronchitis may come on at any period during the fever, and it may 
continue after the fever has subsided. So long as it is confined to the 
larger tubes there is little danger, but sometimes suddenly and insidiously 
it extends into the smaller tubes, and is complicated with pulmonary con- 
gestion and oedema. Under such circumstances it may be the direct cause 
of death. The pneumonia which complicates typhus fever is lobular in 
character, and is frequently preceded or accompanied by bronchitis. It 
has a tendency to terminate in abscess or gangrene. During life it is not 
always possible to distinguish it from hypostatic congestion. If, however, 
the dulness on percussion is confined to one lung, if the respiration is 
bronchial, the diagnosis of pneumonia is readily established. The seat of 
pneumonia is generally at the upper portion of the lung. Pleurisy 
(serous or purulent) may occur. 

Laryngitis is sometimes a very serious complication of typhus. The 
common form is that of acute oedema glottidis. Its occurrence is readily 
recognized by the signs of laryngeal obstruction which attend its develop- 
ment. Whenever there is extensive swelling of the glands about the neck, 
with great tumefaction of the mucous membrane of the pharynx, one 
must be on his guard for the occurrence of this complication. 

On account of the extensive blood-changes which sometimes occur in 
severe cases of typhus fever, the blood readily escapes through the walls 
of the vessels, giving rise to extensive hemorrhages from the mucous sur- 
faces, nose, gums, bowels, the genito-urinary tract, vagina, etc., and into 
the cellular tissue. The occurrence of the hemorrhages is peculiar to 
certain epidemics, and when they occur it is during the first week of the 
fever. 

Meningitis is probably the only cerebral complication which will be met 
with in this fever. This occurs more frequently in children than in adults, 
and is not present in every epidemic. The cerebral symptoms which are 
such constant attendants upon typhus fever do not depend upon menin- 



TYPHUS FEVER. 



771 



geal inflammation ; they belong to the natural history of the disease. If, 
during the course of the fever, there is a deep-seated pain in the head, with 
restlessness, which shows itself by constant attempts to get out of bed, with 
photophobia, contracted pupils, and flushing of the face and eyes, followed 
by somnolence gradually lapsing into coma, it is almost certain that men- 
ingitis is occurring as a complication. This is most liable to occur during 
the second week of the fever. The characteristic symptom which marks 
its development is the constant attempt on the part of the patient to 
get out of bed. He is so persistent in this that unless watched with the 
greatest care he will be found upon the floor, vainly attempting to rise. 
The patient has more muscular power than before the occurrence of the 
meningeal complication, for he will perform acts which previously he was 
wholly unable to execute. Usually the delirium lasts two days, then the 
patient gradually passes into a state of coma from which he cannot be 
aroused ; his respirations may not be more than eight or ten per minute. 
Dilatation of the pupils, and an intermitting and almost imperceptible 
pulse, immediately precede death. 

I regard most of the kidney changes as a part of the history of the fever 
rather than as complications, although in some few instances croupous 
nephritis occurs, and must be included in the list of complications. Its 
occurrence in the course of typhus fever is indicated by the almost entire 
suppression of urine, and by the presence of albumen and exudative and 
blood casts in the urine. 

Glandular swellings are also occasional complications of typhus fever, 
and. sometimes may be of a very serious nature, for they may so interfere 
with deglutition and respiration as to destroy life. The parotid, the sub- 
maxillary, axillary and mammary glands may enlarge and suppurate. These 
swellings usually appear immediately after the crisis of the primary fever. 
They often enlarge with great rapidity, and in some instances terminate 
in extensive suppuration. 

Bed-sores are rather infrequent. Gangrene, necrosis, cancrum oris, sup- 
purative cellulitis, purulent arteritis — all have occurred in various epidem- 
ics, and render the prognosis unfavorable. If menstruation occur in a 
female with typhus, the bleeding is commonly very profuse and may cause 
death from acute ansemia. 

Duration. — The average duration of the fever is thirteen or fourteen 
days. Usually the day of crisis is between the tenth and sixteenth days. 
It is of shorter duration in the young than in the old, in children 
than in adults. 1 Relapses are extremely rare in this fever. I have met 
with, a second and third attack of the fever in the same individual, but I 
have never met with a true relapse. Typhus fever varies very slightly in 
its general character and different cases. A number of different varieties, 
depending upon the mildness or severity of the disease, the prominence 
of certain symptoms, the presence of complications, and the circum- 
stances under which fever appears, have been described, but the general 



1 In 500 cases ending in recovery, thirteen and a half days was the average ; and in 100 fatal cases, the 
duration was fourteen and a half days.— Murchison. 



■4 

772 ACUTE GENERAL DISEASES. 

description already given includes that of (so-called) ' 1 varieties " of 
typhus. 1 

The individual symptoms and signs which render the prognosis unfavor- 
able are as follows : 

A pulse continuing a number of days at more than 120 per minute, 
becoming at times intermittent and irregular, bespeaks an unfavorable 
prognosis. A hurried and difficult respiration, with turgidity of the face, 
due either to cerebral or pulmonary oedema, renders the prognosis unfavor- 
able. 

Delirium which is very active and accompanied by great muscular pros- 
tration, as indicated by subsultus, slipping down in bed, and accompanied 
by that condition known as "coma vigil," lasting for a number of days, is 
almost a certain indication of a fatal termination. 

The " pin-hole pupil," mentioned by old writers, is an unfavorable omen. 
It does not necessarily indicate the presence of meningitis, as was once 
supposed. Great muscular prostration at the very onset of the disease 
renders the prognosis unfavorable. 

Sudden fading of the eruption, and a widely expanded pupil may be 
regarded as unfavorable signs. Marked impairment of the special senses, 
accompanied by very great rapidity of the pulse, is an element of unfavor- 
able prognosis. 

The darker and more abundant the eruption, especially if accompanied 
by petechial spots, the more unfavorable the prognosis. In children the 
eruption is lighter in color than it is in adults, presenting an appearance 
similar to the typhoid eruption. In adults where there is dark mottling of 
the surface confined to the extremities, with evidences of blood extravasa- 
tion, indicated by the presence of petechiaa, the prognosis is unfavorable, 
but the case is by no means hopeless. 

A dry, brown, retracted, tremulous tongue is seen only in severe cases. 
A long-continued high temperature is always an unfavorable symptom. 
Great diminution in the quantity of urine is an unfavorable symptom, as 
also is the presence of casts and albumen in the urine. Eetention of urine 
is a more unfavorable symptom than incontinence ; convulsions and coma 
are liable to follow such retention. It is to be remembered that in typhus 
fever, more than in any other disease, patients pass into an apparently 
hopeless condition, and afterward rally and recover. A patient who seems 
to be overwhelmed with the poison, who has "coma vigil," "pin-hole 
pupils," rolling of the tongue, and a feeble, irregular, and intermitting 
pulse, may recover, although these symptoms warrant an unfavorable 
prognosis ; but "coma vigil " more than any single symptom indicates an 
unfavorable prognosis. 

The first indication of recovery is a diminution in the frequency of the 
pulse. The pulse may have been 120, but on the tenth, twelfth, or four- 
teenth day it begins to diminish in frequency. The tongue has been 

1 Typhus sideram is that form where death occurs in three or four days, after the most intense febrile 
movement and constitutional disturbance. Headaches and a feeling of malaise, etc., during an epidemic 
give rise to what many call " abortive " typhus. Walking typhus is that form where the patient is not con- 
fined to his bed until the second week. 



TYPHUS FEVER. 



773 



brown and dry, subsultus and delirium may have been present, even " coma 
vigil " may have manifested itself ; there has been great muscular pros- 
tration ; the patient, attempting to rise from the bed, may have fallen upon 
the floor ; now, the pulse begins to get slower, the patient falls into a re- 
freshing sleep and awakes perfectly conscious ; his countenance is changed 
from the dusky hue to an almost natural appearance, and he desires food. 
In other words, within twenty-four hours an entire change comes over the 
patient, and that change is first indicated by a diminution in the frequency 
of the pulse, accompanied by a fall in temperature. The fall in tempera- 
ture is not extreme ; perhaps a fall of two degrees is first noticed. In my 
experience, there is an attempt at convalescence upon the eighth day of the 
fever. Especially in those cases that recover, a slight fall in temperature 
will be noticed on this (the eighth day), although the temperature may 
again rise ; upon the twelfth or fourteenth day there is a distinct fall in 
temperature and diminution in the frequency of the pulse that is indicative 
of convalescence. The mode of recovery in typhus and typhoid is, perhaps, 
the most distinguishing clinical feature. In typhus recovery is rapid, in 
typhoid it is markedly slow. 

Of all the conditions which influence the prognosis in typhus fever, age 
and the habits of the patient have as great, if not greater, influence than 
any other. I am convinced of this from an experience in the care of typhus 
fever patients which dates back almost to the very commencement of my 
study of medicine, for very early did I have the care of a typhus fever ward. 
In children, typhus fever is a very simple form of disease. The rate of 
mortality is very low. I remember having the care of sixty children with 
typhus fever, and among these only one death occurred. This is as low a 
rate of mortality as one can expect in measles. Under the fifteenth year 
of life the rate is very low, viz., two or three per cent. From twenty to 
thirty the rate is fifteen per cent., with advancing years the disease is more 
fatal. When the patient has passed the middle period of life, there is great 
danger from typhus fever. So with the intemperate, and those who have 
livid amid unfavorable hygienic surroundings. The bright, educated and 
cultured, those whose brains are active, are less likely to recover than the 
stupid and uneducated. 

Treatment. — The more prominent measures which have been and are now 
employed in the management of typhus fever are in many respects similar 
to those proposed for the management of typhoid fever patients, 3 T et the 
treatment of these two diseases differs in certain essential particulars. 
When the symptoms are mild, very simple measures are all that is required. 
Of these, confinement to bed, cooling drinks, mild aperients, a milk diet, 
and free ventilation are the chief, and, indeed, the only means required. 
It is also important to observe the same rules in regard to the arrangement 
of the sick-room which are recommended in the case of typhoid fever 
patients. The more perfect the ventilation, the greater the amount of 
fresh air around the patient, the better his chances for recovery. The 
majority of cases of typhus fever are ushered in by active and severe 
symptoms, such as would tempt one to adopt a vigorous plan of treatment, 



774 



ACUTE GENE UAL DISEASES. 



symptoms which at one time were thought to indicate the employment of 
heroic antiphlogistic measures. 

Writers usually consider its treatment under two heads — the preventive 
and curative. I prefer to use the terms- prophylactic and remedial, for I 
question our ability to cure this disease. 

Much can be done to prevent its development, and this will constitute an 
important part in its management. How, then, can the development of 
typhus fever be prevented ? Medical skill cannot prevent the importa- 
tion of the disease into localities where it is not indigenous, for this is con- 
trolled by state and national authority. Consequently typhus fever will 
probably continue to be imported into districts where it does not originate. 
For example, we shall occasionally see the disease in all our large cities ; it 
may appear in any commercial seaport, and from there it may be carried 
into the interior. Yet much can be done to prevent its spread after it is 
imported, and to prevent its development as an epidemic when it is carried 
into any locality in the interior. 

It is important that the first cases of typhus fever which are developed 
in any locality should be closely watched. They should be immediately 
quarantined. The dwelling in which the fever has broken out should be 
depopulated — that is, in a tenement-house in which the fever has made 
its appearance, all the families should be removed, and the house should 
be thoroughly disinfected. The disinfection must be thorough, not for a few 
hours, but for one or two days, and afterward the house should remain 
open for the free circulation of air for a considerable length of time before 
persons should be allowed again to inhabit the rooms. If typhus fever 
occur in the dwellings of the wealthy, their houses must be quarantined. 
All persons must be prevented from visiting them, and all persons within 
the dwelling must be prevented from going abroad. After the sick have 
recovered, there must be the same thorough disinfection as in the tene- 
ment-house. Usually, in epidemics of typhus fever there are certain foci 
from which the disease spreads. Perhaps the points from which the con- 
tagion more especially emanates are within an area of half a square mile, 
and yet the disease may have been prevailing for two, three, or even four 
months. Under such circumstances it is possible to prevent the spread of 
the fever by the means just indicated. 

As far as its management in hospitals is concerned, I would say : never 
undertake it within brick or stone enclosures. If possible, patients should 
be placed in broad pavilions or tents, so that the largest possible amount of 
fresh air shall be in circulation about them. It is not sufficient to have 
free ventilation in the ordinary acceptation of that term. The opening of 
a window will not accomplish the desired result. Remove all the windows 
in a room, regardless of the cold, and cover the patients with a sufficient 
number of blankets to keep them warm. Allow fresh air to surround them. 
When typhus fever manifests itself, it can readily be understood how im- 
portant it is that the guardians of the poor should not only enforce cleanli- 
ness, but that they should feed the poor better than at other times. If 
cleanliness is observed, the dwellings thoroughly disinfected, and the poor 



TYPHUS FEVEK. 



775 



well fed, the most virulent epidemic can soon be stayed. The effects pro- 
duced by such measures are sometimes wonderful. In the year 1861, at the 
commencement of the epidemic (as has been stated), the first case occurred 
in a tenement-house in a down-town street, in New York City ; it was six 
weeks before it spread from that locality. The spread of the fever should 
have been stopped at that point ; but very little attention was paid to it, 
and it began to spread from one point to another, until some six or seven 
thousand cases were developed. Many prominent citizens sickened with 
the fever and died. This epidemic could have been prevented had measures 
been taken early to prevent the spread of the disease. It seemed to me that 
the authorities of New York City were responsible for a large proportion of 
the deaths which occurred during the prevalence of that epidemic. 

Medicinal treatment is powerless either to arrest the progress or shorten 
the duration of this fever, but it can undoubtedly save lives that would 
otherwise be lost, and hasten convalescence. The first point under this 
head relates to neutralizing the poison. I have found no medicinal agent 
which can neutralize or destroy typhus poison, or which has power to 
arrest the progress or shorten the duration of this fever. Different agents 
have been proposed for the accomplishment of this result, according 
to the views held in regard to the nature of the typhus poison and its 
effects upon the system. At one time the mineral acids were supposed to 
possess this power, and were administered for that purpose, but have now 
fallen into disuse. 1 The internal use of carbolic acid, chlorine water, 
creasote, and, more recently, salicylic acid has been recommended for the 
same purpose. The inhalation of oxygen gas has also been thought to be 
of service in arresting the blood-changes, and thus preventing the poison 
from having its customary effect upon the system. By the stimulation 
which it produces, the patient may be brought out of an apparent state of 
coma, and revive in a marked degree ; but the relief is only temporary. 
For a time the patient may improve, his consciousness return, and his ap- 
pearance indicate that convalescence is established ; but his unfavorable 
symptoms will return, and it will become quite evident that the oxygen 
has not neutralized the typhus poison. 

Fresh air is the only thing which I have found to have power to neutral- 
ize the poison of typhus fever. It certainly possesses this power when ex- 
ternal to the body. For example : place a patient sick with typhus fever 
in a well ventilated board pavilion, or in a tent, where an abundance of 
fresh air can circulate about him, and it is almost impossible for him to 
communicate the disease to a healthy person. Again, place a patient in 
a closed room, perhaps twelve by fourteen feet square, let a healthy person 
remain with him a single night — probably a much shorter time will be 
sufficient — and the latter, will be almost certain to contract the disease. 
Why is the disease more readily communicated in the one case than in the 
other ? Certainly the fresh air which circulated about the typhus fever 
patient must have prevented contagion. Fresh air, when inhaled, produces 

* Though a very recent work (Wilson on Fevers) says nitro-muriatic acid, alternating with turpentine is 
preferred in the United States, and that mineral acids occupy the highest rank. 



776 



ACUTE GENERAL DISEASES. 



to a greater or less extent the same effect. How do we know this ? As a 
clinical fact, I have seen a typhus fever patient, who was apparently over- 
whelmed by the poison — who within forty-eight hours from the commence- 
ment of the attack was m a state of coma, with high temperature, a rapid 
pulse, etc., and all symptoms indicating that he was fast succumbing to 
the disease — when brought from a crowded tenement house and placed in 
a tent where he could inhale plenty of fresh air, within four or five hours 
from the time of admission begin to rally, and go on to recovery. Eresh 
air was the only remedial agent employed. 

If fresh air does not neutralize the poison, it certainly has some effect in 
eliminating the poison, and thus mitigating the severity of the fever, and, 
perhaps, shortening its duration. It may be regarded as a remedial agent, 
for it certainly is of greater value than any so-called remedial agent at our 
command. To accomplish the best results, place three or four patients in 
a tent twenty feet square ; the fly of the tent should be thrown up, and if 
the weather is cold, the patients should be well covered with blankets. By 
this means all the advantages of free ventilation will be insured. The 
question arises: what therapeutical agents can be employed with advantage 
in order to accomplish the desired results ? 

It is of the greatest importance to reduce temperature and. to sustain 
heart-power. The former is of as great importance in typhus as in typhoid 
fever, and the same rules should govern one with regard to the agents to be 
employed, and the mode of their employment. 

By the beginning of the second week, if not before, there will be evi- 
dence of heart failure, and the question presents itself, Shall alcoholic 
stimulants be administered ? Most writers have regarded a frequent 
feeble pulse, with feeble cardiac impulse, even though cerebral symptoms 
may be present, as certainly indicating the administration of alcoholic 
stimulants. No limit was given as to the quantity to be administered. 
The object to be accomplished was to control the pulse. This could, in 
most cases, be done for a time ; but as the disease advanced and the 
patient became more and more overwhelmed by the typhus poison, alco- 
hol lost the power of giving force to the pulse. 

That stimulants will control the pulse and sustain the heart's action for 
a time, there can be no question ; but I have found that in all severe cases 
there came a time when alcohol, in however large doses it was given, ceased 
to have power. 

Typhus-fever patients under twenty-five years of age rarely require or 
are benefited by alcohol, unless they were of intemperate habits prior to 
the attack. To the old and feeble its occasional administration may be of 
great benefit, and at times be the means of saving life. A copious dark 
eruption, with coldness of the extremities, especially indicates the use of 
alcohol. As a rule, delirium, headache, scanty urine, and intense surface 
heat, contra-indicate the use of alcohol. In any case when it is decided to 
administer spirits, carefully watch the effect of the first few doses ; the 
same rules govern here that were laid down for the administration of 
stimulants in typhoid fever. It is impossible to give any positive rule as 
regards the quantity of stimulants required in each case. It is very rarely 



TYPHUS FEVER. 



777 



necessary, at any time during the fever, to give more than eight ounces of 
brandy during twenty-four hours. If this amount will not sustain the 
heart-power, I am confident larger quantities will fail to do it, and also that 
such administration has hastened the fatal issue. As soon as the symptoms 
on account of which the alcohol may have been resorted to are relieved, 
the quantity must be reduced, or its administration altogether stopped. 

I do not altogether condemn the use of stimulants in typhus fever, but I 
do so as regards stimulants as a " plan of treatment ; " and where the patient 
can be freely exposed to fresh air, I doubt if their use is often required. 
To diminish, the frequency of the pulse, cardiac sedatives have been em- 
ployed, such as veratrum viride, aconite, and digitalis. 

The rapid pulse in typhus fever, after the first onset of the disease, is 
due to the failure of heart-power ; when such is the case, digitalis should 
be employed. From four to six drachms of the infusion of digitalis may 
often be given with benefit during twenty-four hours. If the heart-power 
cannot be sustained by the moderate use of stimulants and by digitalis 
(given as indicated), no more can be done so far as remedial agents are 
concerned. The treatment of the special symptoms of typhus fever requires 
only a passing notice. The headache, when intense, is best relieved by cold 
applications in the form of ice-bags. If it is accompanied by intolerance 
of light, a blister on the back of the neck will be found to give relief. 

Sleeplessness, in any stage of the disease, if it continues for tw 7 o or three 
days, must be relieved, for it is of itself sufficient to cause a fatal termina- 
tion. If sleep does not follow the application of cold to the head, opiates 
may be administered in full doses. I have seen typhus-fever patients that 
had not slept for forty-eight hours drop into a quiet sleep within a few 
hours after they had been exposed to free ventilation. Great care should 
be exercised that their apartments are kept perfectly quiet and darkened. 
When delirium and cerebral symptoms are associated with sleeplessness, 
hydrate of chloral may be carefully employed. Stupor is to be counter- 
acted by promoting the action of all the excreting organs, applying exter- 
nal stimulants, and administering diffusible stimulants, the most service- 
able of which are black coffee, musk, and camphor. In the early stage of 
the disease the cold douche may be employed. 

Two remedies have been recommended for the coma of typhus, namely : 
valerian and phosphorus ; neither of these remedies has seemed to me to 
be efficacious. When there are evidences of great prostration in connection 
with any of these special symptoms to which reference has been made, 
the moderate administration of stimulants may be resorted to, and if relief 
follows the first few doses their use may be continued. In the treatment 
of the complications which are liable to occur during the course of typhus 
fever, one must be guided by general principles and by the symptoms 
in each individual case, it being always remembered that the primary dis- 
ease has a tendency to induce great nervous prostration and depression, and 
that the heart's action forbids the use of all depleting remedies, and indicates 
a supporting plan of treatment. The pulmonary and laryngeal complications, 
as well as erysipelas, bed sores, and gangrene, are to be managed in the same 
manner as was proposed when they occur ns complications of typhoid fever. 



778 



ACUTE GENERAL DISEASES. 



The diet is of primary importance. Though the patient refuse all nourish- 
ment, if possible he must be required or even compelled to take it. As the 
digestive powers are impaired, great care is required in selecting and admin- 
istering the proper nourishment, and it must be given at stated intervals, 
varying from one to two hours. Care must be taken not to overfeed — 
much harm may be done in this way. When the patient clinches his teeth 
and obstinately refuses all food, or is unable to swallow, his life may 
sometimes be saved by pouring liquid nourishment into the stomach by 
means of a long tube passed through the nose. Milk best serves the pur- 
pose as an article of diet. It may be given ice-cold, if desired, and in such 
quantities as the stomach can receive and digest. If more concentrated 
nutrition is desirable, the yolk of eggs may be beaten up and added to the 
milk. 

The management of patients during convalescence from typhus fever is 
a matter of very great importance. As soon as the fever ceases, most pa- 
tients convalesce rapidly unless there is some complication, and the chief 
duty of the physician is to prevent premature exertion and exposure to 
cold, and to restrain the patient in the gratification of an inordinate appe- 
tite. At this time porter or ale may be taken with benefit. The mineral 
acids, Peruvian bark, and iron may also be given as tonics ; these are par- 
ticularly called for when the pulse is slow and feeble. It is important 
to guard against any sudden physical effort during the early period of con- 
valescence, as it may lead to coagulation of blood in the veins. An opiate 
or hydrate of chloral is sometimes required to produce sleep during convales- 
cence. In all cases great benefit will be derived from a temporary change 
of residence and daily exercise in the open air, 

KELAPSING FEVER. 

This has been called famine and seven-day fever, synocha, typhinia, 
mild yellow fever, typhus recurrens, dynamic fever. The French call it 
" Fievre a Eechute ; " and the Germans, iC Hungerpest. " 

Relapsing fever is no new form of disease. It was described more than 
a century ago by Dr. Kutty, 1 and since that time has prevailed as an epi- 
demic disease in most of the countries in northern Europe. 2 There is no 
reliable history of its occurrence as an epidemic in this country until 1872- 
3, when an epidemic prevailed in New York City. It has been reported that 
in the year 1844 a vessel landed in Philadelphia passengers ill of relapsing 
fever. At one time, while typhus fever was prevailing in Buffalo, some twelve 
or fourteen cases of relapsing fever were reported ; but it is altogether prob- 
able that they were cases of irregular typhus fever, for when relapsing fever 
has been introduced into a locality it is not limited to one or two dozen cases. 

Morbid Anatomy. — In this disease there are no pathological lesions that 
are characteristic. There are changes present in some of the organs which 
very closely resemble those met with in typhus. 



1 John Rutty, " A Chronological History of, etc., in Dublin, from 1725 to 1765." London, 1770. 

2 Accounts in Hippocratic writings leave no doubt but that it prevailed 2,000 years ago in islands off 
Thrace. 



KELAPSING FEVER. 



779 



Spleen. — In the majority of autopsies, if death has occurred in the ac- 
tive period of the disease, the spleen will be found increased in size, its 
capsule thickened, smooth, tense and slightly clouded, the trabecule of the 
organ increased, and the Malpighian tufts more prominent than normal. 
In some cases the spleen will be found enlarged, soft, flabby, and eyen dif- 
fluent. There is no uniform change in its substance, although it is always 
increased in size during the active period of the disease. After this period 
has passed, it will be found diminished in size, and its surface will pre- 
sent a shrivelled appearance, with the capsule rolled into folds. Infarc- 
tions (not embolic in origin) are often found. In many cases a number of 
rounded or irregular miliary masses, of a dull yellow color, will be found, 
containing granular detritus, cell-elements, and free nuclei. 

Liver. — During the active period of the fever, the liver will also be found 
enlarged. The gall-bladder is generally distended with dark yellow and 
viscid bile. 

Kidneys, — The kidneys are increased in size, the increase being due to 
congestion of the cortical substance. There is a granular infiltration of 
the epithelium of the uriniferous tubes, a change similar to that noticed in 
other fevers. Small hemorrhages stud the whole organ in severe cases. 

The urine often presents a cloudy appearance. 

Intestines. — Usually enlargement of the glandular follicles of the intes- 
tines will be found. The solitary glands are more commonly affected, but 
even the Peyerian patches may present the " shaven-beard " appearance. 
The mesenteric glands are slightly enlarged in severe cases. Their appear- 
ance is similar to that noticed in typhus. 

Mucous Membranes. — In the majority of cases, small spots of blood- 
extravasation will be found upon the mucous surfaces, especially the 
membranes of the stomach and intestines, and they may be found on the 
mucous membrane of the bronchial tubes. The stomach shows small 
blood-extravasations when vomiting has been severe during life, or when 
there has been black vomit. These spots of ecchymosis are perhaps as con- 
stant as any pathological lesions of the disease. 

Blood. — The blood coagulates imperfectly, as in typhus. Spirilli are 
discoverable, oftentimes, provided death occurs in an active stage. The 
heart presents no constant changes. In some cases fine granular infiltration 
or vitreous degeneration of the muscular fibres has been observed. This 
same granular infiltration is also sometimes seen in the voluntary muscles. 
Coagula are rare. 1 Diffuse or circumscribed changes in the marrow of the 
bones occur, according to Ponfick. The lymphoid elements increase, and 
large cells, filled with numerous oil globules, appear along the track of 
vessels. Necrotic softening of the marrow has been seen in severe. cases. 

Etiology. — There have been differences of opinion and much discussion 
in regard to the etiology of this disease. At the present time it seems to 
be the unanimous opinion that it is a contagious disease, and that it is a 
distinct type of fever. Although it presents many phenomena which 
ally it to typhus, and many other phenomena which ally it to malarial 



i Ponfick, in Vircbow's Archiv, B. 60, p. 153, 1874, states that the cardiac degeneration may be so 
extensive as to cause death, resembling the heart of phosphorus poisoning. 



780 



ACUTE GENERAL DISEASES. 



fever, it is neither typhus nor malarial, but is a distinct type of fever 
having a distinct poison. 

From observations which have been made upon the blood of patients 
suffering from this fever, organisms which have the power of developing 
the fever have been found. This parasitic organism (spirillum Ober- 
maieri) is a spiro-bacterium, unlike that sometimes found in water and 
in mucus from the mouth. But Billroth and Manassein have found 
them in fluid from noma and in a cyst of the antrum. Several German 
observers, Oohnheim among them, have given drawings of these organ- 
isms, which seem to be little spiral lines that are constantly undergoing 
a twisting, rotary, rapid motion, and these observers tell us that they are 
distinctive of this form of disease, and are always present during its active 
period. 1 They are absent in the interval between the primary attack and 
the relapse, but are to be seen as soon as the relapse occurs. 

Clinical experience has shown that relapsing fever is a contagious disease, 
and can be propagated by personal contagion. The disease is not neces- 
sarily accompanied by starvation, for it is developed among those who 
are well fed as well as among those who are badly nourished. As in typhus 
fever, there is a connection between the development of an epidemic of this 
fever and imperfect ventilation and bad hygiene. 

I had never seen a case of relapsing fever until 1870, when the epidemic 
prevailed in New York City. At that time patients were brought into my 
wards in Bellevue Hospital with a fever differing from typhus fever by the 
absence of an eruption ; from intermittent, in the order of its develop- 
ment, and not closely resembling remittent fever. It seemed to me an 
irregular form of malarial fever, differing from any with which I was 
acquainted. Eight cases were brought in. From these my house phy- 
sician contracted the fever, and during his illness I reached the diagnosis of 
relapsing fever. Subsequently we had large numbers of relapsing fever 
patients, and a hospital was established for their reception on Hart's 
Island. In every case that occurred at that time, where the origin of the 
fever could be traced, it was found that there had been direct exposure, and 
it was established beyond doubt that the first cases were brought from Ire- 
land. The contagious character of the affection was also established by 
the fact that all the nurses and all the physicians who were in immediate 
attendance upon the sick contracted the fever. If a patient was placed in 
a bed previously occupied by a person sick with relapsing fever, before it 
had been cleaned, he was almost certain to contract the disease. The closer 
the contiguity the more certain is the individual to contract the fever. 

At the time of this epidemic we found no evidence that the fever was 
conveyed by clothing, although some British writers have claimed that it can 
be done. When our patients were admitted into the hospital, their clothing, 
as it was removed, was simply washed, not disinfected in any special manner, 
then packed away, and not a single person who was thus brought in imme- 
diate contact with the clothing contracted the disease. There is no immu- 



1 Vide Centralblatt, 18T3, and Virchow's Archiv, Bd. 47. Also Obermeier's article in Berliner Klin. 
Wochen., No. 35, 1873. It is from two to six times as long as a red blood disc, and no thicker than the 
finest fibrin-fibril. It is readily destroyed by nearly every reagi-nt. 



KELAPSING FEVEK. 



781 



nity from a second attack. The period of incubation ranges between five 
and seven days, rarely nine. 1 

Symptoms. — The symptoms which usher in relapsing fever are usually 
well marked. If there are any prodromes, they are the same as in typhoid 
fever (q. v.). 

It is sudden in its advent. This is marked by a severe rigor or by a dis- 
tinct chill. Accompanying the chill there is frontal headache, vertigo, pain 
in the limbs and joints, more or less pain in the back, nausea and not in- 
frequently vomiting. 8 A rapid rise in temperature follows the chill, and 
with the pyrexia the headache increases, as does also the pain in the limbs, 
especially about the joints. Sweats may, at first, follow the rigors. There 
is vomiting, at first only of the simple contents of the stomach, afterwards 
of yellowish material. This may be followed by the ejection of a dark- 
colored material, which very closely resembles the black vomit of yellow 
fever. In this disease the rise in temperature is always rapid, and usually 
attains its highest point within the first twenty-four hours; during this 
time it may rise to 104° F., or even as high as 109° F. From this time, 
for two or three days, there is usually very little variation. With the occur- 
rence of the chill and fever there is also a rapid increase in the frequency 
of the pulse. In no disease does the pulse so quickly become rapid as in 
relapsing fever. It is not uncommon for it to reach 140, 150, or even 160 
beats per minute within the first twenty-four hours. It is usually small 
and compressible, sometimes dicrotic. The mind is clear. There is nothing 
peculiar about the countenance of the patient, but it presents the ordinary 
appearance noticed in an active febrile excitement. Sleeplessness is often 
present on account of the severe pains in the limbs. As the disease pro- 
gresses the patient becomes more and more prostrated ; by the second day 
he may be unable to turn in bed. The arthritic pains increase in severity 
and often become the most distressing symptoms of the fever. 

As early as the second day, patients begin to complain of a feeling of 
weight and uneasiness in the upper part of the abdomen, more severe in 
the left than in the right hypochondrium. Profuse sweats are common 
about the second day, but they afford no relief to the urgent symptoms. 
Usually, there is considerable enlargement and tenderness of the liver. The 
spleen, also, becomes rapidly enlarged, and its enlargement is attended with 
quite severe pain and tenderness. Moderate meteorismus is not uncommon. 
The muscles of the body are, however, the seat of the most severe pain, 
which is increased by movement and by pressure ; the pain is piercing and 
lancinating in character. On accor.nt of this pain, the patient usually lies 
perfectly quiet ; he is not restless but sleepless. Delirium is not an infre- 
quent symptom, and is sometimes very active ; yet in the majority of mod- 
erately severe cases the mind remains undisturbed. There may also be 
present irregularities of the pupils, photophobia, and other symptoms 
which might lead one to the diagnosis of meningitis were it not for the 

1 In some cases the fever begins a few hours after exposure. Lebert found 75 per cent, of cases to have 
an incubator}' period within seven days, and of these more than one-half sickened within three days after 
exposure. 

2 This headache persists till the remission ; it is unvarying and intense ; the vertigo is so severe that 
the patient has to take to his bed as much from giddiness as pain. 



782 



ACUTE GENERAL DISEASES. 



character of the pulse. The muscles of the eyes are often stiff and im- 
movable ; the conjunctivae are reddened and the eyelids are swollen. 

As the disease progresses, in a certain proportion of cases, jaundice is de- 
veloped ; this is usually accompanied by vomiting and severe diarrhoea ; 
and these symptoms seem to ally the disease to some forms of malarial 
fever ("bilious typhoid"); not infrequently, especially in children, there 
is epistaxis. The skin may be covered with herpes or sudamina. The 
great prostration and rapid rise in temperature ally it to typhus fever, but 
the rise is more rapid and reaches a higher point within the first twenty- 
four hours than it does in typhus fever. There is sometimes a slight rose- 
colored eruption resembling roseola, but having none of the characteristics 
of typhus eruption. The patient goes on from day to day gradually getting 
worse ; the fever becomes more and more intense ; loss of strength and 
emaciation are progressive, and the muscular pains are more severe. In 
some cases the patient rejects everything taken into the stomach. The 
pulse reaches 160 per minute, the tongue is brown and dry, extreme nausea 
and bilious vomiting are present, and the severity of the symptoms indi- 
cates that death may speedily occur ; when, on the seventh or eighth day 
of the fever, a remission suddenly occurs, attended by a profuse perspiration, 
by a critical diarrhoea, or, rarely, by bleedings from mucous surfaces. 

With the occurrence of the profuse sweating the temperature falls; in a 
few hours it may fall five, six, or even seven degrees ; the pulse becomes 
less frequent ; the respirations, which have been hurried and difficult, be- 
come regular ; the pains in the head and limbs pass away, the thirst disap- 
pears, the tongue becomes moist ; the engorgement of the liver and spleen 
rapidly diminishes, as is shown by the rapid diminution in the size of these 
organs as determined by per.cussion. The bowels are constipated. Within 

twelve hours from the com- 
mencement of the remission, 
the temperature may fall to less 
than 100° F., perhaps below the 
normal standard, and the pulse 
may fall to 80 or 90 beats per 
minute. 

As soon as the remission occurs, 
the patient feels perfectly well, 
except a sense of weakness. He 
gets out of bed, and, if he is in 
a hospital, perhaps insists upon 
his discharge ; his appetite be- 
Eig. 164. gins to return, and he appears 

. Temperature Record in a case of Relapsing Fever. to be rapidly Convalescing, but 

in many the pulse at this period 
is as slow as 40 to 60 per minute, and the first sound of the heart is very 
faint, the second being intensified. 

His apparent convalescence is of short duration ; sometimes in three or 
four days, usually at the end of a week, certainly by the twelfth or four- 
teenth day of the disease, all the phenomena of the primary fever are sud« 




RELAPSING FEVER. 



783 



denly developed, or what is termed the relapse occurs. 1 Sometimes the 
relapse occurs in the morning, sometimes in the afternoon, but more fre- 
quently it comes on at night. The relapse may be ushered in by a chill, or 
it may occur without a chill. The pulse may begin to increase in rapidity, 
and in twelve hours reach 140 per minute. With the rapid pulse, the 
temperature rapidly rises to 106° F. Usually the fever which attends 
the relapse is more intense than the primary fever, the liver and spleen 
becoming as enlarged as during the primary fever. The relapse usually 
lasts three or four days. In a few cases I have seen it last six or seven 
days, and in some it does not continue more than forty-eight hours. 
After it has continued a certain period, a second remission is developed ; 
this, like the first remission, comes on suddenly, is accompanied by a pro- 
fuse perspiration, and in twenty- four hours from its commencement the 
pulse and temperature have reached their normal standard. From this 
period, the patient usually goes on to complete recovery. 

As many as three or four relapses may occur, but ordinarily the conva-. 
lescence becomes complete after the second remission. Convalescence from 
relapsing fever is usually slow, the patient for a long time remains in a 
weak condition, suffering more or less from arthritic and muscular pains. 
The appetite returns slowly. An anaemic murmur, which is of ten very dis- 
tinct during the active period of the fever, is heard for two or three weeks 
after the commencement of convalescence. (Edema of the feet, due to gen- 
eral anaemia, is often quite marked during convalescence. The period of 
convalescence is usually as long as both the period of fever and remission ; 
not infrequently six or eight weeks elapse before relapsing fever patients are 
able to resume their accustomed avocations. At the commencement of con- 
valescence, the decrease in the size of the spleen is rapid, but frequently it 
is a long time before the organ reaches its normal size. 

Complications. — Few complications have been noticed during the course 
of relapsing fever. In some epidemics pneumonia has occurred quite fre- 
quently ; at other times it has been exceedingly rare. When it does occur, 
it is often double, and terminates in gangrene in a number of cases. 

Sudden collapse may occur as a complication of relapsing fever, either 
during the primary fever or during the relapse. The pulse suddenly be- 
comes small, irregular, or intermittent, sometimes imperceptible. The 
cardiac impulse is feeble, the heart sounds are lost, and the patient rapidly 
passes into a condition of collapse and dies. The collapse may come on 
suddenly in cases previously mild ; with fatty heart, death in relapsing fever 
is nearly always from this cause. 

Post-febrile ophthalmia is another yery remarkable complication or 
sequela of this fever. It has been observed in most epidemics. It presents 
two distinct stages, the amaurotic and the inflammatory. During the first 
stage the patient complains of impaired vision, with motes and luminous 
circles floating before the eyes. The inflammatory stage is characterized 
by intense circumorbital pains and lachrymation, without injected conjunc- 
tivae or marked constitutional disturbance. Eecovery is tedious, and, unless 
the case is carefully treated, may end in complete loss of sight. Both eyes 



1 It is very rare for the disease to end in one single paroxysm. 



784 



ACUTE GENEKAL DISEASES. 



are rarely attacked ; the right eye is most frequently affected. Iritis, 
choroiditis, and retinitis are not uncommon. 

Diarrhoea and dysentery are common complications, and in some epi- 
demics they are the chief cause of death. They are most likely to come on 
during the relapse. In our epidemics the most frequent complication is 
hemorrhage from the mucous surfaces, especially from the stomach and 
intestines. In two cases that came under my observation hemorrhagic 
pachymeningitis was the cause of death. In very rare instances, abscess of 
the spleen, accompanied by pysemic symptoms, has occurred during the 
relapse and convalescence. Pregnant females, no matter at what stage of 
pregnancy, usually abort during an attack of relapsing fever. 

Differential Diagnosis. — The diagnosis of relapsing fever is not difficult if 
one has the entire history of the case ; but at the commencement of an 
epidemic, during the primary fever the diagnosis will necessarily be doubt- 
ful. The diseases with which it is possible to confound relapsing fever 
are typhus, typhoid, remittent, yellow and dengue fever, small-pox (before 
the eruption), and measles. It differs from all but typhus in the sudden- 
ness of its invasion, in the short duration of the primary fever, in its termi- 
nation in a crisis, and in the almost uniform occurrence of a relapse be- 
tween the third and fifth days. Then the muscular and arthritic pains, 
which are such constant attendants of relapsing fever, distinguish it from 
the other forms of fever. 

In typhus, the dusky face, contracted pupils, absence of all abdominal 
pain, peculiar smell, stupor, apathy of mind, and the pathognomonic eruption 
on the fifth or seventh day will be sufficient to distinguish it from relapsing. 

In typhoid, the slow invasion, the "step-ladder " rise in temperature, 
the eruption, the characteristic diarrhoea, and the continuance without re- 
mission or intermission, will enable a diagnosis to be reached. 

A severe form of relapsing fever, attended by jaundice, resembles very 
closely, in its general appearance, yellow fever. In yellow fever the pulse 
is rarely over 110, the spleen is normal; but the high temperature and rapid 
pulse which attend the development of the former readily distinguish it 
from the latter ; besides, when the intermission comes on, there can no 
longer be any question as regards diagnosis, for yellow fever is a disease 
in which only a remission occurs, not an intermission. 

Small-pox simulates relapsing fever only during the period of invasion. 
One need make no doubtful diagnosis after the third day, when the red 
spots appear along the edges of the hair. 1 

In measles the eruption following the symptoms of a common cold and a 
bronchitis will suffice for a diagnosis. 

Prognosis. — The prognosis in relapsing fever is always good. During our 
epidemic about three per cent, of all the cases treated in hospitals termi- 
nated fatally. This is a lower rate of mortality than we have with measles. 
Usually deaths from relapsing fever occur, not from the disease, but from 
some complication. During the epidemic in this city, syncope during re- 
lapse was the most frequent cause of death. Eelapsing fever patients may 

• 1 In dengue fever the pains in the joints are severe ; there are glandular swellings not found in relaps- 
ing ; the paroxysm is shorter (three days) than in relapsing (seven days) ; and there is an eruption (like 
scarlatina) on the palms and neck. 



SMALL- POX. 



785 



die of hemorrhage from some of the mucous surfaces. A fatal termination 
may occur from bronchitis, pneumonia, or other pulmonary complications. 
Diarrhoea and dysentery occurring during convalescence sometimes cause a 
fatal termination ; purpura also. Sudden suppression of urine, dependent 
upon renal congestion, may give rise to acute uraemia, and thus cause death. 
My own experience leads me to the belief that the greatest danger in this 
disease arises from sudden syncope. I remember one very marked case, 
that of a young physician who seemed to be doing well in his second re- 
lapse, when suddenly he passed into a state of syncope and died. At the 
post-mortem examination no condition of the internal organs was found 
which would account for his death. 

Treatment. — Dr. Butty stated more than a century ago that all those 
cases of relapsing fever which were abandoned to whey and the good provi- 
dence of God recovered. The experience of a century has furnished no ac- 
cepted plan of treatment. The profession are still unsettled as to the best 
course to be adopted in the management of this disease. When this fever 
appeared in our midst, we thought we could control it by large doses of 
quinine, but we soon found that quinine was of no service in its treatment. 
Then arsenic, aconite and veratrum were employed in full doses as anti- 
pyretics, but after a time these were abandoned as useless. Cold baths were 
resorted to, as also was sponging of the surface in order to reduce the tem- 
perature, but in their use we were disappointed. The temperature was re- 
duced while the cold was beiug applied, but rose again very soon after the 
patients were removed from the baths, and there was no evidence that it 
diminished the severity or shortened the duration of the primary fever, or 
prevented the occurrence of the relapse. Opium in full doses was then 
tried, but with eaually unsatisfactory results, although its free use was 
found to give more comfort to the patients than did any other plan. In 
some cases stimulants were administered quite freely, but without any ap- 
parent beneficial results. 

The conclusion arrived at was, that relapsing fever patients were as well 
without as with medication. I would insist that relapsing fever patients 
should be kept quiet in bed during the primary fever, and should not be 
allowed to leave their rooms until the period of relapse, shall have passed 
and that the greatest care should be exercised to guard against the occur- 
rence of syncope. If there is any evidence of heart-failure, digitalis and 
stimulants should be administered according to indications. Beyond this I 
have nothing to suggest. My experience leads me to place relapsing-fever 
patients under the best hygienic management, with free ventilation and a 
milk diet, and then carefully watch lest some complication should occur. 

SMALL-POX. 

{Variola.) 

There are three recognized types of variola, viz., — " variola discreta," 
" variola confluens," and " variola hemorrhagica." 1 ' 

1 Small-pox is a very ancient disease. Before the Christian era a Goddess had been worshipped in India 
as a protectress against it. The Arabians gave the first detailed account of variola. During the thirteenth, 
fourteenth, and fifteenth centuries it prevailed in Europe, and two centuries later it appeared on the 
American continent. During the eighteenth century one-sixth to one-twelfth of tlie total mortality in 
Europe was caused by small-pox. 
50 



786 



ACUTE GENEKAL DISEASES. 



Morbid Anatomy. — Besides those anatomical lesions which occnr upon 
the mucous membranes and skin, there is more or less intense congestion 
of the lungs, brain, liver, spleen and kidneys.' In the hemorrhagic form 
of small-pox small hemorrhages occur in nearly all the viscera, with ecchy- 
moses in the serous membranes and blood-stained fluid in the serous cavi- 
ties. The mucous membrane of the stomach and rectum is oftenest the 
seat of these extravasations. 

The characteristic anatomical lesion of small-pox is to be found upon the 
mucous membranes and upon the skin. This lesion is usually spoken of 
as the eruption. It does not differ essentially in the different varieties ; 
the modifications which are met with are due rather to its duration and 
the order of its development. These surface lesions pass through regular 
stages of development and decline. 

The first step in the formation of a small-pox pustule is congestion of 
the skin in discrete spots ; the vessels of the corium are dilated and tortu- 
ous, and the connective-tissue of the papilla?, in the centre of the congested 
zone, shows more or less oedema. The non-elevated red spot (looking at 
first like a flea-bite) is a macule. Next, the skin is elevated at these (macu- 
lar) points and a papule forms, from changes in the cells of the rete Mal- 
pighii. Soon the papule becomes a vesicle ; in its centre the epidermis 
becomes distended with serum and cells. As the effusion increases the 
cells change ; the horny layer above is raised, and the summit of the papule 
becomes the centre of the vesicle. The changed cell elements are pressed, 
separated, and- massed into groups from pressure of the effusion, and a 
stringy mesh-work is formed in the vesicle. Meanwhile proliferation of 
the adjoining cells forms a peripheral wall for the vesicle, the contents of 
which soon become turbid. 

Umbilication of the vesicles now occurs. Trabecule slowly spread from 
roof to floor of the vesicle, and hold down its centre, while marginal cell 
proliferation and the accumulation of serum bulge out its periphery. 2 
After the vesicles are fully formed, pus-cells appear in them, and as a re- 
sult the vesicles change in color, and become pustules. At the same time 
an inflammatory process, more or less extensive, is going on in the walls of 
the pustule, and in the surrounding cellular tissue, which terminates in a 
destruction of tissue at the point where the papillary congestion first oc- 
curred. If only the superficial layer of the skin is involved, the infiltra- 
tion of pus-cells into the vesicle and the formation of the pustule may take 
place without extension of the inflammation into the cellular tissue beneath, 
and necrosis or death of the part will not follow ; but if the inflammation 
extends into the deeper tissues, a slough will be produced which necessarily 

1 Enlargement of the spleen is rather an infrequent event in small-pox. Weigert states that the blood- 
vessels of the lymphatic glands and abdominal viscera are often filled with micrococci, that necrosis of the 
cells about these colonies induces pus accumulation, the direct result of "coagulation necrosis" (see 
Inflammation) : but that abscesses rarely form ; some find an analogy between these and the skin dis- 
eases. 

2 Some explain it by saying that each papule and subsequent vesicle holds imprisoned at its centre 
either a hair-follicle or the duct of a sweat-gland, and that when this epidermidal layer of the papule is 
elevated by the serous exudation or infiltration, the portion immediately about the hair-follicle or the 
sweat-duct, is held down, and a depression is produced by the exact point where the hair-follicle or duct of 
the gland may be situated ; but since umbilication is present when neither structure is found, this view 
cannot be accepted. 



SMALL-POX. 



787 



will be followed by a cicatrix and pitting. After the pustule is formed 
the inflammatory products begin to dry down, and a cvust is formed which 
contracts in the central portion, and the same umbilicated appearance is 
presented that is seen in the umbilicated vesicle. The incrustation begins 
at the centre. The crusts are made up of dried pus-cells and detritus. 
After a time these crusts are separated by the ordinary changes which 
occur in the subsidence of an inflammatory process, and recovery is com- 
plete, except that there is left behind a cicatrix which undergoes the same 
changes as does a cicatrix formed under any other circumstances. These 
pustules may be formed upon any mucous membrane. They occur often- 
est in the nose, mouth, trachea, bronchial tubes and larynx. 

There is nothing specific or essentially different in the development of 
the pustules in hemorrhagic small-pox, except that they contain blood in- 
stead of serum or pus. In the hemorrhagic variety, larger or smaller 
hemorrhages take place into the cellular tissues and into the cutis ; in 
the milder forms they take place only in the layer beneath the papillae ; 
while in the severer forms they take place beneath all the cutaneous 
layers ; even the subcutaneous fat may be infiltrated with blood. Xo 
changes in the walls of the vessels have as yet been discovered which will 
account for these hemorrhages. These extravasations more frequently oc- 
cur in those cases in which death takes place before the period of pustula- 
tion is reached, In hemorrhagic variola blood extravasations occur into 
the substance of all the organs, the marrow of the bones, and on mucous 
and serous surfaces, and infarctions in the lungs are the rule. Hyper- 
semia and oedema of the brain sometimes occur. 

Etiology. — The disease is propagated only by contagion ; it is a disease 
which can only be produced by its own specific poison, and is communica- 
ble only to persons who are not protected from its influence. There has been 
considerable question as to where the virus of small-pox is located. Some 
claim that it is exclusively in the pustule, and that it is not possible for a 
person suffering from small-pox to give the disease to an unprotected in- 
dividual unless some of the virus from the pustule is brought in con- 
tact with a cutaneous or mucous surface. This is a mistake. That small-pox 
can be conveyed by means of virus taken from a pustule there can be no 
question, — "contagion by inoculation, " — but the cutaneous surface of an 
unprotected person may be rubbed with pus taken from a small-pox pus- 
tule, and unless there is an abrasion of the surface the person will not be- 
come inoculated with the disease ; but if the virus is brought in contact 
with a mucous surface of an unprotected person he will almost certainly 
contract the disease. It is equally certain that the disease can be com- 
municated from one person to another by means of the breath and exhala- 
tions from the skin. 

There is no evidence that the disease can be conveyed by the discharges 
from the bow T els. Perhaps if a pustule should be developed somewhere 
along the line of the intestine the discharges might become so contamina- 
ted as to have the power of communicating the disease. Small-pox can 
also be conveyed from one individual to another through the atmosphere. 
In the open air the distance of contagion is about two and one-half feet. 



788 



ACUTE GENERAL DISEASES. 



In a small room the atmosphere may be so contaminated that an unpro- 
tected person will contract the disease upon a single entrance into the 
room. The disease can be conveyed in clothing, and the poison will re- 
main for a long time in clothing unless it has been exposed for a consider- 
able , time to the air. In other words, there is no doubt but that it is a 
portable disease. In order that the disease may be transferred by means 
of the clothing or merchandise, it is necessary that the clothing or mer- 
chandise contain the pus or crusts from the small-pox pustules ; how long 
a time may elapse before the virus loses its vitality is not known. There 
are well-authenticated cases in which it has retained its virulence for 
more than a year. 

No period of life is exempt from the contagion of small-pox ; even intra- 
uterine life is in danger from infection. Rarely does an individual have a 
second attack. I remember one exception, that occurred in the person of 
a young Swedish woman, who, under my observation, passed through three 
well-developed attacks of the disease ; the last attack was the most severe. 
Concerning the exact nature of the small-pox virus nothing definite is 
known. 1 Some claim that the earliest period at which one suffering from 
this disease can infect the unprotected, is the period of suppuration ; others, 
that the infecting period is during the stage of desiccation. There are well- 
authenticated cases, however, which prove that infection may take place 
during any stage of the disease, even during the period of incubation. 
There is little doubt but that the suppurative stage is the most infectious 
period. 

There are many views as to the manner in which the small-pox poison 
gains entrance into the system ; the most probable of these views is, that 
it is principally absorbed by the mucous membrane of the respiratory tract 
during respiration, and it is also probable that exceedingly fine particles 
detach from the pustules and crusts, which are suspended in great numbers 
in the air surrounding small-pox patients, and that these convey the con- 
tagion. There are no facts to sustain the views as to the parasitic nature 
of this contagion. 

The length of time which elapses after exposure to, and reception of, 
the variola contagion before the disease is developed varies from five to 
thirty days, giving the extremes. This is called the period of incubation, 
during which the recipient of the poison usually presents no abnormal 
symptoms. If the poison is introduced into the system through inocula- 
tion, only forty-eight hours elapse before the characteristic phenomena of 
the variola are manifested. It is not known what change takes place in 
the body of the infected person during this period of incubation. Usually, 
twelve to fourteen days after exposure, one who has contracted small -pox 
begins to feel chilly ; this feeling of chilliness increases until he has a dis- 
tinct chill. This has been termed the initial stage, or the stage of initiatory 
fever. Measles and small-pox poisons may be latent at the same time in 
the same individual ; also scarlet fever and small-pox. 



1 Cohnheim and Weigert state that the micrococci in the vesicles are the contagious, specific elements. 



SMALL- POX. 



789 



Symptoms.— The transition from the stage of incubation to that of the 
initiatory fever is sometimes abrupt and sometimes gradual ; usually it 
occupies two days, and is followed by the eruption. In this stage there is 
greater variation in the intensity than in the duration of the symptoms. 
The intensity of the symptoms bears no relation to the severity of the 
attack. Not infrequently, the most violent symptoms in the initial stage 
are followed by a mild attack of variola; while mild symptoms in the 
initial stage may be followed by the gravest form of small-pox. The head- 
ache, which usually precedes the fever, grows more intense, only subsiding 
as the eruption appears. With the chill, which may be more or less severe, 
there is pain in the head and back, especially in the middle of the back 
and loins, 1 with this pain there will be rapid rise in temperature. The 
chill is more severe than in any other exanthem. During the first day the 
temperature may rise to 
104° F., during the sec- 
ond day to 105° F., and 
by the third day it may 
reach 106° F. or 107° F.; 
in some cases it has been 
said to have reached 
109° F. Sweating be- 
gins with the first rise in 
temperature, and con- 
tinues till the period of 
eruption. With this rise 
in temperature there will 
be an acceleration of 
pulse ; it may reach 100 
or 120 beats per minute. 

Jn the Strong and robust Temperature Record in a case of Discrete Small-pox. 

person, the pulse will be full and not easily compressed. In females, and 
in the weak and feeble, the pulse has less volume and usually is more fre- 
quent ; it may reach 140 beats per minute. In children, 160. 

At the onset, there is usually more or less nausea and vomiting, and 
soreness of the throat. This soreness of the throat may have preceded the 
chill by twenty-four hours, but now in many cases it will be quite severe, 
and the patient will complain of more or less dysphagia, and pain in the 
pharynx. The extent of the throat symptoms will depend upon the sever- 
ity of the attack. In the severer forms of the disease, by the third or even 
before the end of the second day, there may be delirium. In all cases, 
the face will be flushed, the conjunctivae congested, and there will be throb- 
bing of the carotids. With these symptoms, there will be great restlessness, 
and an anxious expression of countenance, with somnolence. The respira- 
tions will bo short, frequent, and labored, many complaining of dyspnoea 
in whom there are no lung complications. Many suffer from extreme 



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^complete paraplegia has occurred, disappearing, however, with the appearance of the eruption. 



790 



ACUTE GENEKAL DISEASES. 



vertigo, and in children convulsions are not infrequent. By the evening of 
the second, or morning of the third day, swelling and diffuse redness of the 
tonsils and soft palate are present ; not infrequently the swelling and red- 
ness of the mucous membranes extend into the larynx, causing hoarseness 
and huskiness of the voice and a stridulous cough. 

During the fever of invasion patients are languid and weak in propor- 
tion to the severity of the fever. 1 Frequently within twenty-four hours 
after the ushering-in chill, the strongest and most vigorous will be unable 
to get out of bed. Paralysis of the bladder may occur in this stage. The 
tongue is coated. There is epigastric pain and tenderness. If vomiting 
occurs it is present at the very beginning, and continues with great ob- 
stinacy throughout its entire course. In the hemorrhagic variety the 
matters vomited may contain blood. There is constipation, but diarrhoea 
is not infrequent in children. 

Stage of Eruption. — By the third day of the disease, at least after the 
initial fever has continued three full days, an eruption will make its ap- 
pearance upon the face, especially along the edges of the hair. 2 

The eruption, as it develops in a moderately severe case of discrete 
variola, first appears in the form of slightly elevated maculae. These are 
of a pale red color, varying in size from a millet-seed to a pin's head, or 
even larger. These little red spots look very much like flea-bites. In most 
cases the forehead, nose, and upper lip are first covered ; they gradually in- 
crease in size, the increase being attended by a sensation of itching and burn- 
ing of the surface. Usually, about twelve hours after their appearance 
upon the face, similar small red points appear upon the neck and wrists, 
then on the chest, arms, and legs. In children they may first appear on the 
loins, nates, genitals, or about an excoriated or a blistered surface. They 
are always less abundant on the body and extremities than on the face. 

On the second day of the eruption, these spots assume a darker red color, 
become elevated, and have a distinctly papular feel, like shot under the skin. 
In a majority of instances, as they enlarge a depression is formed, which 
gives them an umbilicated appearance. The appearance of the eruption 
is attended by a subsidence of the febrile symptoms, the patient no longer 
complains of pains in the head and back, the temperature falls two or three 
degrees, and the pulse diminishes fifteen or twenty beats in frequency, some- 
times to normal. Vesicles are also seen in the mouth, pharynx, upper part 
of the larynx, etc., etc. 

Stage of Suppuration. — About the sixth day of the eruption the contents 
of the vesicle, from the admixture of pus-corpuscles, gradually become 
turbid, and by the eighth day the pustules become fully formed, and the 
disease enters on the stage of suppuration. The integument in the im- 



1 Trousseau and many others state that the longer the skin manifestations are delayed, the more harm- 
less the disease, and the more rapidly the eruption comes on the more dangerous is it. 

2 Prior to the eruption a diffuse scarlatina-like redness sometimes covers all the body, and a few suda- 
mina may appear in the erythema. At this point haste may lead to a diagnosis of scarlet fever or measles. 
Pctechise and ecchymoses are less frequently seen ; they are not necessarily followed by variola hemor 
rhagica. 



SMALL-POX. 



791 



mediate vicinity of the pustule now becomes red, oedematous, and tumefied, 
each pustule being surrounded by a broad red base, the " halo," and where 
they are thickly set they become confluent. The face swells to a shapeless 
mass, and the patient becomes frightfully deformed. The eyes are closed, 
and the hands and feet look like round balls. The itching now becomes 
almost unbearable and causes the patient to scratch himself, thus causing 
ultimate disfigurement. During this period a characteristic sickish odor 
is emitted. The eruption passes through its stages two or three days later 
on the extremities than it does on the face ; consequently, suppuration may 
be complete on the face while it is incipient on the extremities, and the 
eruption may be perfectly discrete on the trunk while it is confluent on the 
face. About the eighth or ninth day of the eruption the pustule is fully 
formed ; the stage of suppuration is complete. Then commence the retro- 
grade changes. The pustule either ruptures, discharges its contents, dries 
up and forms a yellowish crust, or it shrivels and dries up without ruptur- 
ing ; this is the period of desiccation. 

Stage of Desiccation.— -Desiccation commences in those parts in which the 
eruption first appeared, and commonly on the twelfth day of the disease. 
As the drying down of the pustules takes place, the redness, tenderness and 
oedema of the skin lessen, and the countenance begins to assume a more 
natural appearance. At first the crust adheres quite firmly to the surface, 
but about the fourteenth day of the eruption it becomes separated and 
falls, leaving a stain of reddish-brown color, with elevated edges and de- 
pressed centre, which remains visible for five or six weeks. These spots 
gradually become lighter in color, until finally, if there has been destruc- 
tion of the cutis, and if excoriation, ulceration and renewal of the scab 
have occurred, a pit will be formed of greater or less depth, of a white 
color, giving to the face a " pock-marked " appearance, which will remain 
during the life of the individual. 

On the eighth day of the eruption the secondary fever comes on. It 
often commences with a distinct chill. The fever is highest in the even- 
ing; it is of a distinctly remittent type, the pulse becomes frequent, the 
temperature rapidly rises, perhaps reaches a higher elevation than it did 
during the initial fever, sometimes rising as high as 108° or 109° F. ; it 
reaches its maximum when suppuration is at its height. As desiccation 
commences, the temperature begins to fall, and by the time the crusts are 
fully formed the temperature reaches very nearly a normal standard. If 
the temperature rises again, its rise is diie to some complications such as 
erysipelas or some phlegmonous process. With the fall of the crusts, the 
patient's appetite returns, and he is able to sleep ; convalescence is now 
fully established. 1 The dividing lines between the different varieties of 
small-pox are not sharply defined ; one variety gradually passes into 
another. It is unnecessary to consider all the forms into which this dis- 
ease has been divided by some writers ; frequently the basis of the division 



1 The menses appear in the initial stage in the large majority of women with small-pox, even though 
it be not the proper time. (Quincke, Leo, Knecht, Curshmann, Buck, Obermeier, and others.) 



792 



ACUTE GENERAL DISEASES. 



is merely arbitrary. Our attention will therefore be confined to the more 
common and well-recognized varieties. 

Confluent Small-pox, or Variola Confluens. — This is a much more severe 
form of the disease than variola discreta. It develops far more rapidly and 
is much more fatal in its results. The fever of invasion is usually much 
more severe, and of shorter duration, frequently not lasting more than forty- 
eight hours. 1 The eruption spreads rapidly over tiie entire body, often 
appearing simultaneously on the face and the other portions of the body. 
The red dots which mark the first appearance of the eruption are very 
numerous, especially on the face and hands ; on the first day of their ap- 
pearance they are almost confluent. The conjunctivae are early involved 
and suppurative keratitis is not uncommon in this variety ; — the whole eye 
may be converted into an abscess. On the second day the skin is intensely 
red and swollen, and so thickly studded with large flat vesicles that they 
rapidly unite, suppuration speedily follows, and flattened, yellowish-colored 
confluent patches are formed upon a dark, reddened, swollen skin. Gradu- 
ally these patches run together over a still larger surface, and the epidermis 
is elevated in the form of large, flat bullae, which are filled with a sero- 
purulent fluid and are tense and elastic. In this way the entire skin of the 
face is covered by an immense bulla, and the patient is as unrecognizable 
as though he wore a mask. While the eruption may be completely con- 
fluent on the face and hands, on other parts of the body it remains discrete, 
and never becomes confluent except over limited spaces. 

The period of desiccation is slowly reached. Large concentric crusts are 
formed over the confluent patches ; these adhere firmly to the skin, while 
beneath them suppuration of the papillary layer continues. The true skin 
is more or less extensively destroyed, and when the crusts have fallen, 
there is left extensive loss of substance in the cutis, giving rise to pits and 
ugly scars, which have a tendency to contract, often producing permanent 
and unsightly disfigurements. In this variety of small-pox, the eruption 
is often confluent upon the mucous membrane of the mouth and throat ; 
it may involve the mucous membrane of the posterior nares and extend 
into the larynx. In some cases the attending pharyngitis is so severe as to 
render deglutition impossible. The pharyngeal inflammation is submu- 
cous, and is frequently accompanied by more or less enlargement of the pa- 
rotid and sublingual glands. When this condition exists there is danger 
of the sudden development of oedema glottidis, for the occurrence of which 
one should be on the watch. 2 

In confluent small-pox hemorrhage may occur in the pustules ; this is 
not variola hemorrhagica, but a hemorrhagic pustular confluent small-pox. 
In confluent variola the skin may exhibit erysipelas, phlegmon, gangrene 
or multiple abscesses. In confluent small-pox the severity of the consti- 
tutional symptoms corresponds to the severity of the local manifestations. 

1 The thermometer not infrequently shows a fever of 106° to 110° F. for a short time, which sinks to 
103° to 104° till suppuration, then rising even higher than before. 

2 During the year that I had charge of the Small-pox Hospital, there were three cases in the hospital ol 
oedema glottidis : one case terminated fatally before I reached the patient ; life was saved in the othei 
two cases by the performance of laryngotomy. 



SMALL-POX. 



793 



The temperature during the initial fever often reaches 106° ¥. or 107° F. 
and in very severe types of the disease it may rise as high as 110° F. The 




Fig. 166. 

Temperature Record in a case of Confluent Small-pox. 

pulse is correspondingly frequent and feeble. After the appearance of 
the eruption the temperature falls slowly to 103° F. or 104° F., where it 
remains until the stage of suppuration is reached ; then it again rises, in 
some cases even higher than during the period of invasion. Violent delirium 
is very frequently present during the fever of invasion, as well as during the 
period of secondary fever, and not infrequently patients pass quite sud- 
denly into a state of coma. Uncontrollable vomiting and obstinate diar- 
rhoea are not infrequent, coming on during the fever of invasion and con- 
tinuing throughout the course of the disease. 

In all severe cases typhoid symptoms manifest themselves soon after 
the appearance of the eruption, and patients often lie for days in a semi- 
conscious state, with dry, brown tongue, subsultus, a low muttering deli- 
rium, and all the attendant phenomena of intense nervous depression. In 
such cases albumen appears temporarily in the urine. Complications oc- 
cur much more frequently in confluent than in discrete small-pox. Inflam- 
mations of the serous membranes, especially pleurisy and pericarditis, are 
the most common. Croupous and catarrhal pneumonia and acute laryn- 
gitis frequently complicate the severe bronchial inflammation from which 
so few patients with confluent small-pox escape. Permanent alopecia often 
follows confluent small-pox. 

Variola hemorrhagica 1 is a form of small-pox which can hardly be 
regarded as a distinct variety, but rather as a modification of other vari- 
eties, called the black or malignant small-pox. It differs from the varie- 
ties already described, not in the manner of its development as far as the 
initial fever is concerned, but in the appearance of the eruption. This hem- 
orrhagic tendency is often manifested as early as the first appearance of the 
eruption, by the dark color which the eruption assumes. Sometimes the 



1 Zulzer found that in eighty-five to ninety percent, of his cases of hemorrhagica, the period of incuba- 
tion was only six to eight days, i. e., half as long as in simple small-pox. 



794 



ACUTE GENERAL DISEASES. 



papules become hemorrhagic from the very moment of their development 
at other times they first become vesicles, and then become hemorrhagic. 
Again, at other times, the hemorrhage first shows itself after the vesicles be- 
come pustules. In some cases the eruption over the whole body becomes 
hemorrhagic ; in other cases, it is hemorrhagic in spots. In the majority of 
cases, the eruption becomes hemorrhagic as soon as the papules have at- 
tained the size of a lentil, and the hemorrhagic change comes on slowly, 
generally commencing on the lower extremities. Petechias and ecchymoses 
often appear between the points of eruption. 

In connection with the hemorrhagic eruptions, hemorrhages from the 
various mucous membranes of the body will simultaneously occur — from 
the mucous membrane of the nose, perhaps from the bronchial mucous 
membrane, and sometimes large ecchymotic spots may be seen upon the 
mucous surfaces of the mouth and throat. Haematuria, conjunctival 
hemorrhages, melaena, hsematemesis, haemoptysis, bleedings from the gums, 
and particularly epistaxis are met with. It is rare for this form of 
small-pox to reach the stage of suppuration, for before this stage is reached 
patients die. During the initial stage of this variety of small-pox, the 
constitutional symptoms do not differ from those which attend the de- 
velopment of the other forms of this disease. It is impossible, from their 
character and intensity, to predict, with any degree of certainty, the subse- 
quent development of hemorrhagic variola. It has been said that the pains 
in the back and limbs are more severe ; but these are not characteristic. 
Frequently the fever of invasion is exceedingly violent, while during the 
eruptive period, and during the entire subsequent course of the disease, the 
temperature is comparatively low. In cases in which extensive hemorrhages 
have occurred, the temperature often falls below the normal, while the 
pulse ranges from 140 to 160, and is exceedingly feeble in character. - Only 
when comparatively few of the vesicles become hemorrhagic does the case 
terminate in recovery. 

Differential Diagnosis. — The first question that arises is : how early can 
small-pox be recognized ? One who has seen very many cases of the disease 
may be able to reach a diagnosis on the third day, that is, the first day of 
the eruption, although at that time there is nothing characteristic about 
the eruption or the ushering-in symptoms. It is, however, better and safer 
to wait until the second or third day of the eruption before making a posi- 
tive diagnosis, for there is little to be feared from infection until the vesi- 
cles are fully formed. 

The eruption of measles, in its early stages, is liable to be taken for 
small-pox. If one defers making the diagnosis until the vesicles are fully 
developed, no such mistake will be made. In measles there is coryza, a 
cough, sneezing, redness and suffusion of the eyes. These symptoms are 
not present in small-pox. The range of temperature is two to three 
degrees higher in small-pox than in measles. In these respects the two 
diseases differ sufficiently to enable a differential diagnosis to be made. 
Again, if one waits until the vesicles become umbilicated, it will be impos- 
sible that a mistake in diagnosis should be made. 



SMALL-POX. 



795 



During the period of initial fever it is possible to mistake small-pox for 
typhus fever. In both diseases there may be delirium, pain in the head, 
vertigo, high temperature, and evidence of great disturbance of the nervous 
system. There is no system which will enable a positive diagnosis to be 
made during the very early period of the disease. Of course, if typhus fe- 
ver is prevailing, or if small-pox is prevailing, and the patient has been ex- 
posed to either one of these contagions, one will be able to make a diag- 
nosis without difficulty. Usually there is greater loss of muscular power 
in typhus fever than in small-pox, but this symptom is not always well 
marked. By the third day, the appearance of the eruption upon the face, 
where it is first seen, settles the question of diagnosis. The eruption of ty- 
phus fever is first seen upon the abdomen, and may extend over the whole 
body without appearing on the face. It rarely appears before the fifth day 
of the fever. Therefore, the differential diagnosis between small-pox and 
typhus fever can be readily made as soon as an eruption appears. The 
temperature falls as soon as the eruption occurs in small-pox, and does not 
in typhus. 

Meningitis is another disease which small-pox, in its initial stage, resem- 
bles. There is always considerable cerebral disturbance and a full, hard, 
bounding pulse in the initial stage of small-pox. Photophobia, intense 
pain in the head, nausea and vomiting may be present in both diseases. 
Unless it may be the expression of the. face, there is often no distinguish- 
ing mark between the two diseases in their early stages. In meningitis, 
there is usually a pale, anxious expression of countenance, whereas early in 
small-pox the face is flushed, and day by day the flush deepens until the 
eruption appears. The fever in meningitis is lower than in small-pox by 2° to 
3° F., the pulse is smaller, less compressible, and not as rapid as in variola ; 
and the vomiting is projectile in meningitis, while it is retching in char- 
acter in variola. On the appearance of the eruption, the differential diag- 
nosis between these two diseases is readily made. 

Prognosis. — The prognosis in any case of small-pox depends upon the 
amount of the eruption ; the more abundant the eruption, the greater the 
danger to life. The prognosis also depends upon the type of the disease. Un- 
less some complication arises, most cases of discrete small-pox recover ; while 
of confluent smail-pox nearly one-half the cases prove fatal. 1 The best record 
obtained in the small-pox hospital on Blackwell's Island was one death in 
every five cases. Only a very few cases of the hemorrhagic variety recov- 
ered, and when recovery did take place it was only reached after the patient 



1 In twenty years the " London Small-pox Hospital " gives the following definite statistics : 



No. Mortality. 

Patients admitted with small-pox 4,879 

A. With 1 vaccine scar 2,001 7 7-10 per cent. 

B. " 2 " scars 1,446 4 7-10 " " 

C. " 3 " " 518 1 9-10 " " 

D. " 4 or more scars 544 1-2 " " 

E. Said to have been vaccinated, but no scar visible 370 23 1-2 " " 



In the "London Small-pox Hospital " the mortality is: 4 per cent, of discrete, simple variola; 8 per cent 
of semi-confluent variola ; and 50 per cent, of confluent variola. 



79G 



ACUTE GENERAL DISEASES. 



had passed through an apparently fatal condition of coma. The ratio oi 
mortality is always lower at the end than at the beginning of an epidemic. 
The disease is more fatal in the summer than in the winter. 

The age of the patient greatly influences the prognosis. In infancy and 
old age the ratio of mortality reaches its maximum. Among adults the 
prognosis is worse in females than in males. In the intemperate the prog- 
nosis is always bad, for with this class of persons the disease is liable to 
assume a hemorrhagic type. The intemperate die in discrete small-pox 
when the temperate would almost certainly recover. In the overworked 
and badly-nourished the prognosis is bad. The robust and healthy pass 
through a severe type of the disease much more safely than those enfeebled 
by chronic disease. The severity of the fever of invasion is not a safe guide 
in prognosis. Sometimes a severe initial stage precedes a mild form of the 
disease ; sometimes patients with this disease pass into a state of complete 
unconsciousness, remain in that condition for some time; then the erup- 
tion begins to change in color, and finally recovery takes place. Such 
cases, however, are exceptional. However well-developed the eruption 
may be, or however well-filled the vesicles, it is to be remembered that the 
eighth day is the commencement of the suppurative fever, which is the 
period of the greatest danger. Upon this day the patient may pass into a 
state of collapse, the result of the depressing influence upon the nervous 
system produced by the large extent of surface involved in the suppurative 
process. In most cases in which patients do not die until the second week 
of the disease, the fatal result is due to exhaustion, although death may 
occur from complications. Usually they pass into a typhoid condition, the 
result of the excessive drain upon the system by the suppurative process. 

Pregnancy is a bad complicating condition ; in the confluent, the ab- 
sorption that is so liable to occur is likely to be attended by fatal bleeding. 
The most frequent complications which cause death are those which occur 
in the throat and air-passages. In somo instances swelling of the glands 
of the neck and mucous membrane of the throat takes place to such an 
extent as to seriously interfere with deglutition and respiration. When 
this occurs it becomes an element of great danger, and materially affects 
the prognosis. The tongue may become swollen to such an extent that the 
patient will be unable to protrude it, or, being able to protrude it, will not 
be able to retract it. Under such circumstances deglutition is almost im- 
possible. There may be laryngeal ulcers, and ulcers occurring in the 
trachea and in the bronchial tubes. 1 Whenever, in the course of the 
disease, the urine becomes scanty and hi^h-colored, but especially when it 
becomes so at the commencement of the secondary fever, it is certain that 
kidney complication exists. Under these circumstances the patient may 

1 Keratitis, choroiditis, iritis, conjunctivitis, inflammation of the middle ear, ulcers in the nose, acute 
arthritis (of the large joints), pericarditis, ulcerative endocarditis, pycemia, and erysipelas — these are all 
occasional complications. Diphtheria is a common complication of hemorrhagic variola. Cerebral hemor- 
rhageisnot an infrequent complication of small-pox; aphakia may also occur, and thrombosis of the 
basiliar artery may induce a "dementia-like" condition. (Collie.) Boils, abscesses, and phlegmons of 
the skin are frequent sequelae of small-pox. Blindness and deafness also not infrequently follow, as also 
paralysis of the bladder and paraplegia, due (according to Westphal) to acute disseminated myelitis thai 
has complicated the fever. 



SMALL-POX. 



797 



pass into a condition in which convulsions will be developed, and coma 
and death ensue. 

Treatment. — In vaccination, properly performed, we undoubtedly possess 
a means by which we may prevent one from contracting the disease when 
exposed to its infection. But the question arises, have we any power to 
arrest the development or mitigate the severity of the disease after the 
initial fever is established ? No reliable affirmative answer has been given 
to this question. It has been proposed to accomplish this by blood-letting, 
emetics, diaphoretics, purgatives, cold baths, and more recently by the 
subcutaneous injection of the vaccine virus. All of these means have been 
tested, and have failed to accomplish the desired result. The assertion 
that large doses of quinine, given during the stage of invasion, will shorten 
the duration and modify the course of the disease, is verified only by the 
experience of its author (Stiemer)., Quite recently it has been claimed 
that carbolic and salicylic acids destroy the septic poison of the variola, and 
thus shorten and modify the course. My own experience as regards their 
use has not been sufficient to decide the question, and I am unable to find 
any statistics which sustain such an assertion. 1 

During the fever of invasion all that can be done is to treat special symp- 
toms. Place the patient in bed in a large well-ventilated apartment ; if 
possible, keep the temperature of the room below 60° F. I remember that, 
in the Small-pox Hospital, those patients did best who were placed in bar- 
racks, which were so open, that frequently, during the winter months, 
when I made my morning visit, I would find little snow-drifts on the floor 
between the beds. When the body temperature ranges as high as 107° F. 
or 108° F., it is recommended to employ cold to the surface, and to give 
antipyretic doses of quinine to reduce the temperature. If the headache 
is severe and the face flushed, iced compresses and ice-bags to the head will 
usually afford relief. If the vomiting is severe and constant, iced carbonic 
acid water may be given, and if the vomiting is attended by great restless- 
ness, hypodermic injections of morphine are indicated. Administer such 
food as can be readily assimilated. I have found nothing better than iced 
milk and seltzer water. If the bowels are constipated, it is well to relieve 
them by enemata of cold water. In those cases in which the eruption is 
tardy in making its appearance, and the temperature is higher, sometimes, 
if the patient is kept in a warm bath for fifteen or twenty minutes, the de- 
velopment of the eruption is hastened. * 

When the eruption has appeared, the measures to be employed will vary 
with the character of the eruption. The milder forms of discrete variola 
require no interference. In the severer forms the attendant symptoms 
will decide the means to be employed. Sooner or later, sometimes very 
early in the severer forms of the disease, the patient will be found sinking 
from the depressing effects either of the small-pox poison or of the sup- 
purative process which is taking place upon the surface of the body. 
Under such circumstances stimulants are indicated. There is no question 



1 Zulzer (one of the authors in Ziemssen) states that xylol given internally coagulates the contents of 
the pustules and cuts short their development. 



798 



ACUTE GENERAL DISEASES. 



but that the free use of stimulants for a few days, just at the period of 
suppuration, in very many cases does much to save life. At this time the 
patient has a dry tongue, a frequent, feeble pulse, blue lips and finger ends, 
giving evidence that he is rapidly passing into a state resembling that met 
with in the later stages of typhoid fever. Active delirium is frequently 
present ; the patient insists upon getting out of bed. Under these circum- 
stances, life will often be saved by the judicious use of stimulants. If the 
delirium is excessive, hypodermics of morphine may be combined with 
the administration of stimulants. 

During the stage of desiccation, warm baths employed every day or every 
other day give great comfort, and assist in the removal of the crust. After 
the baths the surface should be freely oiled. Complications will be treated 
according to the general rules which govern their treatment. If abscesses oc- 
cur in the subcutaneous tissue, they should be freely opened at once. We are 
powerless when we come to deal with the hemorrhagic form of small-pox. 
Although tonics and stimulants have been highly recommended, they do 
little good. Transfusion has been proposed and practised with no definite 
results. If the mouth and pharynx are very much involved, and there is 
difficulty in deglutition, ice-cold carbonated water with a weak solution of 
the muriated tincture of iron used as a gargle will often give great relief. 
Sometimes the stronger antiseptic gargles, such as carbolic acid and the 
permanganate of potash, will be of service. 

There is still one point in the treatment of small-pox which is deserving 
of attention, and that is, what means may be employed to prevent the 
pitting, especially upon the face, which is so frequent a result. The erup- 
tion first makes its appearance upon the face; there it is usually most 
abundant, and is most liable to be followed by pitting, and there it passes 
more quickly through all its stages than upon any other part of the body. 
In order to prevent pitting it has been proposed by some to exclude 
light and air from the surface covered by the eruption. For this purpose 
a great many substances have been employed, such as collodion, gutta- 
percha, certain forms of plaster, liquid paper, etc., etc. All these sub* 
stances are to be so applied as to form a mask for the face, which completely 
excludes light and air from the surface. 1 The pitting is due to the forma- 
tion of a slough, and the slough is seated in the areolar tissue ; if by any 
means you can so interfere with the inflammatory process as to prevent the 
formation of a slough, you will prevent the pitting. It was claimed by 
those who advanced the theory that excluding light and air prevented the 
pitting, and that it did this by preventing the occurrence of sloughing. 2 

1 Gold leaf, mild mercurial ointments, bismuth, chalk and sweet-oil, linseed meal poultices, collo- 
dion, carbolic acid and white lead paint have all been extensively used. 

2 When I had charge of so many small-pox patients, I took pains to test all those applications whict 
at that time had been and are still recommended for the purpose, and I satisfied myself that about 
the same results were obtained in the use of every remedy, and in no case was pitting prevented. Certain 
patients were much more scarred than others, but that was the natural result of the disease. Some have 
Proposed to coagulate the serum in each vesicle by nitrate of silver, and to paint each papule with iodine, 
and so arrest the inflammatory process and prevent pitting. But the use of these means has been 



INOCULATION AND VACCINATION. 



799 



INOCULATION AND VACCINATION. 

There are two recognized methods of protection against the infection of 
small-pox : inoculation and vaccination. Inoculation was first introduced 
into England by Lady Montague, who first practised it upon her own child. 1 
Subsequently it was quite generally practised throughout Great Britain. 
Pus from a small-pox pustule was introduced beneath the epidermis of one 
who had been prepared by diet and general hygienic measures for the safe 
development of the disease. It was claimed that the disease resulting from 
inoculation was a modified small-pox, differing from the original disease in 
that it ran its course more rapidly, was attended by few pustules, perhaps 
no more than twenty or thirty, and was said to rarely terminate fatally, the 
ratio of mortality being about one in one hundred. Those who were inocu- 
lated were as fully protected from small-pox as those who had the disease 
in the ordinary manner. The disease developed by inoculation passed 
through the regular stages of small-pox. 

Early in 1776 Edward Jenner observed that in some of the northern coun- 
ties of England persons employed in dairies, who suffered from a certain 
form of ulcer upon their hands, did not contract small-pox when exposed 
to it. 2 He also found that these ulcers upon the hands resembled pustules 
found upon the udder of the cow, and seemed to have been caused by con- 
tact with them. Jenner made a thorough investigation of the subject, and 
arrived at conclusions sufficiently satisfactory to himself to warrant the ex- 
periment of taking matter from one of these pustules found upon the udder 
of the cow and introducing it into the arm of the individual who was sup- 
posed to be unprotected from the contagion of small-pox. After the sore 
upon the arm had run its course, he exposed the individual to the infec- 
tion of small-pox, and in this way he established its protecting power. In 
1796 he made his first vaccination on man. In 1798 he published his first 
paper on the subject. 3 Vaccination was introduced into this country in 
the year 1799, by Waterhouse of Boston, and very soon became the practice 
of the profession. In 1800 it was first practised in France. At the pres- 

attended by the same unsatisfactory results. The only means which I found of certain value was a simple 
cold-water dressing applied over the face, after having ruptured each vesicle before it became a pustule. 
In this way, I was able to diminish the intensity and extent of the inflammation. This plan of treatment 
I adopted in twenty cases of confluent small-pox, and it not only gave the patients very great comfort, re- 
lieving them to a certain extent from the intense itching, thus avoiding rupture of the vesicles by scratch- 
ing, but not in a single case that recovered was there bad pitting. In the treatment of small-pox, the pre- 
vention of pitting is of greatest importance to certain patients, especially young unmarried females. 

1 In 1717 Lady Montague, writing from Adrianople, in Turkey, where the practice of inoculation was in 
vogue, says : " They take the small-pox here for diversion ; I have tried it on my dear little son ; I am 
going to brinir this useful invention into fashion in England." In 1718 it did become the fashion. 

2 In 1771 a Holstein schoolmaster vaccinated three pupils, and in 1774 an English farmer vaccinated his 
wife because of his belief in the power of bovine virus as seen in his dairymaids. 

3 During six years no member of the profession ever received more anathemas or more scurrilous abuse 
than Jenner. He was attacked by the leading physicians and surgeons of Great Britain, and persecution 
and ridicule so followed him that placards with caricatures of Jenner were posted throughout the streets 
of London and the priivlpal towns of Great Britain ; Jenner kept steadily at work and repeated his ex- 
periments, until he became fully convinced that by vaccination perfect, protection could be obtained 
against small-pox. Within the short space of six years Jenner compelled the profession to admit hie state- 
ments and adopt his practice, and within the five or six years following its first recognition, the practice of 
vaccination became generally recognized and practised. 



800 



ACUTE GEKERAL DISEASES. 



ent time there is no question among the intelligent portion of the pro- 
fession but that vaccination, properly performed, is a perfect protection 
against the infection of small-pox ; if persons contract small-pox after they 
have been vaccinated, then it has not been properly performed. 

There are two methods of performing vaccination. One method is to 
take the virus directly from the cow ; this is called bovine virus ; the other 
method is to take the virus from a vesicle developed upon the human body, — 
perhaps a vesicle removed from the original by several vaccinations, — this 
is called humanized virus. To-day good humanized virus is warmly advo- 
cated ; first, because it is more successful (98 per cent.) than bovine virus 
(only 70 per cent.) ; and secondly, because it is a surer safeguard. Jenner 
found that there were several pustules developed on the udder of the cow 
which closely resembled each other, but that only one contained the virus 
which afforded protection from small-pox. In obtaining bovine virus it is 
of the greatest importance that the genuine vesicle be selected. In order 
to make the selection, it is necessary one should be familiar with the pe- 
culiarities of each variety. If humanized virus is used, there is danger of 
introducing into the system the infection of other diseases. I have in my 
possession facts which prove beyond the possibility of a doubt that syphilis 
can be conveyed from one person to another by vaccination. Cutaneous 
eruptions may also be conveyed by humanized vaccine virus, which cause 
the development of very extensive and serious cutaneous diseases. Again, 
if any chronic or acute skin disease exist at the time the vaccine vesicle is 
running its course the protective power of the vaccination will be altogether 
destroyed or very greatly modified. 1 The vaccine virus is usually intro- 
duced by scarifying the surface so as to redden it, scarcely drawing blood ; 
then the surface of the quill containing the virus is applied to the scarified 
part, or the lymph is conveyed from one to the other by direct transmis- 
sion. 

Any irregularity in the development of the vesicle destroys in a greater 
or less degree its protecting power. When an individual has been once 
vaccinated, a second vaccination is liable to run an irregular course. 

A primary vaccination, such as the first vaccination of a child, should 
pass through the following regular stages, and if it does not it fails to give 
protection : upon the third day after the introduction of the virus there 
will be noticed at the point where it was introduced a little red spot, — a 
papular elevation. By the fourth day this little red spot will be occupied 
by a bluish- white vesicle, and at the commencement of the fifth day there 



1 In obtaining vaccine virus for use, both the bovine and the humanized virus should be taken from the 
vesicle on the eighth day. The lymph should be taken from the vesicle before the inflammatory process 
has commenced which is to change it into a pustule. Jenner's " Golden Rule " was, any vesicle which 
manifests an areola must be discarded in the matter of withdrawing lymph. A few years ago it was the com- 
mon practice in this city to use the vaccine crusts, but this practice has fallen almost entirely into disuse 
because of the great danger of thereby transmitting other diseases. J prefer bovine virus when it is possible 
to obtain it. If compelled to use the humanized virus, use the lymph. The vesicles must be punctured in 
such a manner that the lymph cannot be contaminated by the blood ; this is best done by introducing the 
instrument parallel with the arm. The vesicle must be tapped in several places. The lymph which spon- 
taneously flows from such a puncture can be preserved upon the convex surface of a piece of quill, and 
conveyed from one individual to another. Vaccine virus secured from the human arm in this manner is 
less liable than any other form of humanized virus to do permanent harm to the vaccinated individual. 



INOCULATION AND VACCINATION. 



801 



will appear around the vesicle a little yellow margin. This vesicle goes 
on increasing in .size up to the eighth day, when it will become umbilicated 
and there will appear around it a distinct areola ; about the seventh day 
there has been a trifling areola present ; on the eighth or ninth day it be- 
comes very distinct. Now a change is to take place in the vesicle, and by 
the next day it will be noticed that the areola has extended, perhaps so as 
to measure an inch in diameter ; this areola goes on extending itself 
through the ninth, tenth and eleventh days, when it will have reached its 
maximum extent, which may be one or two inches from the vesicle in all 
directions. It is now a deep red color. The part over which the areola 
has spread is more or less elevated, the arm is considerably swollen and 
painful, and the adjacent glands more or less enlarged and tender to the 
touch. The extent of the enlargement of the gland adjacent to the vac- 
cine vesicle, — the axillary gland, if the vesicle is upon the arm, the inguinal, 
if it is upon the thigh, — varies considerably in different persons. 1 In some 
it is very great, in others it is scarcely noticeable. The maximum degree of 
inflammation in the vesicle has now been attained, and there is a -distinct 
infiltration of the tissues about it. 

On the twelfth or thirteenth day the pustule ruptures, and the contents 
escape. The rupture belongs to the natural course of the vaccine vesicles, 
and is independent of mechanical violence. From this time the inflamed 
areola becomes less and less distinct, and by the fourteenth or fifteenth day 
the crust has assumed a dark, brownish appearance, which goes on deep- 
ening until on the seventeenth day a deep-brown crust is formed having a 
central depression and no areola of inflammation. It may be attached 
to the surface only in one or two places, and can be readily removed. If 
permitted to remain, it usually falls off on the eighteenth to the twenty- 
first day. This is the course pursued by a perfect vaccine vesicle. The 
shape and size of the crust will correspond to the shape and size of the 
vesicle. If the eighth day a pustule is formed instead of a vesicle, it is 
evident that the regular development of the vesicle has been disturbed, and 
that it will not afford complete protection. 

The inflammatory process around the vesicle is usually more active when 
the dovine vines is used, than when the humanized virus is introduced, and 
there is more constitutional disturbance. Ordinarily, during the develop- 
ment of the vaccine vesicle and pustule, there is but little constitutional 
disturbance ; this is usually self-limiting, and not sufficiently severe to 
require treatment. In children, eruptions, transitory in character, are 
liable to occur about the eighth or tenth day. About the eighth or ninth 
day the person vaccinated may feel a little chilly, and have severe headache ; 
in most cases there is a slight rise in temperature. 

The regular course of the vaccine vesicle may be interfered with by the 
occurrence of an erysipelatous inflammation, and if such an inflammation 
does occur during the course of its development, it entirely destroys the 
protecting power of the vaccination. Again, if a large quantity of pus has 
been discharged, and healing of the ulcer does not take place for two or 

1 Tne axillary swelling is sometimes so intense that abscess results.— Quairi's Diet. 
51 



802 



ACUTE GENERAL DISEASES. 



three months, it is probable that something besides genuine vaccine virus 
has been introduced into the arm, and that the vaccination is not pro- 
tective. As I have already stated, the presence of a vesicular eruption upon 
the surface at the time vaccination is performed will interfere with its de- 
velopment, therefore I would advise never to vaccinate one who has an ec- 
zematous eruption upon any part of the body, unless he has been exposed 
to the contagion of small-pox, for it is very probable that the vaccination 
will not be a protective one. It is better never to vaccinate a person having 
any form of skin disease, especially if the eruption is vesicular in character. 
The best time for the first performance of vaccination is in infancy, between 
the third and fifth months. 

Revaccination should be performed after puberty, and always after or 
preceding a new exposure to the contagion of small-pox, for the period dur- 
ing which revaccination will afford complete protection is not the same in 
every individual. In some cases a single vaccination will afford complete 
protection for a lifetime. In other cases it is necessary to frequently repeat 
the vaccination, perhaps every two years, in order to secure the desired 
protection. 1 

VARIOLOID. 



During every epidemic of small-pox there is a certain number of cases 
concerning which there will be doubt as to whether they are cases of variola 
or varioloid. Certain persons who have never been vaccinated may, through 
a naturally slight susceptibility to the infection of small-pox, have so mild a 
form of variola that it is difficult to distinguish it from varioloid. 

Varioloid differs from small-pox in the rapid development and decline of 
the symptoms, in the small number of the pustules, and in the short time 
required for the formation and separation of the crusts. The entire period 

of the eruptive stage often does not 



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m size 



last more than a week. Rarely are 
cicatrices or pits left after the erup- 
tion. In varioloid the period of in- 
cubation is about one-half as long as 
in variola, hence the onset of the 
graver disease may be anticipated by 
vaccinating one who is known to 
have been exposed, and who, other- 
wise, would go on and have the un- 
modified disease. 

In varioloid and variola the pus- 
tules pass through similar stages. We 
first have the small red spot, then 
vesicles form, often within twelve 
hours after the appearance of the erup- 
iton. These vesicles rapidly increase 
sometimes they are umbilicated ; by the end of the third day their 



Fig. 167. 

Temperature Record in a case of Varioloid 



1 The best plan is to vaccinate at intervals until the individual has four good scars. 



CHICKEN-POX. 



803 



contents sometimes become purulent, without any tumefaction of the sur- 
rounding skin. Many vesicles abort ; they do not become pustules. On 
the fifth day desiccation commences, which is often complete by the seventh 
day. The majority of the pustules simply dry up, without previously 
bursting, and form brown crusts which are thinner and smaller than those 
of variola. In varioloid there is no regular period of development as in 
variola. In variola there is the period of eruption, during which the vesi- 
cle is perfected ; this is succeeded by the period of suppuration, then by 
desiccation, about fourteen days being required to complete the process ; 
while in varioloid the course of the eruption is irregular, and is usually 
completed within one week. Secondary fever is slight or absent. Again, 
in varioloid there is but little constitutional disturbance after the appear- 
ance of the eruption. By the end of the first or commencement of the sec 
ond day the temperature is usually normal. It resembles variola in the 
severity of the symptoms during the period of invasion, but as soon as the 
eruption appears there is an entire cessation of all the active febrile symp- 
toms. During the period of invasion varioloid may be said very closely to 
resemble variola. When an unprotected individual is exposed to varioloid, 
the most severe confluent small-pox may be the result. This fact proves 
that varioloid is a modified form of small-pox. Varioloid is small-pox hav- 
ing a shorter duration and a milder course than usual. 1 

Prognosis.— Usually the prognosis is good. The rapidity with which the 
vesicles are developed, their shorter duration, the subsidence of the fever, 
and the appearance of the eruption, together with the usual duration of an 
attack, are sufficient to distinguish it from variola. 

Treatment. — The treatment for varioloid is the same as for a mild or mod- 
ified form of small-pox. The patient should be placed in a large, well- 
ventilated room, and quarantined the same as though suffering from vari- 
ola. If the form of invasion is severe, saline cathartics may be adminis- 
tered. When delirium is present, and the pain in the back is very severe, 
the moderate use of opium is admissible. As soon as the eruptive period 
of varioloid is reached, no further treatment is required ; the patient passes 
on to a rapid and complete convalescence. 

CHICKEN-POX. 

{Varicella.) 

Varicella is an acute contagious febrile disease accompanied by a vesicu- 
lar eruption, which chiefly affects children. It has been called " spurious 
variola," swine-pox, etc., etc. 

Morbid Anatomy. — The only lesion of this disease is the eruption, which 
consists of small slightly elevated rose-spots, varying in number from twenty- 
five to two hundred, which in from ten to twenty-four hours become small 

s It may be said that we modify small-pox by inoculation. We do not : we only modify it? intensity. 
There is the same regular development of the disease after inoculation that we have in the ordinary form 
of small-pox ; while by vaccination we not only lessen the severity of the disease but we are able to so 
modify the stages of its development as to shorten its duration. 



804 



ACUTE GENERAL DISEASES. 



vesicles with clear contents. They vary in size from a pin's head to a pea. 
They are usually discrete, but may run together and form bullae three- 
fourths to two inches in diameter. They rest on a hyperamric zone of skin. 
In many cases the areola is absent. As the vesicles enlarge, they become 
globular or ovoid in shape and their contents are translucent, glistening 
and opalescent, never acid as in sudamina. Sometimes the vesicles are di- 
vided into compartments. On the third day pustulation of a few vesicles 
may occur. On the fourth day the vesicles commence to dry up ; on the 
sixth crusts are formed. One crop occupies rarely more than six days, and 
as a second crop appears or starts also on the second and third day of the 
first, crop, the whole number of days of the eruption is from seven to nine. 

According to the shape of the vesicles, varicella is called lenticular, glob- 
ular, conoidal, 1 etc. Pitting rarely occurs ; should cicatrices remain, they 
disappear in two years. 

Etiology. — Opinions are still divided as to the identity of variola and vari- 
cella. Hebra claims that there is one poison for the two diseases. Senator, 
Thomas, and others regard it as a specific disease. It occurs sporadically 
and epidemically. Inoculation has given negative results. The period of 
incubation varies from eight to seventeen days. 

Symptoms. — Twenty-four hours preceding the eruption there is usually 
lassitude and a feeling of malaise. The eruption appears first on the back 
or cheek, and then on the face or scalp. It spreads irregularly to the abdo- 
men and extremities. About the second day vesicles may appear upon the 
tongue, lips, cheeks, palate, and on the mucous membrane of the genitals. 
On the second day after the first crop of the eruption a new crop appears,- 
and in many cases there is a third crop on the following day. The tem- 
perature rarely rises over 100° or 101° F. 

Differential Diagnosis. — The points of differential diagnosis between 
varicella and variola are as follows : — varicella runs rapidly through its 
stages ; small-pox has three distinct periods — the papular, the vesicular, 
and the pustular. The eruption of varicella is complete by the third, while 
the eruption of variola is never complete until the ninth day. In both 
natural and modified small-pox prodromata occur before the eruption ap- 
pears, and then the temperature falls ; in varicella there are no prodromata, 
and a rise in temperature follows the eruption. Varicella spreads irregu- 
larly. Small-pox vesicles are umbilicated and multilocular ; those of 
chicken-pox are globular or pointed, unicellular, and collapse on pressure. 
Small-pox is inoculable, varicella is not. 2 The stage of incubation is much 
longer in chicken-pox than in small-pox, and vaccination does not protect 
against it ; and during its progress a child can be successfully vaccinated. 
It is very doubtful whether varicella ever attacks the same individual twice. 

Prognosis. — The prognosis is always good. 

Treatment. — The treatment is rest in bed, cleanliness, a non-stimulating 
diet, and cooling drinks. 

1 Conoidal is also called swine- pox. 

2 SmalUpox and vaccinia are often early followed in the same individual, say within two or three 
years, by chicken-pox, or vice versa. Chicken-pox, vaccinia, and srnall-pox have been known to follow 
in immediate succession in the same individual. 



SCARLET FEVER. 



805 



SCARLET FEVER. 

Scarlet fever or scarlatina is a contagious disease accompanied by an 
inflammation of the tegumentary investment of the entire body, both cu- 
taneous and mucous. This name has been given on account of the bright- 
red appearance of its eruptions. It is a disease of childhood, but may 
occur at any age. 

Its development and course are divided into three periods : first, the 
period of invasion, which lasts {from twenty-four to forty-eight hours ; 
second, the period of eruption, which lasts from five to seven days ; third, 
the period of desquamation, during which the entire epithelial surface is 
removed. Some classify the disease according to its severity ; others ac- 
cording to the prominent organs of the body which are involved ; others 
according to the prominent phenomena which attend its development. 
The more common classification, and certainly the simplest, is that which 
divides it into scarlatina simplex, scarlatina anginosa, and scarlatina 
maligna. I shall adopt this classification. 

Morbid Anatomy. — It has no characteristic anatomical lesions, except 
those which occur in the skin and mucous membranes. The eruption is 
its distinguishing lesion ; it makes its appearance on the second or third 
clay after the commencement of the febrile symptoms. At that time it con- 
sists of very numerous and closely aggregated points about the size of a 
pin's head ; between these the skin is of its natural color. In typical cases, 
these points are equally distributed over the entire body, except the face. 
These red spots are usually circular in shape, slightly elevated, above the 
surrounding skin, and so close to each other that they give a confluent red- 
ness to the entire surface. In mild cases the red points remain isolated, 
and do not become confluent ; as the eruption develops, these red points 
unite. In severe cases the skin becomes turgid and swollen, and presents 
a uniformly red and glistening appearance. In malignant cases the hyper- 
emia of the skin is often accompanied by more or less extensive hemor- 
rhages, causing petechia? and extensive ecchymosis. The redness of the 
eruption gradually increases up to a certain point, which is not the same 
in all cases, then remains unchanged for twelve or twenty-four hours, after 
which time the redness slowly passes away. During the course of the dis- 
ease, the color often changes with the exacerbations and remissions of the 
fever. As a rule, the degree of redness depends upon the intensity of the 
fever, and may vary from a pale red to a deep scarlet. If the respiration 
becomes impeded, the eruption assumes a bluish-red hue. During the first 
forty-eight hours after the appearance of the eruption, when the respiration 
is unimpeded, the redness completely disappears under firm pressure, and 
reappears as soon as the pressure is removed. After this period, the pressed 
point does not entirely lose its red color. In a certain proportion of cases, 
the eruption only appears in spots on the surface of the body, on the trunk, 
or face, or about the flexor surfaces of the joints. "When it only appears on 
the face, the diagnosis is difficult. 



806 



ACUTE GENERAL DISEASES. 



In addition to the cutaneous hyperemia which gives the redness to the 
surface, there is more or less serous and lymphoid exudation into the " rete 
Malpighii," which is followed, on the decline of the redness of the surface, 
by an abundant epidermic exfoliation. Blood extravasations into the sweat- 
glands often occur. The exfoliation marks the period of desquamation, 
which may immediately follow the decline of the redness or may be delayed 
a few days. This is due to an excessive production of newly-formed epi- 
dermis, and the process may last only a few days, or if the eruption is abun- 
dant it may continue for several weeks, and may recur a second time on the 
same surface. After the desquamation has ceased, it does not reappear, ex- 
cept in cases of relapse ; these are followed by renewed and sometimes by a 
very complete desquamation. Desquamation has not infrequently occurred 
on skin that has never been the seat of the eruption. 

In connection with these cutaneous changes the scarlatina poison causes 
changes in the mucous membrane of the mouth and throat, the most fre- 
quent of which is catarrhal pharyngitis, which at first gives to the mucous 
surface of the tonsils and pharynx a red, swollen, and dry appearance. After 
a little time, these mucous surfaces become covered with a tenacious mucus. 
Upon the reddened mucous membrane small elevations arise, like the smaller 
follicles in an ordinary catarrh. In mild cases, all these changes disappear 
in a few days ; in the severer cases, the mucous surface assumes a dark, 
livid color, the parts become more or less oedematous, and are covered by 
an abundant secretion. Follicular ulcers also form. The oedema may be 
so extensive as to render deglutition difficult ; the tonsils are often so 
swollen that they touch each other. 

Besides the redness and oedema of the mucous membrane of the mouth 
and throat, there is often inflammation of the parotid and sublingual 
glands as well as of the connective-tissue of the neck. This glandular in- 
flammation may end in resolution, but often it terminates in suppurative 
or diffused necrosis. It may give rise to extensive gangrene of the tonsils 
and adjacent soft parts ; sometimes it is followed by extensive abscesses 
and destruction of the cellular tissue about the neck ; the skin in the region 
may slough, and not infrequently fatal hemorrhage results from the de- 
struction of small vessels ; or the whole region may lie open as if dissected 
out. 

Diphtheria is so often a complication of scarlatina anginosa, that it has 
been assumed that there is some necessary relation between the two dis- 
eases. 1 Yet diphtheria is as frequently met with in the mild as in the 
severe types of scarlatina, and occurs in every stage of the disease ; it is 
often present during the period of incubation, so that the symptoms of the 
two diseases appear simultaneously. Again, it is met with during the 
period of convalescence. In some instances, scarlatina seems to complicate 
diphtheria. 

In a mild form of scarlet fever, when the disease runs a regular course, 
the nasal mucous membrane is usually pale, and its secretion is not in- 

1 Hubner states that the pseudo membranes are much thinner in scarlatinal than in ordinary diphtheria, 
and that in the former, fibrin is found between the epithelia and in the mucous and submucous connective- 

t issue. 



SCARLET FEVEE. 



807 



creased. When the disease is severe, the nasal mucous membrane becomes 
secondarily, never primarily, involved. This is the result of a catarrhal 
affection of the throat. It is a purulent catarrh of the posterior nares, 
which gradually extends to the anterior nares, and gives rise to a very 
troublesome form of coryza. During the eruptive period of scarlatina, 
affections of the ear frequently occur in connection with those of the throat. 
Usually these have their seat in the middle ear, pus being the product. 
They are always tedious and may become chronic. The eye maybe involved; 
keratitis and ulcers are not uncommon. 

Next to the skin and mucous surfaces, the kidneys are the organs most 
frequently affected in this disease. There is no question but that, in a cer- 
tain proportion of cases, recovery takes place without any kidney lesions ; 
but these are the exceptions and not the rule. In some epidemics the 
scarlatina poison induces a so-called " croupous" inflammation of the urin- 
iferous tubules. The tubules of the cortical substance of the kidneys are 
most extensively affected ; the morbid processes commencing at the Mal- 
pighian tufts 1 follow the course of the convoluted tubules. If the tubules 
are only slightly affected there will be no symptoms except a slight albu- 
minuria. The kidney changes are rarely well marked before the second or 
third week of the disease, and usually terminate in complete recovery. The 
character and extent of these kidney changes vary in different epidemics. 
During some epidemics, the kidney changes are slight ; during other 
epidemics almost every case, whether mild or severe, will be attended- by 
extensive kidney lesions. 

At the post-mortem examination of one who has died of scarlet fever, 
there will be found more or less extensive congestion of the internal organs, 
the brain, liver, spleen, etc., but these congestions do not differ from those 
met with in other acute infectious diseases. The changes in the constitu- 
ents of the blood are such as to diminish its coagulating power. The Peyer- 
ian patches will often be found presenting the " shaven-beard appearance." 
There may be parenchymatous degeneration of the gastric tubules. 

Etiology. — The cause of scarlet fever is a contagion, which is transferable 
from the sick to the healthy. No specific microbe of the disease has as 
yet been discovered. It has been claimed that sporadic cases do occa- 
sionally occur ; but there is little doubt that if the history of every case 
of supposed spontaneous scarlet fever could be carefully taken, it would 
be found that at no place and at no time had the disease ever been of spon- 
taneous origin. It may be conveyed directly from the affected to the 
healthy by contact, through the atmosphere and by clothing which has been 
thoroughly saturated with the scarlet fever poison ; therefore it may be 
considered a portable disease. Animals that have been around those sick 
with scarlet fever may convey it. I recall an instance in which the scar- 
let fever poison was conveyed in this way : — For a number of days a little 
dog had been around children sick with scarlet fever, and by a single visit 



1 There is proliferation of epithelial nuclei in the glomeruli, distending them to twice their size, 
and thus compressing the vascular tuft. There is hyaline degeneration of the capillaries (Klein). 

2 Micrococci are found in the blood. 



808 



ACUTE GENERAL DISEASES. 



of the dog to the children of another family the disease was conveyed. 
There has been considerable discussion as to whether the disease can or 
cannot be conveyed in milk. This is possible. 1 

The infection of scarlatina is not so certain as that of measles or small- 
pox. "When one member of a family is sick with measles, usually every 
other member of that family who has not had measles will contract the dis- 
ease ; whereas one member of a family may be sick with scarlet fever and 
every other member may escape. Some seem to have a certain idiosyn- 
crasy, so that when they are brought in contact with the poison of scarlet 
fever they do not contract the disease. The poison which they receive into 
the system has power to produce some of the symptoms but has not power 
to fully develop the disease. 

Scarlet fever can be communicated from one individual to another by in- 
oculation. If some of the watery material or serum that can be obtained 
from the minute vesicles occasionally seen upon the surface of the body in 
connection with the scarlet fever eruption, be taken and introduced into 
the body of an individual who has not had scarlet fever, it will develop the 
disease. It has been proposed to inoculate those who have not had scarlet 
fever in the same manner as one would inoculate those who have not had 
small-pox, and, by so doing, produce a modification of the disease. But it 
has been found by experiment that those who have been inoculated for 
scarlet fever have suffered more severely than those who contracted the dis- 
ease by any of the common methods of contagion. There is no question 
but that the scarlet fever poison can also be introduced into the system 
through the respired air, but whether it can be taken into the system 
through the medium of food or fluids is still an unsettled question. 

A question of great practical importance is : if the disease can be con- 
veyed by clothing, is it safe for a physician to visit patients sick w T ith scar- 
let fever, and go from them directly to those who have not had the disease ? 
Unquestionably it is possible to so convey the disease, but in my own ex- 
perience I know of no case where it has been so conveyed. The clothing 
in order to be sufficiently impregnated with the poison to render it a means 
of contagion must be longer exposed than is the case when a physician 
makes a visit of ordinary length. Unquestionably, nurses who. have been 
with a scarlet fever patient for a number of days, and whose clothing has 
become filled with the poison, may carry the disease. These should change 
their clothing before they go from the sick to the healthy. The real nature 
of the scarlatina poison is undetermined. The period at which this disease 
is most infectious is probably the desquamative period, although some main- 
tain that it is most infectious during the eruptive period. 

An individual is almost certain never to have a second attack. 

The period of incubation varies from two to ten days, the average dura- 
tion being from three to five. It may be only three hours. Age has a 
great influence on individual predisposition. The greatest susceptibility 
to the influence of the poison exists between the second and seventh years : 



1 Qnain says : "Milk is a great medium for carrying scarlet fever, and cream, even more than milk, 
often carries it from sick to well." 



SCARLET FEVER. 



809 



it rapidly diminishes after the ninth year, so that adults, and especially the 
aged, have only a slight predisposition to the infection. Those who have just 
undergone surgical operations seem to be especially prone to contract the 
disease. Scarlet fever may be endemic or epidemic. No reason can be as- 
signed for its variations in type or severity. For years the type of fever 
which appears in a given locality will be exceedingly mild in character, 
when suddenly, without any assignable cause, a most malignant epidemic 
will prevail. Usually epidemics of scarlatina prevail in the autumn and 
spring. 1 

Symptoms. — The symptoms of scarlet fever vary with the type and with 
the severity of the fever. In moderately severe cases, before the appear- 
ance of the eruption, the patient will have a more or less severe headache, 
pain in the back and limbs, and at first coldness' of the surface. Epistaxis 
is not rare. In some cases rigors will occur, and perhaps distinct chills. 
In children convulsions and coma often occur. These ushering-in symp- 
toms are immediately followed by a sensation of intense heat, with great 
acceleration of the pulse, which at this time often beats 120 or 130 per 
minute. There will also be nausea and vomiting, frequently most per- 
sistent and distressing. Besides, there will be a rapid rise in temperature. 
It may reach 103° F. or 104° F., within a few hours. 

Within a period lasting from twelve to forty-eight hours, the average 
being thirty-six hours, the eruption makes its appearance, and the fever 
increases. The elevation in temperature is accompanied by restlessness, a 
burning sensation, perhaps delirium; the nausea and vomiting become 
more urgent, and now the papillae of the tongue become swollen, and the 
organ presents the appearance of a strawberry : — (the " strawberry tongue" 
of scarlet fever). This appearance is not commonly seen in the milder cases, 
but, as a rule, is present in all the severer cases. With the appearance 
of the eruption, all the symptoms, perhaps excepting the pain in the head, 
increase in severity. The urine, if it has been scanty, will now become 
more so, and may be nearly suppressed ; if it has been sufficiently abun- 
dant, not infrequently, as the eruption makes its appearance, it becomes 
scanty and high-colored. In some cases the disease is so mild that there 
is but little disturbance, except that caused by the eruption, the tempera- 
ture being not over 102° F. In other cases the disease is ushered m by 
violent nervous symptoms, such as delirium and coma, accompanied by 
extreme exhaustion, and the patient dies before the eruption makes its ap- 
pearance. In other words, the patient dies during the period of invasion, 
from the overwhelming of the nervous system with the scarlet fever poison. 

During the earlier stages of the disease the throat symptoms are quite 
characteristic. Adults and older children complain of a pricking sensation 
in the throat, and difficulty in deglutition ; the tonsils, uvula, and posterior 
wall of the pharynx are red and cedematous, and from their appearance, 
with the attendant symptoms, in most instances, one is able to very early 

1 Trojanowsky and Thomas describe a variety called '' recurrent," where two series of eruptions over- 
lap, as it were, and finally merge into one attack. But the latter's cases all occurring in marshy districts, 
he inclines to the view that the poisons of malaria and scarlatina were combined and perhaps modified by 
such an union. 



810 



ACUTE GENERAL DISEASES. 



decide that the case is one of commencing scarlatina. There are cases 
in which the throat symptoms are altogether absent at first, and do not 
come on until later in the disease. The symptoms which mark the de- 
velopment of this disease remain to be studied in detail. 

As already stated, the whole course of scarlet fever may conveniently be 
divided into three stages. First, the stage of invasion, or the febrile 
stage. Second, the stage of eruption. Third, the stage of desquamation. 

The duration of the stage of invasion varies with the type of the dis- 
ease. In most cases, it is from twelve to twenty-four hours ; it may be 
four or five days. Usually the onset is marked by chilliness and slight 
rigors, followed by a rapid rise in temperature. The skin becomes dry, the 
face flushed, and the pulse accelerated. At the same time there is slight 
soreness of the throat, the face appears red and dry, the neck is stiff, the 
eyes suffused, and there is some tenderness about the joints. Vomiting 
and thirst are prominent symptoms. The tongue is red at its tip and 
edges, the papillae are enlarged, and it presents the so-called strawberry 
appearance. Lassitude, pain in the head, aching of the limbs, and rest- 
lessness are generally present. There may be some delirium at night. 
Twenty-four hours after commencement of the fever of invasion, the 
eruption may make its appearance. The period which elapses between the 
exposure and the appearance of the eruption varies. In some cases the 
eruption is said to have appeared as early as twenty-four hours after ex- 
posure, while in others one or two weeks have elapsed after the exposure 
before the disease was developed. No definite statement in regard to the 
duration of the period between the exposure and the appearance of the 
eruption can be made. The eruption first makes its appearance upon the 
neck and upper portion of the chest, and is first seen as little red dots, 
varying in size from a line to a line and a half in diameter. These gradu- 
ally coalesce and the eruption extends over the entire surface of the body, 
perhaps on the face, and lastly it appears on the lower extremities. It 
presents its brightest appearance upon the evening of the fourth day. 
After the second day of the eruption, if not before, the entire surface 
will present a uniform redness, the color varying with the severity of the 
disease. 

In the milder cases one will have a bright rose-red eruption or rash, while 
in the severer types the eruption will assume an appearance resembling the 
deep-red color of the boiled lobster. The darker the eruption, the more se- 
vere the form of the disease and the greater the danger. When the erup- 
tion is fully developed, it will be noticed that the surface is somewhat ele- 
vated, the parts present a swollen appearance, the vessels of the skin seem 
to be congested, and there will be soreness of the throat more marked than 
in the febrile stage. Miliaria appear when the rash is most intense, and 
sudamina are common. 

Usually, vomiting is present at the commencement of the disease, but 
becomes more severe and a more marked symptom as the stage of eruption 
is ushered in ; if not present at the commencement, it is certain to make 
its appearance with the appearance of the eruption. The vomiting is pe- 



SCARLET FEVER. 



811 



culiar, not on account of the matters ejected, but the act of vomiting is 
projectile. in character. 

In scarlatina the condition of the throat depends upon the severity of the 
disease. In some cases there is simply a blush of redness over the posterior 
portion of the pharynx and uvula and anterior pillars of the soft palate. In 
other cases a general tumefaction and oedema of all the soft parts of the 
throat will be seen, and the tonsils will be the seat of a more or less intense 
parenchymatous inflammation, which gives rise to a swelling that encroaches 
more or less upon the pharynx. Again, ulcerative pharyngitis will occur, 
or upon the surface of the enlarged tonsils and swollen mucous membrane 
of the pharynx there may be an exudation, which will be more fully de- 
scribed hereafter. 

In this, the ordinary form of scarlatina, when it runs its ordinary course, 
there will not be much swelling of the glands about the neck, nor very much 
tumefaction of the soft tissues in the pharynx. On the morning of the fourth 
day, if the finger-end is drawn across the surface, a clear, well-defined line 
will be made, which will remain for some time. This distinct white line 
is a point of some importance in distinguishing scarlatina from roseola. 
Usually the eruption begins to fade upon the fourth day, and by the sixth 
day it has entirely disappeared, and desquamation has commenced. During* 
the time the eruption is developing, the temperature continues to rise until 
perhaps it has reached 106° F. or 107° F. In the meantime the pulse may 
increase to 120 or even 140, or ]3erhaps 150 beats per minute, and not in- 
frequently there is some delirium during this stage ; there may be also more 
or less stupor. There is an intense itching and burning upon the surface, 
and a great restlessness. 

Between the fifth and eighth days of the eruption, the temperature be- 
gins to decline, and at the same time 
the eruption fades. This fading of 
the eruption goes on rapidly, so that 
by the end of the eighth, certainly 
early on the ninth day, sometimes as 
early as the sixth day, it is no longer 
visible. With the disappearance of 
the rash, desquamation commences, 
and with this there will be a still 
more marked fall in temperature, and 
diminished frequency of the pulse, 
xlll the febrile symptoms disappear, all 
the throat symptoms subside, there is 
no longer any difficulty in deglutition, 
there is no more pain in the throat, 
no more swelling of the external 
glands, if previously it had existed. 

The period of desquamation lasts 
about two weeks, during which time 
there is the greatest danger of communicating the disease. At the end 



Day. 



104 



res 



102 



lor 



loo 



99 



1. 



^5 



7U- , 



I 



o. 



m 



7 



t?3 



Fig. 168. 

Temperature Record in a case of Scarlatina. 



812 



ACUTE GENERAL DISEASES. 



ot that period, if no complication occur, the patient is well. The fine 
scales which are so abundantly thrown off contain the specific poison, and 
they are so delicate that they are blown about with every breath, and car- 
ried in every current of air, and are in the most favorable condition to be 
taken into the system in the respired air. Some have maintained that the 
contagious period in this disease does not occur until the period of des- 
quamation. This statement is not sustained by clinical facts. The 
amount of the desquamation depends upon the intensity of the eruption. 
The skin has a dry feel before desquamation commences. Where the skin 
is thin the epidermis comes off in thin scales, "branny" desquamation. 
Where the skin is thick, as on the palms of the hands and the soles of the 
feet, it peels off in extensive patches, "scaly" desquamation. With the 
desquamation, the fever subsides more or less rapidly. The entire period 
occupied by a case of scarlet fever, when it runs its regular course, is from 
two to three weeks. 

Scarlet fever is liable to irregularities which it is important to consider. 
It is claimed by some that these irregularities depend upon the organ or 
set of organs primarily affected by the scarlet fever poison. They are 
rather due, to some peculiarity in the type of the disease, to the degree of 
poisoning, and in some instances to the particular set of organs that are 
involved in the different epidemics. In some epidemics even milder forms 
of the disease than have been described are seen. The attack may be so mild, 
and there may be so little fever that if the eruption was not present one 
would not be able to recognize the scarlet fever ; and even that may be so 
light that the stage of eruption and the stage of desquamation may pass 
unnoticed, and one may be scarcely able to decide whether the patient has 
or has not had an attack of scarlet fever. 

The most frequent irregularity in the manifestation of the disease is 
noticed in that class of cases where we have complications resulting from 
the overwhelming of the cerebro-spinal system with the scarlatina poison. 
This is due to some peculiarity of the poison, and is characteristic of cer- 
tain epidemics. In a large number of cases in the febrile stage, especially 
in young children, convulsions may occur, but they do not depend upon 
the peculiarity referred to. In the class of cases to which reference has 
been made, where complications arise from the overwhelming of the cerebro- 
spinal system with the scarlatina poison, from the very onset of the disease 
there seems to be a tendency to stupor and delirium, a peculiar restlessness, 
an apparent wandering, a picking at the bed-clothes, accompanied by a 
peculiarity in the appearance of the eruption, which may cause it to assume 
the boiled-lobster appearance, or even a darker hue. The eruption is slow 
in its development, and there is not that uniform redness over the entire 
body that is seen in ordinary cases ; it appears in patches, and with it there 
is exhibited a tendency to blueness of the finger-ends, indicating that there 
is acting upon the nervous system a poison which possesses the power of 
very greatly lowering the vitality of the patient. These symptoms pre- 
dominate in some epidemics. 

There is a class of cases in which there is not much swelling of the 



SCARLET FEVER. 



813 



throat, nor is the pulse more frequent than 130 or 140 per minute, but 
during the second day of the eruption the temperature ranges very high, 
reaching 10 T° or 108° F., and then the pulse becomes intermittent. Under 
such circumstances the disturbance of the nervous system is due to the 
high temperature which may have been present for two or three days ; 
these disturbances may be prevented if the temperature is not allowed to 
rise above 103 c or 104" F. 

Again, in cases where there is marked swelling of the throat, and a 
general infiltration of the tissues and glands of the neck, the development 
of the nervous phenomena is due to an interference with the return circu- 
lation. The condition which gives rise to the cerebral symptoms is one of 
mechanical cerebral congestion. 

There is still another class of cases in which the marked nervous phe- 
nomena appear still later in the course of the disease. Under such cir- 
cumstances they often indicate a typhoid condition. This typhoid condi- 
tion is not induced, nor are the nervous phenomena developed, on account 
of the peculiar effect produced upon the nerve centres by the scarlet fever 
poison, nor are they due to the effects produced by a high temperature, 
nor by an interference with the return circulation, but they are due to 
septic poisoning, a poisoning entirely different from scarlet fever poisoning. 
The nervous phenomena develop after the eruption. During the develop- 
ing period, there may be noticed a peculiar ichorous discharge from the 
nostrils, and frequently it is said that the patient has become repoisoned 
by scarlet fever poison — but this is not the case ; he has become repoisoned 
by the septic element of these discharges. During the period of desqua- 
mation the nervous system may be involved in consequence of the presence 
of uremic poisoning. 

The mere terms, scarlatina simplex, scarlatina anginosa, and scarlatina 
maligna, do not indicate all that may be embraced under each of the divi- 
sions. 

Scarlatina maligna is that form of the disease in which the cerebro- 
spinal system becomes early involved. What the changes are that produce 
these nervous phenomena, when high temperature is present, is still an un- 
settled question. 

Again, scarlet fever may run an irregular course in those cases in which 
there is present an extensive infiltration of the tissue of the neck, with 
inflammatory products, swelling of the glands, and extensive suppuration. 
Not infrequently these cases terminate fatally ; doubtless in some cases the 
extensive suppuration in the areolar tissue about the neck produces this 
result, and in other cases it is produced by the interference with respira- 
tion caused by enlargement of the glands and swelling of the tissues of the 
neck. Exhaustion from sloughing is a cause of death. In these cases 
there is danger from tedema glottidis, the consequence of extension of the 
inflammation from the adjacent tissues. 

There are cases in which the eruption is not very well marked ; the pa- 
tient passes safely through the stage of eruption, and the stage of desqua- 
mation is fully established ; but, instead of making a good recovery from 



814 



ACUTE GEXEKAL DISEASES. 



this point, immense abscesses are rapidly developed in the cervical region, 
blood-changes begin to manifest themselves — changes that favor hemor- 
rhages. Hemorrhages are then petechial in character and occur on the 
mucous surfaces, and the patient passes into a typhoid condition, with hem- 
orrhages occurring from the nose, mouth, intestines, etc., and death en- 
sues. Such a result is produced by the peculiar action of the septic poison 
developed during the suppurative process, and perhaps from outside influ- 
ences (as bad hygiene). 

I regard scarlatinal coryza, in which the discharge contains elements 
capable of producing septic poisoning, as an unfavorable symptom. The 
clear serum which runs over the lip never causes death ; but the fact that 
it sometimes produces excoriation and ulceration of the tissues with which 
it comes in contact, indicates that there are nasal and pharyngeal changes 
which may destroy life ; especially is this the case in young children. 
Sloughing ulcers sometimes develop in the mouth and throat; and when 
they do occur, the patient is said to have ulcerative stomatitis ; but these 
ulcerations are really due to a peculiarity of the scarlatina poison. Under 
such circumstances the patient may go on through the period of eruption, 
enter the stage of desquamation, and then rapidly sink and die, with symp- 
toms similar to those which attend diphtheria. Although the odor of the 
breath may very closely resemble that noticed in some cases of diphtheria, 
there is no diphtheritic exudation present. 

Scarlatina may also run an irregular course by the development of in- 
flammation of the internal ear. This inflammation extends from the 
throat up the Eustachian tube, involves the middle ear, and gives rise to a 
train of symptoms, such as intense pain, delirium, and rolling of the head, 
all of which suggest the presence of acute meningitis. I recall several in- 
stances in which the diagnosis of acute meningitis was made, where from 
the after-history of the case there was no question but that the symptoms 
were due to such an inflammation of the middle and internal ear. 

Complications and Sequela}. — The most common sequela is anasarca. 
The anasarca of scarlatina usually appears at the time the patient is conva- 
lescing, during the period of desquamation, or just as desquamation is being 
completed. It has been thought that anasarca is due to some exposure to 
the influence of cold during this period. It is possible that the changes in 
the kidney which give rise to the anasarca may sometimes be produced by 
the influence of cold, and undoubtedly anasarca is occasionally developed in 
this manner; but in the majority of cases it is due to some peculiarity in 
the scarlet fever poison, or to some peculiar atmospherical condition. Dur- 
ing some years anasarca is a very common sequela of scarlet fever ; while 
during other years in equally severe cases, scarcely a case of anasarca occurs. 
While we recognize the fact that it is possible for kidney lesions to be de- 
veloped which shall give rise to anasarca in consequence of exposure to 
cold, it is also of importance that we recognize the fact that the lesions and 
the anasarca may be developed independent of such exposure. The ana- 
sarca first shows itself on the face, and from the face it extends over the 
entire body, and if it becomes general more or less ascites is developed. 



SCARLET FEYER. 



815 



In most cases, at the time of, or previous to, the occurrence of the anasarca, 
certain premonitory symptoms occur, and it is of great importance to be 
familiar with these symptoms, and be on the watch for their appearance. 
For two or three days previous to their development a certain restlessness 
will be noticed, with nausea and vomiting. These symptoms are almost 
universally present. The nausea and vomiting so commonly present dur- 
ing the early periods of the disease have subsided, and now, during the 
period of desquamation, or perhaps after it has been completed, the vomit- 
ing returns. The patient has some pain in the head, has loss of appetite, 
is annoyed by the light, does not sleep well, and the temperature is raised 
perhaps two or three degrees. But the pulse now grows remarkably slow : — 
50 to 60 in children. When a patient complains in this manner during the 
desquamative stage of scarlet fever, our suspicions should be aroused, and 
if the urine has not yet been examined, an examination should be made 
at once. 

The urine may be entirely suppressed for a day, and then it will usually 
be found scanty and high-colored, will contain albumen and casts. Hema- 
turia and hemoglobinuria both occur quite frequently. If previous exam- 
inations of the urine have been made before the development of these symp- 
toms, a cloudiness will have been noticed (non-albuminous) due to epi- 
thelia and hyaline material, but now there are present casts which indicate 
the existence of scarlatinal nephritis. After the anasarca has been present 
two or three days, and the abdomen has become tense, swollen and painful, 
if the case is to have a favorable termination it will begin to decline, will 
be less and less marked about the face and feet, the tendency to stupor 
which has accompanied it will begin to disappear ; and as the dropsy sub- 
sides, and the patient is not so lethargic, the appetite begins to return, the 
urine increases in quantity, the albumen diminishes, the casts disappear, 
and convalescence is fully established. Anasarca may have been developed, 
all the symptoms have disappeared, and the patient have recovered within 
two weeks from the commencement of the attack. If, however, after the 
anasarca is developed, the case is to go on to an unfavorable termination, 
the anasarca instead of diminishing will increase ; the face will become 
more and more puffy, the legs more and more oedematous, the abdomen 
more and more distended, the pulse more and more frequent and feeble, 
the temperature more and more elevated, until a condition of coma is 
finally reached, which condition is sometimes preceded by convulsions, and 
followed by death. 

Another sequela of scarlatina is inflammation of the serous membranes. 
The serous membrane most liable to be involved is the endocardium, and 
this inflammation may pass unrecognized unless its occurrence is closely 
watched, and there may be no rational symptoms present. Endocarditis, 
when it does occur, is liable to be ulcerative in character. Inflammation 
of the pericardium may occur as a complication of scarlet fever, but it does 
so much less frequently than inflammation of the endocardium. Inflam- 
mation of the pleura, and occasionally inflammation of the peritoneum, is 
met with as a sequela of this disease. • If peritonitis does occur it is usually 



816 



ACUTE GENEBAL DISEASES. 



subacute in character. It is possible to have peritonitis developed as a 
sequela to scarlet fever and to be entirely recovered from. Rheumatism 
may be developed during the desquamative period of scarlet fever. Under 
such circumstances it assumes the ordinary appearances of inflammatory 
rheumatism. It is not a serious sequela, and a complete recovery usually 
occurs within ten or fourteen days from the commencement of the attack. 
Suppurative inflammation of the joints is sometimes a sequela of scarlet 
fever. 

Another serious complication of scarlet fever is diphtheria. It may 
occur at any period of the fever ; usually it occurs during the period of 
desquamation. There is developed the characteristic exudation of the dis- 
ease, with the attendant depression noticed in a case of diphtheria devel- 
oped independently of scarlet fever. It differs in no respect from primary 
diphtheria, except in the rapidity of its development and in its fatality. 
In scarlet fever there is no more serious complication. Usually it appears 
quite suddenly, and perhaps does not occur more frequently m those who 
have a severe form of the disease than in those who have a mild scarlet 
fever. The lymphatic glands may be enlarged and swollen, i. e., a lym- 
phadenitis may be a sequel of scarlatina. Keratitis, retinitis, and total 
blindness are rare sequelae of scarlet fever. Anaemia, paralysis of single 
nerves, spinal disease, chronic Bright' s, deafness, chorea, epilepsy (melan- 
cholia and mania in adults), valvular diseases, etc., are also named as 
sequelae. 

Differential Diagnosis. — The diagnosis of scarlet fever is usually not diffi- 
cult after the eruption has made its appearance, for, in well-marked cases, 
that alone will readily distinguish it from other eruptive fevers. At the 
very onset of the eruption, and sometimes in irregular cases, the differ- 
ential diagnosis is difficult. The eruptive diseases which are most liable to 
be mistaken for scarlet fever are measles, small-pox, roseola, and an erythema 
which sometimes appears in surgical cases. In all doubtful cases a care- 
ful study of the history of the patient is necessary before making a diag- 
nosis. 

In measles the appearance of the eruption is preceded by a cough and 
coryza. These symptoms are never present in the ushering-in stage of scar- 
latina, but may follow the eruption. Besides, the eruption of measles 
first appears on the face, whereas the eruption of scarlet fever first makes 
its appearance upon the neck and chest. The incubation period is shorter 
in scarlet fever and the early pyrexia is higher than in measles. After 
these diseases are once fully developed, the course of the one so differs from 
that of the other that there will rarely be any chance for doubt after the 
first week of the disease. The minute punctate appearance of the scarla- 
tina eruption before it becomes confluent is an important element in its 
diagnosis. 

Although the eruption of confluent variola, for the first twenty-four 
hours, may sometimes resemble that of scarlatina, yet the development of 
the first vesicle settles the question. 



SCAKLET FEVEE. 



817 



The appearance of erythema bears a close resemblance to a perfectly de- 
veloped scarlatina eruption ; it is not, however, present on the extremities, 
neck, and portions of the trunk, and it spreads in a very irregular manner, 
whereas in scarlatina such is not the case. But if, on account of the scanti- 
ness of the scarlatina eruption, any doubt arises as to the nature of the erup- 
tion, the fact that in scarlatina the throat symptoms are rarely absent, that 
the tongue presents the strawberry appearance, and that at an early period 
there is usually some swelling of the cervical glands, will decide the case. 
In those cases in which, during the early part of the disease, it is impossible 
to make a differential diagnosis, the diagnosis will be readily made when the 
period of desquamation is reached. 

The differential diagnosis between roseola and a very mild form of scar- 
latina is sometimes attended with great difficulty. If scarlatina is prevail- 
ing, and a child has an eruption which lasts for two or three days, then 
disappears, and is not followed by desquamation, it may be thought that the 
case is one of scarlatina ; and yet the sequel proves that the case was one of 
roseola. Such a form of roseola sometimes prevails epidemically, and 
attacks children in a certain locality, whether they have or have not had 
scarlatina. Under such circumstances, adults and children are said to have 
had a second attack of scarlet fever. In making a differential diagnosis 
between this form of roseola and scarlatina, the duration of the eruption 
and the character of the throat symptoms must decide. In scarlatina the 
posterior part of the pharynx is affected, while in roseola the redness is con- 
fined to the anterior portion ; besides, the throat affection in roseola is 
much milder than in scarlatina. In roseola the white line that the finger 
leaves disappears immediately ; while in scarlatina it remains — indeed, a 
letter may be traced on the skin in well-marked cases. 

One can hardly mistake erysipelas for scarlatina, for erysipelas com- 
mences at one point and gradually extends from it ; there is also marked 
oedema of the connective-tissue, and there is a very marked difference in 
the constitutional symptoms of the two diseases. 

Malignant cases of scarlet fever, in which no eruption appears, prove 
rapidly fatal. In such cases, the fact that an epidemic of scarlet fever is 
prevailing (which is usually the case), the rapid development of the disease, 
the very high range of temperature, and the very grave nervous phenomena, 
will aid in the diagnosis, and these can only be accounted for on the ground 
that the patient is overwhelmed by some very active blood-poison. In this 
class of cases the entire surface of the body should frequently be examined, 
for the eruption is sometimes very transient, perhaps appearing only for a 
few hours on the neck or extremities. 

It is sometimes difficult to draw the line of distinction between scarlatina 
without an eruption, but with swelling of the cervical glands and ulcera- 
tion of the throat, and diphtheria. If a patient has swelling of the 
cervical glands and well-marked febrile symptoms, which have come on 
gradually — that is, have been two or three days developing — and yet no 
scarlatina eruption has appeared, but a gangrenous ulceration has developed, 
involving the tonsils, the posterior wall of the pharynx, and the anterior 



818 



ACUTE GEKEKAL DISEASES. 



pillar of the soft palate, and if scarlet fever is prevailing in the locality, it is 
very difficult to decide between it and diphtheria. There can be no doubt 
but that scarlatina poison may excite a tubular nephritis without an erup- 
tion appearing on the surface of the body, or without any of the other 
ordinary symptoms of scarlatina. 

Prognosis. — The prognosis in scarlet fever is always uncertain. It will 
be influenced more by the character of the prevailing epidemic than by any 
other circumstance. According to statistics, the rate of mortality ranges 
from one death in five to one in twenty. Some epidemics are very mild. 
During one epidemic, in one month, I treated fifty cases of scarlet fever, 
with only two deaths. During the same month of the following year, 
I treated twenty cases, with seven deaths. In giving a prognosis one must 
always take into account the type of the prevailing disease. Even when 
the disease is mild in character, and is running a perfectly regular course, 
dangerous symptoms may suddenly arise without any assignable cause. 

The conditions of a favorable prognosis are as follows : when the erup- 
tion appears within forty-eight hours from the commencement of the 
attack, and rapidly completes its course, reaching its maximum on the 
second day ; when the throat symptoms are mild, little difficulty being ex- 
perienced in swallowing; when the cervical glands are but slightly enlarged; 
when the temperature does not rise higher than 104° F., and the pulse beats 
only 120 per minute ; when the cerebral symptoms are not severe, and are 
of short duration ; and when the disappearance of the eruption is attended 
by a steady decline in temperature. Even if there is a slight affection of 
the joints and a moderately severe nephritis during the period of desquama- 
tion, a favorable termination may be predicted. The nephritic symptoms 
will almost always entirely disappear during the third or fourth week. 

The conditions for an unfavorable prognosis are an irregular course ; a 
temperature rising above 105° F., 1 with dyspnoea and extreme frequency of 
the pulse ; symptoms of collapse attended by a cold surface and a small 
pulse, an eruption of a livid hue, and abundant hemorrhages in the skin ; 
ulcerative pharyngitis, especially when it extends to the nasal passages, ac- 
companied by copious coryza and infiltration of the glands and tissues of 
the neck ; severe nervous symptoms, with typhoid symptoms and long con- 
tinued vomiting with diarrhoea coming on at the commencement of the 
attack; early nephritic symptoms and general dropsy, excessive haema- 
turia, or almost complete suppression of urine, with high temperature. 
The occurrence of any of the more serious complications, such as pneu- 
monia, diphtheria, pericarditis, oedema glottidis, etc., always renders the 
prognosis bad. 

Before making a prognosis, decide whether the scarlet fever is regular or 
irregular in its course, and if irregular, what are the causes of the irregu- 
larity. It is also important to determine the patient's power of resisting 
disease. Autumn is the most unfavorable season. Favorable hygienic sur- 



J A temperature of 110° has been reached and yet followed by recovery ; it rose to 115° F. in a fatal case. 
Scarlet fever is an intensely febrile disease ; hence the temperature is not such a very important element 
in the prognosis. - • 



SCARLET FEVER. 



819 



roundings, good nursing, and well-directed medical treatment will greatly 
lessen the death rate in scarlet fever epidemics, and these should be con- 
sidered elements of the prognosis. Patients with scarlet fever do better 
when left to themselves than when badly nursed, even if under the care of 
skilful medical attendants. 

Age is an important element of prognosis. The period of greatest mor- 
tality is from infancy to five years of age. Beyond this period until adult 
life, the prognosis is decidedly better. Five per cent, of the whole mortality 
falls in the first year, fifteen per cent, in the second, twenty per cent, in 
each of the next two years, and then decreases progressively. In adults, 
the mortality is greatest in pregnant women, and those who are suffering 
from some organic disease, especially some disease of the heart or kidneys. 

Treatment. — In connection with the treatment of this affection, the first 
question that presents itself relates to prophylaxis or prevention. 

The prophylaxis of scarlet fever is a system of the strictest quarantine. 
The sick must be removed from the healthy. All useless articles of furni- 
ture must be removed from the sick-room. Fresh air renders the contagion 
of scarlet fever less powerful ; therefore, free ventilation is of the utmost 
importance. All the clothes and excretions of the patient should be dis- 
infected in the same manner as in typhoid fever. To prevent the dissemina- 
tion of the dusty particles of the desquamating epidermis, during the period 
of desquamation the surface of the body should be frequently sponged, and 
after each sponging the surface should be rubbed with olive oil. Those con- 
valescing from this disease should not be allowed to leave their apartment 
until desquamation is completed, which usually requires at least three 
weeks after the commencement of the period of desquamation. The 
sick-room and everything which has been used about the patient should 
be thoroughly disinfected, and the windows and doors of the apartment 
should be allowed to remain open for a long time before it is again 
occupied. 

To prevent the spread of the disease, nurses and attendants upon the 
sick should not be allowed to have any intercourse with the healthy until 
the period of desquamation is passed, and after that time not until there 
has been thorough cleaning and disinfecting. The funeral of those dying 
of scarlet fever should not be public. There is no known prophylactic 
treatment, except isolation, and a thorough disinfection of everything con- 
taminated by the contagion. 

A theory has been advanced that belladonna has power to prevent the 
development of this disease in those who have been exposed to its con- 
tagious influence. This drug has been very extensively administered in 
order to test its effects as a preventative in scarlet fever. After having 
carefully examined the subject, both in its literature and clinically, I am 
convinced that belladonna has no power to prevent the development, or 
mitigate the severity, of the fever in those who have been exposed to its 
infection. Fresh air is the only agent which can render the contagious in- 
fluence of this fever less powerful. 

Medicinal Treatment. — The medicinal treatment of scarlet fever is al- 



820 



ACUTE GENERAL DISEASES. 



most entirely expectant. It is a disease which cannot he aborted, and if 
left to its natural course tends to recovery if the fever and the local symp- 
toms remain within certain bounds. It has certain stages to pass through, 
and one cannot safely interfere with its regular course. To stand by and 
watch, and, as far as possible, to guard against complications are the physi- 
cian's chief duties. There are certain details which it is important to attend 
to. The bed and body linen should be frequently changed. As soon as 
the period of desquamation has been reached the patient should have a 
warm bath once or twice during the day, the surface of the body being 
well washed with carbolized soap. The baths hasten the process of des- 
quamation and aid in bringing the skin into a healthy condition as rapidly 
as possible ; the kidneys will also be relieved, and serious lesions of these 
organs may thus be prevented. Such general means as are applicable in 
the treatment of all fevers may be employed. 

If the temperature of the patient rises above 104°, certainly if it rises 
above 105° F., it is important that some measures be resorted to for its re- 
duction. The temperature should never be allowed to remain at 105° F. 
longer than twenty-four hours. The means which are to be employed to 
accomplish this reduction are the antipyretic measures already referred to. 
There is a strong prejudice against the application of cold to the surface 
of the body in scarlet fever. I am by no means certain that cold baths 
are always safe, or that in all cases the application of cold to the surface 
is judicious treatment. It is said that the kidneys will be most readily 
relieved of the scarlet-fever poison when cold is used for the purpose of 
reducing the temperature. It is claimed that when the temperature of a 
patient is kept below 103° F., scarlatinal nephritis rarely occurs. This 
statement is not sustained by facts ; it has been found that kidney com- 
plications are as extensive in the cases where cold is employed as in those 
cases where the temperature ranges higher and cold to the surface is not 
employed. We should be governed by the same rules in the application 
of cold to the surface in scarlet fever as govern us in the treatment of 
typhoid fever. 

With regard to the use of other antipyretics I need add nothing to what 
has already been said in connection with the treatment of other fevers. 
Unless the temperature in a case of scarlet fever ranges above 105° F„ do 
not apply cold to the surface or give antipyretics. With such a tempera- 
ture there probably will be delirium, but it must be regarded as one of the 
phenomena of the disease, requiring no special treatment. If the tempera- 
ture rises above 105° F., perhaps reaching 106° or 107° F., and the patient 
manifests the nervous phenomena which have been referred to, such as 
restlessness, tossing, blueness of the surface, tendency to coma, etc., the 
temperature is to be reduced either by the application of cold to the sur- 
face or by the administration of antipyretics. 

In all cases the patient is to be sponged frequently with tepid water, 
and if there is intense burning of the surface, a saline is to be added to the 
water. Sponging in this manner will give the patient very great comfort. 



SCARLET FEVER. 



821 



Some advise that the surface be anointed with oil for the relief of the 
burning. My own experience has led me to rely upon simple tepid saline 
water. I have found that it gives patients greater relief, is more easily 
applied, and is every way more agreeable than any of the substances which 
have been used for this purpose. I have not found that the application of 
oil to the surface has any effect in controlling the temperature, nor does it 
seem to have any effect on the process of desquamation. As soon as 
desquamation commences the process should be assisted by frequent wash- 
ings with soap and water. 

For the throat complications, which will give more or less trouble in all 
severe cases, especially when there is much enlargement of the glands at 
the angle of the jaw, causing difficulty in swallowing, leeches were for- 
merly employed, but their use has now been almost entirely abandoned. 
Of all the remedies which I have employed for the relief of throat compli- 
cations, cold carbonic acid water proved best. Whether it does more than 
afford relief, I am not able to say, but I am certain that cold carbonic acid 
water or pieces of ice held in the mouth, and brought as much as possible 
in contact with the swollen mucous membrane of the throat, if used early, 
afford most marked relief. 

In the advanced stages of the disease, where there is great infiltration 
of the glands and tissues of the neck, cold applications do not afford the 
same relief as when they are used in the early stage ; then cloths wrung out 
in tepid water and applied to the surface seem to be of service. During 
this stage, hot applications are generally much more agreeable to the pa- 
tient, and the hot cloths may be covered with oil-silk. These applications 
will not hasten the suppurative process, unless suppuration is already estab- 
lished. While using hot applications externally, warm water gargles and 
steam inhalations may be used internally. Of these methods of treating 
throat affections, the one which seems to be the most rational plan of treat- 
ment should be chosen. In scarlet fever I favor the use of hot water rather 
than cold applications. The superficial and deep ulcers which are some- 
times seen in the throat of scarlet fever patients can best be treated by 
spraying them with carbolic acid, muriated tincture of iron, chlorate of 
potash, tannic acid, or any of that class of remedies. Whatever remedy 
maybe chosen, it can be much more successfully applied by means of spray 
than by a camel's-hair brush or a probang. Such local remedies thus ap- 
plied afford great relief. The pain from these ulcerations is sometimes 
very severe, and cocaine, ether, or other anodyne applications in a form of 
spray may be used with satisfactory results. 

In a certain class of cases, where there is marked disturbance of the 
nervous system accompanied by great depression of the vital forces and 
feeble heart action, stimulants will be demanded early. . It is not necessary 
to wait until a certain stage of the eruption or of the disease is reached 
before commencing their administration. It may be necessary to resort to 
their use within twelve hours, or even within a less time, from the com- 
mencement of the attack. In some cases the beneficial effect that may be 



822 



ACUTE GENERAL DISEASES. 



produced by the free and early administration of stimulants will be the 
physician's sole reliance. 

The approach of kidney implication in scarlet fever will be indicated by 
the development of those premonitory symptoms which precede the ana- 
sarca ; and whenever such symptoms are developed, dry or wet cups, accord- 
ing to the condition of the patient, should be applied over the region of the 
kidneys, upon either side of the spine ; three or four cups are to be applied 
on each side, and their application followed with hot fomentations over the 
kidneys. At the same time the temperature of the sick-room is to be raised 
to 73° or 74° F.,the body of the patient covered with flannel, hot-air or 
warm baths are to be administered, and the administration of diuretics is 
to be commenced early. Of these, digitalis will act most favorably. If the 
anasarca does not disappear under the influence of the digitalis and the 
other means employed, calomel may be combined with the digitalis and 
its use continued for a few days. Pilocarpin is recommended by some ; 
my experience with it has not been satisfactory. The action of diuretics 
is increased by having a mercurial combined with them. In certain 
cases, when the patient is going from bad to worse, when the anasarca is in- 
creasing, the tendency to coma is becoming more and more marked, indi- 
cating an unfavorable termination to the case, cups have been applied, and 
hot baths and diuretics employed with no satisfactory result — if then small 
doses of calomel are combined with the diuretics, and its use continued for 
two or three days, the entire phase of the case may be changed. When 
toxic symptoms are marked, some advise carbolic acid, the sulpho-carbo- 
lates, the hypopbosphites, inhalation of ozone, etc. In conjunction with 
the measures recommended, the patient may drink as freely as possi- 
ble of water. If convulsions occur, or threatening symptoms indicating 
the approach of convulsions are developed, opium, either hypodermically 
or by the mouth, may be given. Under such circumstances, the effect of 
opium is often most satisfactory. It not only arrests the convulsive tenden- 
cies, but produces the most profuse diaphoresis, and aids in restoring the 
renal functions. 

MEASLES. 

Measles, or rubeola, is a disease from which few persons escape. It is 
essentially a disease of childhood, but it may occur at any age ; it is, how- 
ever, less liable to occur in young infants than in children after the period 
of dentition. A second attack is of rare occurrence. It is characterized 
by an eruption of red spots, accompanied by a catarrh of the mucous mem- 
brane of the air-passages, and a more or less severe fever. It is con- 
tagious. It may prevail as an epidemic, but occurs more frequently as a 
sporadic disease. 

Morbid Anatomy. — Its anatomical lesions, with the exception of the erup- 
tion, are similar to those of small-pox and scarlatina. There are similar 
changes in the blood, and the same tendency to congestion of the internal 
organs. The spleen and liver are moderately enlarged. The mucous mem- 
branes of the nose, pharynx, larynx, and larger bronchi, and the conjunc- 



MEASLES. 



823 



tivae, are more or less intensely congested and present all the lesions of acute 
catarrh. In the majority of instances this catarrh is most severe just be- 
fore and during the early period of the eruption ; generally, it begins to 
disappear when the eruption has reached its height, and within two or 
three days entirely disappears. Where death has resulted from measles, 
in the majority of autopsies, evidence of capillary bronchitis is found, and 
not infrequently of catarrhal pneumonia also. 

Strictly these are not anatomical lesions of measles, but complications ; 
they are, however, such frequent attendants of this disease, that they are 
almost a part of its history. 

The eruption is papular ; the papules first show themselves upon the 
face, especially upon the chin ; gradually they extend to all parts of the 
body, and lastly appear upon the back of the hands. When the eruption 
is well developed the spots are slightly elevated, and have a diameter vary- 
ing from two-fifths to one-twentieth of an inch ; in form they are crescent- 
shaped, their margins are sharply defined, usually their color is bright- 
red, sometimes shading off into blue. In most cases the spots are distinct 
and separated from each other by pale tracts of skin ; they may become 
confluent, and thus give to the surface a uniform redness. When this 
occurs the surface presents an appearance similar to that seen in scarlatina. 
The earlier papule in each spot usually occupies the place of a hair-follicle ; 
hence some regard inflammation of a sebaceous follicle of the skin as the 
first event. The spots disappear on pressure, but immediately return when 
the pressure is removed. Sometimes each spot contains several papules. 
The diversity in form and appearance of measle-spots in different cases 
depends upon variations in size, elevation, and grouping of the papules. 
When the spots assume a dark-red color, and do not disappear on pressure, 
capillary hemorrhages have taken place into the papules, and the eruption 
is called hemorrhagic. When the eruption is very abundant, little vesicles 
sometimes appear upon the papules, especially upon the trunk when there 
has been profuse perspiration, called by, some vesicular or miliary measles. 
As soon as the spots have reached their maximum of development, their 
color begins to fade ; the fading is progressive, the centres of the spots 
retain their redness longest ; the elevations subside with loss of color. In 
a varying time, from one to five days, the spots entirely disappear, leaving 
a yellowish or brownish stain. This staining is due to pigmentation of the 
skin, and is sometimes visible for two weeks. 

Exfoliation of the epidermis or desquamation takes place only upon the 
sides of the measle-spots ; it is never so extensive as in scarlet fever. The 
skin does not desquamate in layers, but in fine brown scales, i. e,, is fur- 
furaceous, not squamous, hence it is called the bran-like desquamation. It 
may commence before the redness of the eruption disappears, but it does 
not usually occur until the eruption has entirely faded. In most cases the 
period of desquamation is short, rarely lasting a week. 

Etiology. — It is essentially a contagious disease. So far as has yet been 
determined, it is only propagated by contagion. There are places, extensive 
districts, and countries thickly inhabited, where this disease has never pre- 



824 



ACUTE GENERAL DISEASES. 



vailed. The poison of measles is located either in the mucous secretion, 01 
in the exhalations from the body of the infected, and the air becomes so 
contaminated about the sick that when persons who have not had the dis- 
ease are brought within its influence, measles will be developed. It has 
been proved that the blood, the mucous secretions, especially the nasal, and 
even the tears, have the power of conveying the disease by inoculation. 1 
There is little question but that the disease can be conveyed in cloth- 
ing, or, in other words, that it is a portable disease. One not protected 
when exposed to measles is much more certain to contract the disease 
than is an unprotected person to contract small-pox or scarlet fever. It 
is possible for the infection to be conveyed from one place to another 
in clothing and in fluids. Its microbe has not yet been definitely deter- 
mined. 

The average period of incubation is eight days. During this period the 
poison remains latent, giving its possessor no knowledge of its presence. 
In most cases a slight exposure is sufficient to induce the disease ; in some 
cases it is contracted only after prolonged exposure. Susceptibility to this 
contagion is almost universal. All classes are equally subject to the in- 
fection. Second attacks are exceedingly rare. The exact time in the 
course of the disease when measles is most infectious is not definitely deter- 
mined. Statistics furnish almost absolute proof that it may infect through- 
out its entire course. 

Symptoms. — Measles, like the other exanthematous fevers, if uncompli- 
cated, runs a definite course. 

Premonitory or precursory Stage. — At the end of the stage of incubation 
or latent period of the disease, which is without fever, and free from local 
symptoms, or from eight to ten days after exposure, the patient begins to 
suffer from coryza, is languid, chilly and exceedingly irritable. Sometimes 
a subnormal temperature precedes the first symptoms. Occasionally, in 
young children, convulsions occur. The coryza and other catarrhal symp- 
toms, at first, may or may not be accompanied by fever, or the sudden 
initial fever may be very intense. Very soon, in either case, occurs a 
marked febrile movement. The eyes will be injected and watery, there 
will be a burning sensation and an aversion to light, and the eyelids will be 
red and tumefied. There is a constant, irritating, watery discharge from 
the nose, with frequent sneezing and pain over the frontal sinuses. Sore 
throat is complained of, and the voice is a little husky. Bronchial catarrh 
is indicated by uneasiness and constriction over the chest, with a frequent 
dry, hoarse cough, hurried respiration, etc. The suffused, red appearance 
of the eyes is peculiar, and distinguishes measles from scarlet fever and 
other forms of eruptive fever. 

After the early symptoms have continued perhaps for twenty-four hours 
an initial fever will be developed which, with the catarrhal symptoms, con- 



1 An organized ferment, bacterium or tarnea (which develops to a certain point in a proper medium and 
then suddenly ceases its career), has been found in blood and breath and in glycerine on which children 
with measles have breathed. They have been found in the true skin, lymph-spaces and sweat-glands ; in 
<hape they are rod, spindle and canoe shaped, also spherical and ovoid. They are also found in the lungs. 



MEASLES. 



825 



tmues from forty- eight hours to four days ; then the eruption makes its ap- 
pearance. 

Eruptive Stage. — The eruption is first seen upon the face (about the 
chin, forehead, mouth, and side of the nose), theu upon the neck, then 
upon the chest and over the body, afterwards upon the legs and arms, and 
lastly upon the back of the hand. The eruption on the face feels like 
small shot early in the disease. The eruption may appear first on a part 
of the skin that has been the seat of injury. Usually it is about four days 
from the time of the appearance of the eruption upon the face before it has 
passed over the entire body, and it begins to fade from one part about thirty- 
six hours after its appearance upon that part ; first, it begins to fade from 
the face, then the neck and chest, and finally from the back of the hands. 
If closely examined, the eruption will be found composed of little, fine, red, 
crescentic dots, which, after a little time, will be seen crowded together in 
patches of irregular shape. Between these patches the skin usually has its 
natural appearance. The odor is peculiar during this period. The erup- 
tion of measles presents more of a papillary appearance upon the face than 
upon any other part of the body. With the appearance of the eruption there 
is more or less swelling of the surface, with itching and burning, and the 
color of the eruption will vary from a bright rose-red to a dark mahogany 
hue. The difference in color depends upon the condition of the individual 
and the peculiarity of the type of the disease, rather than upon any change 
in the skin itself. The respirations are hurried, and convulsions may, in 
children, prove fatal. Epistaxis is common, and the lymphatic glands 
are enlarged. As the eruption disappears it loses its bright red color and 
becomes a yellowish red, until finally nothing but a staining of the sur- 
face is left ; then desquamation commences. Increase in fever and rise 
in pulse and nocturnal delirium often follow the first outburst of the 
eruption. 

Desquamative Stage. — The desquamation which follows the eruption is 
not like the desquamation of scarlet fever — scaly or " peely," — but it occurs 
in very fine dust-like flakes, which may pass unobserved. The eruption 
reaches its height by the third day from the time of its appearance, and 
generally has disappeared by the end of the sixth day. As a rule, during 
the development of the eruption the catarrhal symptoms and fever are in- 
creased in intensity ; the patient will sneeze and cough, and frequently 
with such severity and with such a coarse, grating tone, that it has re- 
ceived the name of "iron cough.' 7 It is not the cough of croup (though a 
true croupy cough is sometimes present) ; there is no stridulous breathing 
accompanying it, but it is the result of an ordinary catarrhal laryngitis, 
which causes the patient to cough perhaps for two or three days without 
expectoration, or any attempt at expectoration. During this period the 
pulse will range from 100 to 120 beats per minute, and in young chil- 
dren it may reach 160. In the majority of cases the temperature does 
not rise above 103° F., but it may rise as high as 106° or 107° F. As 
soon as, or even before the eruption begins to decline the temperature often 
falls two or three degrees. As the decline in the eruption goes on, the 



826 



ACUTE GENERAL DISEASES. 



temperature gradually falls, until by the time the eruption has entirely 

disappeared the patient will be 
fully convalescent. 

Measles, like scarlet fever, is lia- 
ble to irregularities in its develop- 
ment. When it is prevailing in a 
locality, cases occur in which all 
the catarrhal symptoms of the dis- 
ease are present without an erup- 
tion : again, there is an eruption 
closely resembling that of measles, 
with no catarrhal symptoms ; from 
the appearance of the eruption one 
will not be able to say whether the 
patient has or has not measles ; if 
the subject has been exposed to the 
contagion of the disease, the case 
will probably be regarded as one of 
measles, and yet if there are no 
catarrhal symptoms, but simply an 

Temperature Record in a Case of Measles. eruption, Such a diagnosis WOUld be 

made with a question. 

There is a form of roseola which very closely resembles measles in every 
aspect of the disease, except the catarrhal symptoms. There is an irregu- 
lar form of measles which prevails epidemically, which is characterized by 
a tendency to ulceration of mucous surfaces. This form shows its peculiar 
tendency by the development of ulcers at the angle of the mouth, within 
the nose, around the vulva, anus, etc. Sometimes these ulcers spread and 
so interfere with deglutition and respiration as to endanger life. The ul- 
cerations are accompanied by great prostration of the vital powers and a 
tendency to gangrene of the above-named parts and also of the lungs. This 
irregular variety only occurs in those who are poorly nourished, live in badly 
ventilated houses, and are surrounded by unfavorable hygienic influences. 

Again, there is a form of measles in which, at the very onset of the 
disease, there is a very high range of temperature. There will be no 
more severe catarrhal symptoms than in the ordinary forms — no more 
bronchitis ; but there will be a higher range of temperature, perhaps rang- 
ing as high as 106° or 107° F. Associated with this pyrexia there will 
be restlessness, a dry tongue, and, very soon after the appearance of 
the dry tongue, a change in the color of the eruption, which will assume 
a dusky purplish hue. The eruption may present this peculiar appear- 
ance at the very commencement of its development. This type of measles 
is called "Mack measles The color of the eruption simply shows that 
there have been extensive blood-changes. In most cases, these changes 
have taken place prior to the development of the eruption. By some it 
has been claimed that there is at work a peculiar epidemic or endemic in- 
fluence that gives rise to the peculiar type of the disease ; but as I have 



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3. 


4. 


5. 


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7, 


a 


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c. 


104 
103 








































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102 








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too 

.9.9° 
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9- 




































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MEASLES. 



827 



been brought in contact with it, it has seemed to me that it differed from 
the ordinary type only in the intensity of the fever. It is the high range 
of temperature which stamps it as a peculiar type of the disease ; hut as 
soon as the eruption has made its appearance, although at first it may be 
of a bright red color, within a day or two it assumes the peculiar dusky 
black appearance which has given rise to its name. 

There is another irregular form of measles in which the eruption is 
largely made up of petechial spots scattered over the surface of the 
body, due to a hemorrhagic diathesis. It is really a hemorrhagic form 
of measles, and is a very unfavorable type of the disease. At first the 
eruption presents the same appearance as the ordinary eruption of measles: 
but, after the fever has continued a few days, it assumes a dark color, the 
patient becomes restless, the tongue dry, there may be vomiting and 
diarrhoea, and, if death occur, at the post-mortem examination lesions 
very closely resembling those of typhoid fever, such as changes in the 
spleen and elevation of Peyer's patches, will be found. These cases are 
also known by the term C£ black measles." Hemorrhages also occur from 
nose, mouth, urethra, intestinal and other mucous tracts. 

There are thus two forms of black measles — one in which the. eruption 
consists of petechial spots scattered over the surface, and dependent upon 
a hemorrhagic tendency ; in the other form the eruption assumes a dark 
appearance on account of changes which have occurred in the blood, the 
result of a very high temperature at an early period of the attack. There 
is always more or less danger connected with any of the more severe forms 
of irregular development. Although measles is usually not a disease of 
aiuch severity, yet, however mild the type may be, it is liable to complica- 
tion, and the most frequent complications are to be found in the respira- 
tory organs. 

Complications. — Of these the most important is capillary bronchitis. 
Rarely is there a case of measles without more or less bronchial catarrh ; 
but the bronchial catarrh which ordinarily attends it is not of much con- 
sequence. When, however, the bronchitis becomes capillary, the patient 
is in great danger. Upon auscultation, if instead of loud, sonorous rales, 
which indicate that the catarrh is confined to the larger bronchial tubes, 
there are fine crackling sounds, accompanied by an entire loss of, or an 
extremely feeble, vesicular murmur, the catarrhal inflammation has ex- 
tended into the finer bronchial tubes, and there is always danger of lobular 
pneumonia (q. v.). A lobular pneumonia which complicates measles is 
always attended with danger, and when depression of temperature fol- 
lows decline of the eruption, all the pulmonary signs may grow very in- 
tense. With serious lung complications, the eruption may recede. As 
a rule, it attacks both lower lobes at the same time, especially their dor- 
sal aspect, while in the upper lobes only a few tubes are involved. This 
complication may occur at any time during the course of measles, but it 
is more liable to occur just after the eruptive stage. Its development is 
attended by a rise in temperature, in proportion to the extent of lung in- 
volved. The urine is always scanty and may be suppressed. 



828 



ACUTE GENERAL DISEASES. 



Secondary meningitis not infrequently occurs as a complication of measles. 
When it does occur, it is developed during the period in which the eruption 
is disappearing. It is more likely to occur in this disease than in scarlet 
fever. 

A sequela of measles is a mild form of ophthalmia. This ophthalmia 
may considerably inconvenience the patient, and lead to permanent injury 
of the eyes. It is especially important to remember that it appears during 
the convalescing period, that it is a conjunctivitis, and usually entirely 
disappears if the eyes are frequently bathed with warm water and properly 
protected from the light. 

Otorrhoea, or inflammation of the external ear, is another sequela of 
measles. It most commonly appears in those patients who have what is 
called a strumous diathesis, have phthisical parents, are themselves badly 
nourished, or who have suffered from a severe form of measles. This 
otorrhoea is sometimes very obstinate, and if it yields to treatment does so 
very tardily ; it may be followed by permanent deafness. 

In adults acute miliary tuberculosis not infrequently occurs as a sequela 
of measles. The mucous membrane of the intestinal canal may also be- 
come the seat of important complications in measles. A mild form of 
gastric catarrh is of quite frequent occurrence, but is rarely serious in 
character. Severe intestinal catarrhs, giving rise to troublesome diarrhoea 
and dysentery, are sometimes very serious complications, especially in 
very young and feeble children. Occasionally malignant epidemics of 
measles prevail, during which the fatal results are chiefly due to intestinal 
catarrhs. 

Diphtheria does not so frequently complicate measles as it does scarlet 
fever. It generally makes its appearance when the eruption is at its height, 
and when severe its occurrence is marked by a rapid rise in temperature. 
The symptoms of the diphtheria are the same as when it occurs as a 
primary disease. It must always be regarded as a serious complication. 
Not infrequently measles leaves the patient in a state of general ill-health. 
Especially is this the case in scrofulous and rachitic children. 

Differential Diagnosis. — Ordinarily, when the eruption is well defined, 
the diagnosis of measles is not difficult. In some cases, however, the 
eruption presents an appearance which closely resembles that of scarlet 
fever and roseola. In nearly every case of measles the catarrhal symptoms 
accompany the precursory stage, and increase in severity during the period 
of eruption. The presence or absence of these catarrhal symptoms will 
enable one in the majority of cases to make a differential diagnosis. 

In children, the eruption of typhus fever very frequently closely resem- 
bles that of measles, but it does not appear upon the face, and is not 
accompanied by catarrhal symptoms. In typhus fever, nervous symptoms 
are quite frequently present, such as delirium, prostration, and tendency 
to coma. Such symptoms are only met with in the hemorrhagic or typhoid 
variety of measles. Before the appearance of the eruption a careful ex- 
amination of the mucous membrane of the pharynx will settle the question 



MEASLES. 



829 



of diagnosis. In measles the mucous surface will be more or less intensely 
injected ; in typhus fever it will not be so injected. 

The differential diagnosis between measles and small-pox has been con- 
sidered. 

The eruption of measles differs from that of roseola. In measles it is 
partially confluent, in roseola it is non-confluent. In roseola the mucous 
membrane of the fauces is not intensely injected, and the fever does not 
run a characteristic course, the reverse of which occurs in measles. If the 
temperature is normal, if the eruption on the trunk is of a bright color, 
if the surface is smooth, and if catarrhal symptoms are absent, measles 
may be excluded. 

It is hardly possible to mistake syphilitic exanthemata for measles, for 
there are certain glandular changes which attend the development of 
syphilitic eruptions which establish the diagnosis. In the early period of 
the disease, when coryza is a prominent symptom, before the appearance 
of the eruption, measles may be mistaken for an ordinary influenza. 

Prognosis. — The prognosis in uncomplicated measles is always good. 
Any irregularity in its development, and dentition in children, may render 
the prognosis unfavorable. In the hemorrhagic, ulcerative, and in the ty- 
phoid varieties the prognosis is grave. Measles occurring in pregnancy does 
not prove fatal to the extent that scarlet fever does ; but abortion is very 
common. Intra-uterine measles may be recovered from, and the child is 
then proof against a second attack. In severe cases, the deviations from 
the typical course of the disease which render the prognosis unfavorable 
are a temperature of 105° or 106° ~F. during the period of initiatory 
fever, a retardation or an irregularity in the appearance of the eruption at 
the beginning of the eruptive stage, and the occurrence of complications, 
especially broncho-pneumonia, croupous laryngitis and diphtheria. Pro- 
fuse hemorrhages from the mucous surfaces, during any period of the fever, 
render the prognosis unfavorable. Eecession of the rash is very unfavor- 
able when there are any pulmonary symptoms. The hygienic surroundings 
of the patient greatly influence the prognosis. 1 

The prognosis also depends upon the age of the patient ; the rate 
of mortality is much greater among adults than children, and in very 
young children than in older children. The character of the prevailing 
epidemic determines to a very great degree the prognosis. When measles 
is developed in one who is suffering from a severe chronic disease, especially 
some organic disease of the lungs, the prognosis is unfavorable. The 
patient will not probably die durinj the active period of the measles, but 
the chronic pulmonary disease may terminate fatally from the effects of 
the measles. For instance, a patient has evidences of consolidation about 
the apex of the lung, a condition which justifies a favorable prognosis ; let 
measles be developed in such a case and capillary bronchitis, terminating 
in more or less extensive pneumonia, will probably occur, from which 
acute phthisis may be developed. 



1 The presence of sewer-gas renders nearly every case fatal.— Quain. 



830 



ACUTE GENERAL DISEASES. 



In measles, death rarely occurs during the first week of the disease ; it 
usually takes place during the second week ; if serious complications occur, 
it may take place later in the disease. The rate of mortality is estimated at 
from one to four per cent. 

Treatment. — The prophylactic treatment of measles consists in isolating 
the affected person. When measles run a regular course, the principal duty 
of the physician is to watch for, and guard against the occurrence of pul- 
monary and other complications. All that is necessary is to place the 
patient in a large, well-ventilated, darkened room, with the temperature 
of 63° or 65° F., so that the congested conjunctivae may not be exposed to 
light. 

The chief article of diet should be milk. If the patient complains of 
itching and burning of the surface, he may be frequently sponged with 
tepid water ; this causes an alleviation of the itching and burning, and re- 
duces the temperature. In an ordinary case this is all that will be re- 
quired. Hot drinks or stimulants have no power to hasten the appearance 
of the eruption ; the administration of the latter may be followed by very 
injurious results ; convulsions and death may occur. In an ordinary case, 
stimulants should never be administered during the initiatory period of 
the fever, unless there is some special indication for their use, such as great 
prostration or bronchial complication ; then they may sometimes be used 
with benefit. Covering the patient with heavy clothing does not hasten 
the appearance of the eruption. The greatest cleanliness should be ob- 
served ; besides, there should be free ventilation, avoiding all draughts, 
in the sick-room. If there is thirst, cold water may be freely taken in 
small quantities at a time. 

If the case is severe, and the temperature rises to 103 or 104 degrees 
F., it may be reduced by frequently sponging the surface with tepid 
water. 1 

Post-pharyngeal catarrh is liable to extend into the larynx and bronchial 
tubes and give rise to bronchitis. One of the most important duties of the 
physician is to watch for the occurrence of this complication ; he should 
frequently examine the chest, and when the bronchitis is found to have 
reached the capillary tubes, should immediately commence treatment for 
its relief. I have found the inhalation of steam to afford the greatest re- 
lief, and to best control the bronchial inflammation. As soon as the larynx 
has become so involved as to interfere with the respiration of the patient, 
and there is danger of croupous laryngitis, immediately order vapor inhala- 
tions, and insist upon their continuance until the laryngeal symptoms shall 
have subsided. Sometimes this subsidence will take place within two or 
three hours, and, again, not until after two or three days. The value of 
vapor inhalations in the treatment of the laryngeal and bronchial complica- 
tions of measles, I regard as very great. When catarrhal pneumonia is de- 

1 German writers recommend the cold bath in the treatment of measles. I should hesitate to place a 
patient with measles in a cold bath, on account of the great tendency in this disease to pulmonary com. 
plications. 



1 

GERMAN MEASLES. 



831 



veloped, it is to be treated in the same manner as catarrhal pneumonia 
developed under any other circumstances ; the patient should be sustained 
by the free use of stimulants. 

Pulmonary complications in measles are often the result of exposure to 
sudden changes in temperature ; the severity of catarrhal symptoms will al- 
ways be increased by such exposure, therefore it is of great importance in 
the management of every case of measles that the patient should be pro- 
tected against such changes. When there is great restlessness during the 
fever of invasion, or during the early period of the eruptive stage, small 
doses of opium, in the form of Dover's powder, may be administered with 
marked benefit. 

The management of the different varieties of measles will be indicated by 
the general condition of the patient. In the ulcerative, hemorrhagic, and 
typhoid varieties, the free administration of stimulants should be commenced 
early. Usually in these varieties there is great prostration, and the main 
indication is the support of the patient. Diarrhoea at the close of measles 
may take the place of lung complications, and should not be too suddenly 
checked. 



Q-EEMA1ST MEASLES. 
(Rolheln.) 

German measles, or epidemic roseola, has been regarded by some as a 
modified form of measles ; by others as a modified form of scarlet fever ; 
again, it has been thought to be a combination of the two diseases — a hy- 
brid disease. Some maintain that it is not an independent and specific dis- 
ease, but that it may embrace any blotchy exanthem. 1 I am disposed to 
regard it as a different type of measles from that which ordinarily pre- 
vails, and by way of distinction would call it German measles, or epidemic 
roseola. 

Morbid Anatomy. — It is one of the mildest of the eruptive fevers. It 
prevails epidemically and endemically. The study of its morbid anatomy 
has been almost exclusively restricted to the eruption. This consists of ir- 
regular spots, or hyperaemic blotches, varying in size from a pin's head to 
a large pea, usually slightly elevated, so that when the hand passes over 
the surface of the skin it feels somewhat rough. Sometimes these spots oc- 
casion intense itching ; they are quite distinctly separated by healthy skin, 
and disappear under pressure. As a rule, even at the acme of the develop- 
ment of the eruption, their color is a pale rose-red, paler than the intense 
red of the eruption of scarlet fever, or the peculiar bluish hue of the erup- 
tion in severe cases of measles. It appears upon all parts of the body, but 
is most abundant upon the face and trunk. The spots are usually discrete, 



1 Later German writers regard it as an independent affection, a specific, acute, and contagious eruptive 
fever, and have given to it the name of rubeola. 



832 



ACUTE GENERAL DISEASES. 



are round (not crescentic), they often lie crowded closely together, but they 
are not confluent. 

Mild roseola is a punctate rash. The throat is red and the glands in 
the neck may be enlarged. The rash rarely lasts more than two days, and 
it is attended by itching. In some cases there is slight desquamation ; 
it disappears and leaves no trace, except in occasional instances, when there 
is a transient, yellowish discoloration of the skin. 

Some aflirm that the rash may disappear and reappear alternately 
for several days, and when it has finally disappeared the disease has ter- 
minated, and there is nothing to fear from complications or sequelae. In 
certain rare cases vesicles resembling miliaria may be developed upon the 
hyperaemic spots, especially upon the back ; these are chiefly due to external 
conditions. 

Etiology.— Doubtless this disease is contagious. Nothing is known con- 
cerning the nature of its contagion. It is essentially a disease of child- 
hood. In those over forty years of age its development is of very rare 
occurrence. It is conveyed from one person to another in the same man- 
ner as measles. It has been stated that women are more susceptible to it 
than men. 

Symptoms. — Epidemic roseola is so mild an affection, that it is question- 
able whether it has an invasive stage. The duration of the stage of incuba- 
tion has not been determined. Generally, the symptoms which manifest 
themselves two or three days before the appearance of the eruption are 
much less marked than they are in any other eruptive fever. Perhaps in 
many cases they escape notice. The period of invasion is seldom more than 
twenty-four hours. Quite frequently the eruption is the first symptom of 
the disease. 

In most cases there may be nothing more than a feeling of discomfort. 
In other cases the disease may be ushered in by vomiting, diarrhoea, and 
convulsions. In many cases, immediately preceding the eruption, and ac- 
companying its appearance, there is well-marked fever, headache, loss of 
appetite, and sometimes noticeable prostration. When the eruption is 
regular in its appearance it affects first the neck and chest, then the face 
and scalp, and then gradually extends downward over the trunk and ex- 
tremities. Usually, the development and spread of the eruption are rapid, 
perhaps no more than two or three days being occupied in its passage over 
the entire body. Its duration upon any one part of the body before it be- 
gins to disappear is not more than twelve or twenty-four hours. In the ma- 
jority of cases the temperature does not rise more than 1° or 2° F. It may 
rise to 102° F. or 104° F. During the second day, the temperature begins 
to fall. Sometimes it reaches the normal within twelve hours, occasion- 
ally not until the third day. Sometimes it reaches it by crisis, at others 
by lysis. The pulse increases and diminishes in frequency according to 
the rise and fall of temperature. The tongue is usually covered with a 
whitish coating, and is dotted here and there with red and swollen papillae. 
The mucous membrane of the fauces is generally congested and the tonsils 



GEBMAH MEASLES. 



833 



Hag. 



105 



104 



J 03 



JD2 



JOI 



JVC 



9? 

93' 



5. 



6. 



7. 



Fig. 170. 

Temperature Record in 
Measles. 



case of German 



moderately swollen ; there may be some soreness of the throat. The 
mucous membrane of the air-passages is 
usually in a condition of mild catarrh, 
consequently, at the onset of the disease, 
sneezing and coughing are frequently 
present, but they are less marked and are 
of shorter duration than in measles. Suf- 
fusion of the eyes with congestion of the 
conjunctival vessels is rarely present ; there 
may be a slight degree of photophobia. 
The face and eyelids are usually slightly 
swollen at the time the eruption makes its 
appearance, but this swelling rapidly dis- 
appears. 

In most cases, there is moderate swell- 
ing of the lymphatic glands of the neck, 
and enlargement of the glands at the nape 
of the neck. Moderate enlargement of the 
occipital glands may continue for a num- 
ber of days The disease is so mild in char- 
acter that children are with difficulty kept 
in bed. 

Differential Diagnosis. — One of the promi- 
nent features of this disease is the close resemblance which its eruption 
bears to that of measles. In certain cases it may be impossible by the erup- 
tion alone to make a differential diagnosis. When the eruption of measles 
is not typically developed, a complete history of the case must be taken 
into consideration. When this has been done, there is usually no great 
difficulty in arriving at a correct diagnosis. Perhaps that which will best 
aid in making a differential diagnosis between roseola and measles is the 
fact that an attack of one does not protect against the other, any more than 
does an attack of varicella protect an individual from an attack of variola. 
This fact certainly establishes the non-identity of the two diseases. The 
short period of invasion, the eruption appearing first on the chest and neck, 
the very mild nose and throat symptoms, and the loiv temperature are in 
contrast with the symptoms of measles. 

It has been questioned whether a person may not have a second attack 
of epidemic roseola. The latest observations go to prove that a second attack 
is of as rare occurrence as a second attack of measles or scarlet fever. 
Again, one attack does not protect an individual against the contagion of 
scarlet fever ; nor does an attack of scarlet fever protect one against the 
contagion of roseola. An individual may have an attack of epidemic 
roseola very soon after he has been ill with measles or scarlet fever. 

Prognosis. — The prognosis is always good. Complications rarely occur ? 
when they do, they are usually pulmonary. 

Treatment. — The treatment of this affection consists in protection against 

exposure. Tepid sponging will relieve troublesome itching, and reduce 
53 



834 



ACUTE GEKEEAL DISEASES. 



fever. Eegulate the diet, and carefully watch the catarrh of the air-pas 
sages. As a rule, convalescence is rapid. 

MILIARY FEVER. 

This form of fever cannot strictly he regarded as a contagious disease, 
but it so frequently prevails in connection with measles and scarlet fever, 
and has apparently so many elements of contagion, that it is included iu 
the list of contagious fevers. Some deny its existence as a distinct fever. 
Writers have described it under the names of sudamina, sudoral exan- 
thema, miliaria alba, etc. Several diseases which are accompanied by sweat- 
ing, and which exhibit a tendency to the formation of miliary vesicles, have 
been called miliary fever. 

Until the occurrence of the severe epidemic of the disease known as the 
"English Sweating Sickness," its specific type was not recognized. It has 
prevailed epidemically over limited areas, in Belgium, France, England, 
Germany, Italy, and Austria. In some of these epidemics eleven to twenty 
per cent, of the whole population of the invaded district has been attacked. 
The average duration of the epidemics has been from three to four weeks ; 
occasionally they have lasted from three to four months. 

Morbid Anatomy, — Few post-mortem examinations have been made, and 
those few have failed to reveal any characteristic lesion. The miliary 
vesicles which are seen upon the surface of the body, and the cutaneous 
eruption, are developed because the secretion of the sudoriferous glands 
cannot escape. The escape of the contents of these glands may be pre- 
vented by two causes : (1) the gland-ducts may become obstructed ; or, (2) 
the secretion may be so abundant that it cannot be transmitted by the 
gland-duct. In either case, the secretion emerges under the epidermis 
around the sweat-duct, and as the scales are lifted up, a small clear vesicle 
is formed. The liquid contained in the vesicle at first is transparent, has 
an acid reaction, and is said to contain free nuclei and cells which have 
three or more nuclei ; these nuclei remain visible after the cell membrane 
has been destroyed by the addition of acetic acid. The contents of the 
vesicle becomes milky and yellowish from pus (m. alba). It has been 
claimed that the virus of the disease is contained in these polynucleated 
cells. After death, the skin becomes cedematous, and very soon the odor 
of decomposition is perceptible. 

Etiology. — It has been supposed that miliary fever was indirectly induced 
by scarlatina, the puerperal condition, variola, vaccinia, typhus fever and 
like diseases, and that it was not a distinct disease arising from some con- 
stitutional cause. The prevalence of this fever in connection with these 
diseases gave rise to this supposition. Epidemics of this disease have 
generally prevailed during the spring and summer months ; from this fact 
one would be led to think that there is some atmospheric condition pecul- 
iar to these months. Again, the disease has most frequently appeared in 
ivarm, moist weather, and from this fact it has been supposed that some 
peculiar condition of the soil is necessary to its development. Certain 



MILIARY FEVER. 



835 



epidemics have shown a close connection with contaminations of the soil, 
such as arise from neglect of drainage, collections of refuse, etc. Doubt- 
less, such conditions of the soil may increase its severity, and cause it to 
prevail more extensively, but facts do not prove that, directly or indirectly, 
they cause its development. 

The disease usually attacks healthy adults, and occurs more frequently 
among females than males. It attacks all classes, and its spread does not 
seem to be affected by crowding. 1 

Symptoms. — The average duration of the disease is from five to eight 
days. It has three stages: (1) the stage of invasion ; (2) the stage of 
sweating ; and, (3) the stage of eruption and desquamation. 

Hie Stage of Invasion. — The average duration of this stage is from 
forty-eight to seventy-two hours. It is characterized by an excessive irri- 
tation of the skin, thirst, general lassitude and headache. There is also 
more or less febrile movement. Some writers mention a feeling of suf- 
focation, which is usually preceded by a sense of oppression at the epigas- 
trium. These are the characteristic symptoms of the stage of invasion. 

Tfie Stage of Sweating. — This stage is usually ushered in by rigors ; 
rarely, by a well-marked chill. The characteristic symptom of this stage 
is profuse and persistent sweating. The sweating is accompanied by a 
prickling sensation of the skin, distress, and a sense of compression at the 
epigastrium, and by more or less violent palpitation of the heart, with pre- 
cordial pain. Usually the sweat appears on all parts of the body at the 
same time. Sometimes it appears first upon the head and breast, then 
gradually descends, and soon becomes so abundant that every article of 
clothing, bed-clothes and bedding, becomes saturated. The pulse some- 
times reaches 140 beats per minute, the temperature rises to 103° F., 104° 
F., or even 105° F., and the skin, notwithstanding the profuse perspiration, 
feels extremely hot. During this stage the headache and the sense of 
suffocation increase ; the epigastric and precordial pain and the palpita- 
tion increase in severity, and sometimes become alarming, although the 
most careful physical examination fails to discover any lesion in the 
heart or lungs to account for them. The respiration becomes rapid, often 
irregular and intermittent. 

Irregular exacerbations, or even intermissions, in these symptoms may oc- 
cur, but, as a rule, they continue without abatement until the vesicle ap- 
pears, on the third or fourth day of the disease. 

Tlie Stage of Eruption. — This stage is characterized by the appearance of 
a rash. It is first seen upon the neck and breast, then upon the back and 

1 It can hardly be regarded as a contagious disease, in the sense that it can be commnnicated directly 
from the sick to the well. It does not seem to be well established that the disease can be developed by 
inoculation with the contents of the vesicle, notwithstanding it has been supposed that certain cells in 
the fluid hold the contagion of the disease. The infrequency of the simultaneous occurrence of miliary 
fever with epidemics of measles or scarlet fever, is unfavorable to the theory that there is a specific rela- 
tionship between the poisons of these diseases. The view that there is an intimate relationship between 
cholera and miliary fever has been accepted by some writers, and the accession of the latter during 
the course of the former has been supposed to exert a favorable influence over the course of the disease ; 
the opposite, however, does not appear to hold good, but on the contrary, favors a fatal termination. 
Much remains to be learned in regard to the relationship existing between miliary fever aud the other 
diseases which ipe have mentioned. 



836 



ACUTE GENERAL DISEASES. 



extremities, sometimes upon the mucous membrane of the mouth, nose, and 
conjunctiva, sometimes upon the abdomen and scalp. This eruption con- 
sists of irregularly shaped spots, 1-8 to 1-16 in. in diameter. In some 
cases they stud the skin so thickly that it appears like an uniform sheet of 
vivid redness. After the lapse of a few hours, vesicles can be seen in the 
centre of these spots ; perhaps at first they are so small as to necessitate 
the aid of a lens to discover them. These vesicles rapidly increase in size, 
and may reach the size of a millet-seed or a small pea. The contents of 
these vesicles have already been described. Occasionally, as the eruption 
appears, all the constitutional symptoms are increased in severity, but usu- 
ally they are modified and disappear either suddenly or gradually after its 
development. Jn the milder cases the vesicles only, without the efflores- 
cence, are seen. -Vomiting is rarely present, although nausea is a common 
symptom, as is also constipation. 

The urine is usually scanty and high colored ; in some cases there is sup- 
pression of urine. Occasionally, during the stage of eruption, profuse 
secretion of urine takes place. This has been regarded as a favorable 
symptom. The vesicles, clear at first, soon become opaque and yellowish, 
remain for two or three days, then burst and begin to fall off in scales. 
Desquamation is usually completed within forty-eight hours, but convales- 
cence is often quite protracted on account of the debility and emaciation. 

Such is a brief description of miliary fever, when it runs a regular course, 
but there are certain variations in the development of the symptoms which 
should be noticed. In the severest form of the disease, the temperature may 
rise to 107° or 108° F., and there may be delirium and a sense of suffocation. 
Again, even in fatal cases, the eruption, sweating and convulsions may 
be absent. Occasionally sudden and fatal collapse follows the sweating 
stage. The typhoid condition maybe developed in the sweating stage, 
and may be attended by black sordes upon the teeth and tongue, epistaxis 
and uterine hemorrhage, and may terminate fatally, without any consid- 
erable anatomical changes recognizable after death. 

Complications are not of frequent occurrence. Occasionally there is 
bronchitis, pneumonia, and diarrhoea. 

Relapses are of common occurrence, but recovery generally takes place 
after a short relapse. 

Differential Diagnosis. — Miliary fever may be confounded with measles, 
with malarial fever, and with typhoid fever. 

The profuse sweating, the prickling of the skin, the intense oppression 
at the epigastrium, the sense of suffocation, with precordial pain, and the 
peculiarity of the eruption, are sufficient to distinguish it from measles, 
from intermittent fever (although a decidedly intermittent type of the dis- 
ease sometimes prevails), and from typhoid fever. When the disease pre- 
vails epidemically, the diagnosis cannot be difficult. 

Prognosis. — When the disease runs a regular course, with only a moderate 
degree of severity, the prognosis is good ; whereas great severity of the fe- 
brile symptoms, exceptionally profuse sweating, and increasing sense of 
constriction of the chest, with suffocation, render the prognosis unfavora- 



INFLUENZA. 



837 



ble. The accession of profuse hemorrhages, coma, convulsions, active de- 
lirium, or symptoms of collapse, render the prognosis unfavorable. The 
severity of the symptoms is usually mitigated when the eruption makes its 
appearance, and death rarely occurs after that stage is reached. If a fatal 
termination is reached, it usually takes place during an exacerbation, prior 
to the appearance of the eruption. In some epidemics, the mortality has 
been very great ; in other epidemics the disease has been mild in character ; 
eight or nine per cent, is the average death-rate. The character of the 
epidemic affects the prognosis. 

Treatment. — At one time diaphoretics were employed in the treatment of 
this disease, on the supposition that the sweating and eruption were criti- 
cal manifestations, and must be aided by all possible means. The sense of 
suffocation, with that of constriction of the chest, was thought to indicate 
blood-letting ; but it was soon decided that loss of blood aggravated rather 
than improved the patient's condition. Antispasmodics, nervines, quin- 
ine, emetics and counter-irritants at different times have formed the basis 
of various plans of treatment. Of late, subcutaneous injections of mor- 
phine have been used with advantage. Sinapisms and blisters have been 
employed for the relief of the sense of constriction in the chest, and for the 
epigastric and precordial distress, with benefit to the patient. It is now 
acknowledged that the administration of purgatives in large doses should 
be carefully avoided, as well as blood-letting, general or local. 

At present the expectant plan of treatment is regarded with most favor. 
It chiefly consists in the use of cooling drinks, aromatic teas, acidulated 
water, sponging with warm water, or the employment of warm baths. It 
has been thought that the addition of alum or vinegar to the water used for 
sponging or bathing is beneficial. In the treatment of this affection, quin- 
ine seems to be regarded with almost universal favor. If restlessness is 
persistent, opium, ether, valerian, and antispasmodics may be employed in 
moderate doses, carefully watching the effect produced. The patient should 
be surrounded by proper hygienic influences, the diet should be moderately 
nutritive, and in those cases in which convalescence is tedious a steady and 
continued tonic treatment is indicated. In the severest form of the disease 
stimulants may be employed with benefit. 

INFLUENZA. 

(Epidem ic Catarrh . ) 

Influenza is a specific continued fever, generally widely epidemic, and at- 
tended by catarrh of the respiratory and digestive tracts. It has received a 
great variety of names. In 1830 and '31 a severe influenza epidemic swept 
over the whole civilized world. 

Morbid Anatomy. — There are no special pathological lesions of influenza. 
There is generally more or less extensive inflammation of the respiratory 
organs ; the lungs are usually inflated so that when the chest is opened they 
protrude from the cavity instead of collapsing. Sometimes they are very 
dry, at others cedematous. Spots of lobular consolidation appear as de- 



838 



ACUTE GENERAL DISEASES. 



pressions between the inflated portions. The mucous membrane of the 
trachea and larger bronchi is red and covered with frothy or viscid muco- 
pus. The injection is usually most marked in the smaller tubes. The 
bronchial glands are enlarged and softened. Pale, firm clots are found in 
the right heart. The gastric and intestinal mucous membrane is congested ; 
the stomach is usually more congested than the intestines. Hence the name 
gastric influenza. 

Etiology. — All conditions and ages suffer alike; but children are some- 
times remarkably exempt. The disease travels very rapidly ; it has passed 
over the whole of Europe in six weeks. It passes quickly from one country 
to another, visiting whole continents in a short time. It rarely continues 
in one locality more than two months. There is no doubt that influenza 
is -due to some powerful special morbific agent, which is given off by the 
mouth of the infected, and which acts specifically upon the respiratory 
mucous membrane and also upon the nervous system. 1 

Symptoms. — Influenza comes on suddenly. A feeling of chilliness, 
sometimes distinct rigors, flashes of heat, and a feeling of lassitude are fol- 
lowed by symptoms of a severe naso-pharyngeal catarrh, with frontal 
headache, pains in the limbs and back, soreness of the throat, hoarseness, 
and a frequent racking cough, difficult breathing and constriction across 
the chest. The sputa are first mucous and then scanty, later copious and 
muco-purulent. The respirations are accelerated ; there is great prostra- 



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tion, lassitude, apathy, muscular 
weakness, and precordial oppres- 
sion. The fever assumes a remittent 
type, attended by profuse perspira- 
tion. Sudamina appear on the sur- 
face and herpes on the lips. The 
pulse is rarely over 90 ; yet a tem- 
perature of 104° has been observed, 
and the pulse has been feeble, ir- 
regular, and 120 per minute. The 
tongue is moist and covered with a 
white fur ; it may be dry and brown. 
There is anorexia. Nausea and 
vomiting may be early symptoms 
and continue throughout the whole 
course of the disease. The bowels 



Temperature Record in a case of Influenza. a t first are Constipated, later there 

is diarrhcea. There may be hepatic tenderness and slight jaundice. As 
the disease advances the face gets congested and livid, the frontal head- 
ache becomes more severe, the pulse increases in frequency and becomes 
feeble, the tongue becomes brown and dry. There are muscular* tremors 
and subsultus, the patient becomes dull and listless, and delirium is often 
present. 



1 Brimer (in Virchow's Handbuch) thinks it is a miasmatic disease, caused by a living miasm capable of 
being transmitted by the air and having an independent existence. It is probably contagious. 



INFLUENZA. 



839 



On auscultation sibilant and sonorous rales are heard oyer some portions 
of the chest, while at others the inspiratory sounds are dry and harsh. The 
vesicular murmur is always indistinct. Measle-like spots are often seen on 
the palatal mucous membrane. In mild cases the disease is at its height 
on the third day and then gradually declines. In the severe cases where the 
pulmonary symptoms are prominent, convalescence does not commence until 
the tenth or twelfth day ; convalescence is protracted and relapses are fre- 
quent. The urine is less in quantity than normal ; sometimes there is 
complete suppression. It is high-colored and deposits a sediment on stand- 
ing. The different " varieties" of influenza as described by writers are due 
to the different complications. 

Differential Diagnosis. — The large number of persons attacked, the nerv- 
ous debility which accompanies it, and its short uniform course are gener- 
ally sufficient for its diagnosis. 

The Prognosis is good except in the very old, very young, and in those al- 
ready subjects of pulmonary or renal disease. Whenever there is a high 
mortality-rate, the fatality is due to complications which have been en- 
grafted on the influenza. Its complications are chiefly of the respiratory 
tract, the more frequent of which are laryngitis, bronchitis, pulmonary 
congestion and oedema, pneumonia, 1 which is usually lobular, and pleurisy ; 
these complications have given to the disease the name of epidemic catarrhal 
fever. Pharyngitis, parotitis, salivation, hyperemia of the liver, and sub- 
acute gastritis are rare complications of the digestive apparatus. Herpes 
labialis occurs often. The duration of influenza varies from four to twelve 
days ; and an epidemic rarely continues more than from four to six weeks 
in one locality. 

Treatment. — When influenza is prevailing all exposure to cold must be 
carefully avoided, and in its treatment the general hygienic measures of 
the acute infectious fevers are to be employed ; medicinal treatment is not 
very efficacious. Quinine sometimes aborts it, if given in large doses at its 
very onset. In the early stages liquor ammonii acetatis and pulvis ipe- 
cacuanha (one grain of the latter in one-half ounce of the former) every 
two or three hours is all that is required. The bowels should be kept 
freely open with salines ; milk combined with alkaline waters is the only 
food which should be allowed for the first forty-eight hours. If patients 
are restless, Dover's powders may be given in small doses. Steam inhala- 
tions will relieve the laryngeal and bronchial symptoms, and may be con- 
stantly employed during the acute stage. The prostration which occurs 
in the old, young, or feeble must be combated early with stimulants. 

All revulsives, blood-letting and depressing remedies are contraindi- 
cated. Colchicum, carbonate of potash, and opiates are of service in those 
cases of influenza where pain and rheumatic symptoms are predominant. 
When convalescence commences the patient should begin to take quinine 
and iron in small doses with a nourishing diet ; a change of air is often of 
great service, especially if there have been pulmonary complications. It 

1 In one hundred and eighty-three patients at H6tel Dieu over twenty per cent, had lobar pneumonia 
—Copland. 



840 



ACUTE GENERAL DISEASES. 



must be remembered that influenza is often the exciting cause of a phthi- 
sical development m subjects who are so predisposed. 

PEETUSSIS. 

( WJi ooping- Cough. ) 

"Whooping-cough is an acute contagious disease, attended by a peculiar 
spasmodic cough. It should be classed among the diseases of children, 
although it may occur at any age. 

Morbid Anatomy. — The principal, if not the only, morbid changes in 
this affection are those of catarrhal bronchitis. Those who regard the 
disease as of nervous origin claim that there are evidences of inflammation 
of the vagus nerve, or congestion of the medulla oblongata. I am dis- 
posed to regard it as a specific catarrh of the respiratory mucous membrane, 
which differs from other forms of catarrh in being contagious and attended 
by peculiar laryngeal and bronchial spasms. Its complications are cerebral 
oedema and congestion, lobular collapse, lobular emphysema, bronchial 
dilatation, or capillary bronchitis and catarrhal pneumonia. 

The specific catarrh is located chiefly in the bronchi, although some re- 
gard it as at first limited to the pharyngeal mucous crypts, and still 
others regard it as confined to the larynx. The bronchial and mediastinal 
glands may undergo softening, the pleurae and pericardium may be ecchy- 
motic. The mucous membrane of the stomach is congested and sometimes 
studded with petechial extravasations. Follicular enteritis is not uncom- 
mon. The liver and the spleen are often enlarged and fatty. Letzreich 
claims to have found a fungoid vegetation in the epithelium of the air 
tubes. Buhl, Oertel, and Hitter also found them. 

Etiology. — Whooping-cough depends upon a specific poison which is 
given off in the breath of the affected, and conveyed through the air to 
the healthy. A second attack is rare. The period of incubation varies 
from five days to two weeks ; micrococci are sometimes found in the sputum. 
Teething and measles predispose to the reception of the infection. It may 
be carried in clothes. It may prevail epidemically, attacking nearly all 
the children of a neighborhood or township. 

Symptoms. — There are three recognized stages in whooping-cough, a 
catarrhal, a spasmodic, and a stage of decline. 

The catarrhal stage is marked by the ordinary symptoms of a severe naso- 
pharyngeal and bronchial catarrh. It rarely commences with a chill, but 
fever, restlessness, and languor are marked. The fever in the early stage 
is intermittent. It commences with coryza, and a severe dry paroxysmal 
cough, which is soon attended by an abundant, tenacious, viscid, transparent 
mucus. The respirations are shallow and the pulse is rapid. The dura- 
tion of this stage is from two days to three weeks ; nine to ten days is the 
average. 

The spasmodic stage is attended by a characteristic spasmodic cough. 
This cough is very severe and distressing ; the face grows red, and then 
begins a long, clear, piping sound, followed by a series of rapid, convulsive 



PEKTUSSIS. 



841 



and forcible expiratory puffs, which are succeeded by a prolonged, shrill 
inspiratory sound or whoop. If the fit lasts any length of time, the cough 
becomes inaudible, and a considerable quantity of clear, yiscid mucus is 
expectorated or vomited with the contents of the stomach. During the 
paroxysm the patient grows red or purplish in the face, the eyes pro- 
trude, the tongue assumes a dark appearance, and he seems on the yerge 
of suffocation. Bleeding from the mouth, nose, ears, and lungs often 
occurs during a violent paroxysm. The face becomes puffy, and ulcers 
form on the tongue, and hemorrhages occur into the conjunctivae. The 
subsidence of the paroxysm is usually followed by a sense of exhaustion, 
with soreness about the muscles of the chest, and expectoration of whitish, 
viscid mucus. 

A physical examination of the chest during a paroxysm of whooping 
cough shows a feeble or absent respiratory murmur over the whole chest, 
with sibilant and sonorous rales ; during the interval mr.cous rales are 
usually heard. The frequency and duration of the paroxysm vary greatly 
in different cases. There may be one hundred in twenty-four hours. They 
are most frequent, or occur only at night. As a rule the more violent the 
paroxysm the sooner it is followed by another. The disease usually attains 
its height by the end of the fourth or fifth week. In mild cases the pa- 
tient is well in the interval between the paroxysms, but in severe cases 
there may be languor and debility, loss of appetite, headache, and more or 
less fever. Moist or dry crepitations and a weak inspiratory sound are often 
heard during the interval. 

The stage of decline is marked not by any sudden transition, but by a 
gradual diminution in the frequency and severity of the paroxysms. The 
peculiar whoop ceases, the expectoration is less difficult and becomes more 
purulent in character, and finally, after a period of about nine weeks, the 
characteristic cough ceases altogether, and the patient passes into a rapid 
convalescence. Whenever the coughing fits lose their characteristic feat- 
ures and become dry and hacking, and the dyspnoea is greatly increased 
and continues through the intervals with a marked rise in the temperature, 
it indicates some pulmonary complication. Another complication which 
is particularly to be feared in this disease is cerebral congestion. When, 
during a paroxysm, the countenance becomes flushed and swollen, the 
jugular veins turgid, with a gush of blood from the nose, there is danger 
of such an occurrence. When the face is continually flushed, the head 
hot, the patient drowsy or restless in his sleep, moaning and grinding his 
teeth, there is danger of convulsions and coma, and the disease often termi- 
nates fatally. 

Differential Diagnosis. — In its earlier stages, it is not possible to diagnos- 
ticate whooping-cough with certainty ; but its existence may be suspected 
if the cough is of a violent spasmodic character, and if the disease is prev- 
alent. When the disease is fully established, the peculiar cough and ex- 
pectoration distinguish it from all other catarrhs. 

Prognosis. — Whooping-cough is always a serious disease, although it is 
rarely directly fatal ; yet indirectly it frequently causes death. It is dan- 



842 



ACUTE GENERAL DISEASES. 



gerous in proportion to the number and severity of the paroxysms, the in- 
tensity of the fever, and the character and severity of the complications. 
Cerebral or pulmonary complications are always dangerous. Teething 
children are liable to convulsions during paroxysms of the coughing. 
Death may result from laryngeal spasm independent of complications. A 
condition of general debility, rickets, poverty and destitution, a residence 
in a city in badly ventilated apartments, and epidemic influences, tend to 
render the prognosis unfavorable. 

Treatment. — The chief indications in the treatment of whooping-cough 
are, first, to diminish the severity of the paroxysms ; second, to prevent 
and treat as far as possible the complications ; third, to attend to the gen- 
eral health of the patient. There are no known means by which this affec- 
tion may be averted. The paroxysms cannot be altogether prevented, but 
their severity may be lessened. 

All of the internal and external specifics for the prevention of the parox- 
ysms of whooping-cough, which have been proposed, and. in some instances 
strongly advocated, are of very doubtful benefit. The most important and 
reliable remedies for relieving the paroxysms of coughing are the sedatives 
and antispasmodics, the most efficient of which are belladonna, hydrocyanic 
acid, hydrate of chloral, hyoscyamus, cannabis indica, the bromides, chloro- 
form and musk ; all of these remedies must be given in minute doses, and 
their effects closely watched. Recently antipyrine and quinine have been 
strongly recommended. The dilute mineral acids, arsenic, nux vomica, 
cochineal, bromide of potassium, and repeated emetics — emetics are no 
longer given — have each in turn been highly recommended as specifics for 
the control of the paroxysms in whooping cough. Alum is recommended 
by Golding Bird (gr. i-v every four hours) and Meigs 1 says it is the best 
remedy. No form of opium or belladonna is to be used till after the 
catarrhal stage is past. Infusion of chestnut leaves is regarded highly. 
Inhalation of coal gas is recommended by the French Academy of Medi- 
cine. Ergot, the carbolic acid spray, asafoetida, arsenic and quinine are 
highly efficacious, 2 the second and last especially. The nitrite of amyl and 
jaborandi are drugs that I would not give to very young children. Local 
applications to the larynx, such as solution of nitrate of silver, etc., ac- 
cording to my experience, do more harm than good ; and the same is true 
of counter-irritants, such as liniments and plasters. 

I desire to impress this fact, that whooping-cough is a self-limiting dis- 
ease, and, like all other diseases of that class, must be treated expectantly. 
The patient, by warm clothing, should guard against undue exposure. In 
bad weather, he should be confined to the house in a room of uniform 
temperature ; but there is no reason, if the weather is favorable, why he 
should not go out into the open air. The diet should be simple, and the 
state of the alimentary canal carefully looked after. Adults and older 
children should be taught to suppress the cough as much as possible. 

Complications must be watched for, and treated as soon as they occur. 
Bronchitis is the most frequent complication ; when it occurs it should re- 
ceive prompt attention, according to the rules already given for the man- 



1 Dis. of Children. 



2 Binz and Squire. 



HYDROPHOBIA. 



843 



agement of bronchitis, great care being taken that it does not become a 
broncho-pneumonia. If the symptoms of congestion of the brain or of 
pneumonia are developed, they should be met by the most prompt and effi- 
cient remedies adapted to these conditions, and their earliest appearance 
should be watched for. It is important to remember that in any or all of 
the complications of whooping-cough, the treatment should be supporting 
in character. 

During convalescence, tonics, such as iron, quinine and cod-liver oil, are 
indicated ; in fact, in a large proportion of cases these remedies are service- 
able throughout the whole course of the disease. Astringents and restora- 
tives are called for in the third stage and at the commencement of conva- 
lescence. Sometimes this affection assumes a chronic form, continuing after 
several relapses much beyond the usual period. In these cases, the great 
remedy is change of air. In all stages of whooping-cough, benefit is de- 
rived from a short sea-voyage and a temporary residence in a warm climate. 
It has been recently stated by some very judicious observers, that large 
doses of the sulphate of quinine have the power of aborting this disease. 
My experience in this direction is not sufficient to deny or sustain the state- 
ment ; but my impression is that this, like many other so-called specifics, 
after a more extended trial, will be found unavailing. 

HYDEOPHOBIA. 

Hydrophobia, or rabies, is a specific contagious disease special to animals 
of the canine and feline species, which may be communicated to man and 
to all warm-blooded animals. 

Morbid Anatomy. — There are no constant pathological changes. The 
mucous membranes of the alimentary and respiratory tracts, especially' of 
the fauces and pharynx, are congested, oedematous, and possibly show points 
of hemorrhage. The tongue, tonsils, and the salivary glands are enlarged 
and softened, and the lungs and other internal organs are congested. 

Eecent investigations have shown 1 congestion of the nervous centres, most 
marked about the basal ganglia, the medulla and the gray matter of the 
cervical cord. This is accompanied by a diffuse cellular infiltration of the 
adventitia of the veins, with venous injection and thrombosis. Miliary an- 
eurisms and minute hemorrhages have also been noted in the medulla, cer- 
vical and dorsal regions of the cord. 2 

The blood is dark, forming soft clots, and putrefactive changes appear 
early after death. 

Etiology. — The cause of the disease is a specific virus which is most 
abundant and concentrated in the saliva and secretions of the mouth 
and pharynx. Pasteur's experiments show that the poison is present 
abundantly in the nervous centres, and particularly in the spinal cord. 

The poison retains its vitality for some time after the death of the 
affected animal. Although not proven, it is probable that the disease is 
never of spontaneous origin, but spreads among animals by contagion. It 

1 Fitz and Shattuck. 

2 Benedict considers the essential pathological change in the nerve centres to he "an acute exudative 
inflammation attended by byaloid degeneration." 



844 



ACUTE GENERAL DISEASES, 



certainly is communicated to man solely by inoculation, which can take 
place only through some break in the surface. Applied to the skin or swal- 
lowed the virus is inert. 1 

Symptoms. — As in other infectious diseases, there is a period of latency 
following the inoculation, during which the wound heals readily and pre- 
sents no peculiarities. This period of incubation varies from a few days to 
several months, and in some cases even to years. It is seldom, however, 
that the disease appears after five months, and usually within two to six 
weeks the stage of invasion begins. 

This may or may not have been preceded by slight reddening about the 
seat of the inoculation, with pain which radiates from the wound along the 
nerve trunks. In a few cases the inflammation causes suppuration and re- 
opening of the wound. 

The period of invasion, or melancholic stage, is attended by marked de- 
pression of spirits and change in the disposition. The patient is feverish 
and shivering alternately, is restless, uneasy and sleepless, and speaks in 
a sharp, quick manner. The pupils are dilated and the eyes bright, and 
the countenance has a look of anxious anticipation of some unknown 
danger. The pulse is increased in frequency, the skin dry, and there is 
constipation, with perhaps nausea and vomiting. In this stage the respi- 
ration is oppressed, and shows evidences of the approaching spasms. There 
is epigastric heaviness, and with inspiration the shoulders are elevated and 
the epigastrium protuberant. 

There may be also slight constriction of the throat and hesitancy in 
swallowing, with general hyperesthesia and sexual excitement. 

These symptoms increase in severity for two or three days, when the 
patient passes into the convulsive stage. 

The restlessness and undefined dread are more marked, the eyes have a 
wild look, are bright, staring, and constantly moving ; the brows are con- 
tracted, the surface pale, and the patient not only often appears like one 
with acute mania, but the fear and horror may pass on to halluciations and 
delirium. 

The mouth and fauces are dry, congested, and covered with thick, 
tenacious saliva, which gathers about the lips in frothy masses. Thirst is 
intense, but every effort the patient makes to drink, and later the sight 
of water or thought of drinking is followed by increase of the pharyngeal 
constriction at first, and later by violent spasms of the muscles of deglu- 
tition and respiration, attended by general tremors and most terrific mental 
distress. 

At first the convulsions only follow attempts at drinking, but the general 
hyperesthesia increases rapidly and becomes so intense that the weight of 
the clothes, loud harsh sounds, bright lights, or a draught of cold air will 
excite general convulsions that leave the patient utterly exhausted and with 
the most agonizing horror of their repetition. 

In some cases death occurs early in the disease from asphyxia during a 

1 Pasteur's experiments show that inoculation with, a diluted virus affords protection from the actual 
disease. Not over seventy per cent, of those bitten by rabid animals become hydrophobic, owing, doubt* 
less, in many cases to the cleansing which the fangs receive as they pass through the clothing. 



HYDROPHOBIA. 



845 



spasm, but more commonly as the symptoms increase in severity the patient 
is rapidly exhausted ; the pulse becomes feeble, frequent, and irregular, 
and as the spasms are more prolonged, he may die from gradual asphyxia 
or exhaustion. 

In rare cases a paraplegic stage is said to occur, in which the paralysis is 
most marked in the under jaw and lower limbs. 

The ''hydrophobia" which is so characteristic of the disease as to give 
it a name, is due entirely to fear of the distressing spasm which every effort 
at swallowing produces, and is generally absent in dogs and other animals. 
For the same reason the patient is continually hawking and spitting out 
the thick, ropy mucus which is so abundantly secreted. 

The peculiar characteristics of the disease are the intense hyperesthesia 
of the skin and organs of special sense; the exalted reflex irritability of 
the nervous centres, which results in the peculiar spasms ; and the parox- 
ysmal rabid impulses that lead the patient to injure, it may be, his dearest 
friends, even when he is conscious of the nature of his frenzy and is strug- 
gling against it. 

Differential Diagnosis. — Hydrophobia may be confounded with tetanus, 
but in tetanus the mind is clear throughout, there is no fear of liquids, 
the spasms are tonic and the hyperesthesia is not so acute, nor does it in- 
volve the special senses. 

In hysteria the difficulty in swallowing is the only symptom of hydro- 
phobia, and the expressions of fear are out of all proportion to the other 
symptoms. A spurious rabies may be developed by the imagination in 
patients, who suppose they have been bitten by a rabid animal, but the 
course of the disease, its milder symptoms and favorable termination, will 
readily distinguish it. 

Prognosis. — Most authors regard the disease as absolutely fatal, and in 
tables of cases which record a small per cent, of recoveries the possible 
hysterical nature of these cases must be considered. I have never known 
a case to recover. 

The duration of the disease is from two to ten days, but in rare cases may 
be extended to two or three weeks. Death usually occurs from asphyxia, 
rarely from exhaustion or inanition. 

Treatment. — When it can be done immediately, if the injury is upon a 
limb, a tight ligature should be applied above the wound, which is then to 
be widely excised and the part cupped. Venous hemorrhage should be 
encouraged. 

Of the many remedies proposed, curare offers the most encouragement. 
It should be given hypodermically, in doses of one-third grain every fifteen 
minutes, increasing until the spasms are controlled. Recovery has been 
reported in one case where it was used. Pasteur claims that the develop- 
ments of the disease may be prevented and its progress arrested by inocu- 
lations with an attenuated hydrophobic virus derived from the spinal cord 
of an affected animal. His claims have received the support of a large 
number of careful scientific observers. 



SiG ACUTE GENERAL DISEASES. 



MALAEIAL FEVEE. 

Introduction. 

The different varieties of malarial fever are like different branches of 
the same tree ; they have many things in common, yet differ from each 
other so widely in the phenomena which attend their development, 
that they may . be regarded as distinct diseases. They have a common 
origin in a poison which has received the name of miasm. 1 All varie- 
ties of malarial fever depend upon one and the same poison, which is 
subject to certain variations in quantity. The concentration of this poison 
determines the severity and, to a certain extent, the type of the fever. It 
is possible to arrange the different types in a progressive scale, from the 
mildest to the most severe, beginning with simple intermittent and passing 
on to pernicious fever. The extent of the morbid processes and the rapid- 
ity with which they are developed depend upon the intensity of the malarial 
poison, the length of time the individual has been under its influence, 
and, to some extent, upon individual idiosyncrasies. 

Many theories have been advanced as to the nature of this miasm 
or malarial poison. By some it is regarded as gaseous in its nature ; others 
believe it to be a living vegetable organism ; and again, others think it a 
specific poison, having no tangible, chemical or microscopical constituents. 
No one of these theories, nor any of the many others which at different 
times have been advanced, has been sustained either by fact or by reliable 
chemical or microscopical analysis. In 1881 Lavaran, and later, in 1883, 
Marchiafava and Celli, described certain protoplasmic bodies in the red 
blood corpuscles of malarial patients, to which the name (i plasmodium 
sanguinis malarias " was given. It was claimed that these bodies were 
found only in connection with malarial poison. Their presence in a pro- 
portion of cases seems established, but it is entirely undetermined whether 
they are normal, or are the cause or result of the malarial infection. While 
we have no positive knowledge in regard to the true nature of malaria, we 
do know something of the circumstances which are necessary for its pro- 
duction, and the laws which regulate its development. 

First. — There must be a certain amount of vegetable matter, either on 
the surface or in the substance of the soil where the malarial poison is gen- 
erated. It is not necessary that the quantity be large, but a certain amount 
is a necessity. 

Second. — A certain amount of moisture must be on the surface or in the 
substance of the soil ; it need not be excessive ; but some is indispensable. 

Third. — A certain average degree of temperature is necessary for its pro- 
duction. It cannot be developed below an average temperature of 58° F. 
for the twenty-four hours, and will not prevail as an epidemic unless the 
average temperature ranges as high as 65° F. for the twenty-four hours. 

In regions where these fevers prevail, their type, form and intensity, to 
a great degree, depend upon the height of the temperature. As a rule, 
malarial fevers are endemic, rarely extending over large sections of coun- 



1 " Telluric poison " is a term which has recently come into vogue. 



MALARIAL FEVEK. 



S47 



try in the form of an epidemic. We also have some knowledge concerning 
the regions in which malarial fevers are most likely to prevail, and which 
seem most favorable to the development of malarial poison. 

First. — Marshes are especially favorable to the development of this poi- 
son, and may generate it for an indefinite period. The Pontine marshes 
have been malarial for more than two thousand years. Yet all marshes 
are not malarial ; their power to generate the malarial poison varies with 
the amount of water they contain. Where there is an abundance of water, 
malarial fevers are rare ; when they are covered only with a thin sheet of 
water, and are exposed to the direct rays of the sun, malarial poison will 
abound. Marshes that have dried up are especially favorable to the de- 
velopment of this poison, yet as soon as heavy rains submerge the previously 
parched surface, the power to generate the poison is for a time diminished 
or entirely arrested. Scattered here and there over our own continent are 
districts which have been malarial ever since the white man has held pos- 
session of them ; whether such was the case in earlier times, history is too 
uncertain to determine. 

As a rule, salt-water marshes are especially free from malaria, but when 
salt and fresh water are mixed in the marsh, the most favorable conditions 
for the abundant development of malaria occur. Marshes that rest on a 
substratum of sand are far less malarial than those resting on limestone, 
clay, or mud. There are marshes in the higher latitude of New York and 
other States which often, during the heat of summer, become dry, yet no 
malarial poison is generated (although during the day the thermometer 
may reach 90° F.), since during the night the temperature falls below 50° 
F. There are some quite extensive marshes in which, apparently, every con- 
dition of development of malaria exists, and yet none is generated. We 
cannot account for this fact unless we accept the theory that the ozone 
which is claimed to be present in such marshes arrests or prevents its gene- 
ration. Damp " bottom lands " that are exposed to an annual overflow, 
such as are found along the southern shores of the Mississippi Eiver, are as 
fruitful as swampy regions in the generation of this poison. 

Second. — Another condition which seems to favor the development of 
malaria is the upheaval of new alluvial soils, such as obtains when new 
lands are first brought under cultivation. This same state of things also 
occurs throughout the middle and southern portions of this State, and in 
the New England States. Where railroad excavations are made, malarial 
fever is very frequently developed. In New York City, while the Fourth 
Avenue improvements were being made, the entire region along the 
avenue was rendered highly malarious by the excavations. Such excava- 
tions bring decomposing vegetable matters to the surface ; these, under 
the influence of heat and moisture, generate miasm. 

The fact that fevers of this type appear in regions previously free from 
them, as soon r 3 the conditions favorable to their development exist, is 
confirmed by the testimony of many careful observers. 

Third. — Eegions otherwise non-malarial may have malarial poison 
brought to them by the waters of rivers which have their source in, or 
flow through, malarial districts. Examples of this kind are found along 



848 



ACUTE GENERAL DISEASES. 



the banks of our Western rivers, where some of the most pernicious types 
of this fever are developed ; while in places only a short distance from 
these rivers it is unknown. 

Fourth. — Non -malarial regions may be rendered malarial from poison 
transmitted by the wind. There has been considerable discussion as to 
whether this poison can be transmitted in such a manner, and if it can be, 
to what distance ; there is no reliable account of its transmission over a 
greater distance than four and three-quarter miles. 1 The wind may also 
carry malarial poison up along the sides of mountains, to an elevation of 
one thousand feet ; some writers say no higher than six hundred feet. 
American writers give an account of its being carried higher than six hun- 
dred feet, while some German writers give well-authenticated cases which 
show that it must have been carried to the height of one or two thousand feet. 

The circumstances which are inimical to its production are: 

First. — High latitude. In this country malarial poison is not generated 
in higher latitude than that of Quebec. The limit of its development is 
63° north and 57° south latitude. Between these two parallels of latitude, 
both on the eastern and western hemispheres, malarial fevers may be 
developed ; the nearer the approach to the equator, the more severe the 
type. They do not prevail over the entire region embraced between these 
parallels of latitude, but it is possible for them to be developed at any 
point where the altitude is not too great. 

Second. — High elevation is another condition inimical to its development. 
As a rule it is not generated above an elevation of one thousand feet above 
the sea. There are, however, some remarkable exceptions to this rule. 
We find recorded cases of malarial fever which have been developed upon 
plateaus among the Pyrenees, at an altitude of five thousand feet, and in 
South America at ten and eleven thousand feet above the sea-level. 
Among the Pyrenees, there is a marsh which has a clay bottom, and there 
malarial poison is developed which is very persistent. 

Third. — Drainage is another means which diminishes, and in certain 
conformations of soil entirely destroys, malarial generation. In the ma- 
jority of marshes, this generation can be arrested or prevented by free 
drainage. Yet there are marshes upon which millions have been expended 
in drainage and which still remain pestiferous. Perhaps it is possible to 
drain the Jersey flats so as to render them non-malarial in their character, 
out it is hardly probable that this change can be effected, for they have a 
clay bottom, and contain both salt and fresh water, conditions which are most 
favorable to malarial generation. Years of labor and large expenditures of 
money have been bestowed upon the Pontine marshes to render them non- 
malarial, yet they are as pestiferous as they were twenty centuries ago. 

Fourth. — Cold is a powerful agent in arresting malarial generation. If, 
in a pestiferous region, the temperature should fall below the freezing 

* Malarial fever broke out in the crew of a ship, which was anchored just four and three-quarter miles 
from shore where this fever was prevailing. No cases were on board when the anchor was cast, nor did 
any of the crew go on shore. So long as the wind blew from the ship towards shore, the crew remained 
well, but when the wind changed its direction and blew from the shore towards the ship, within six days 
from the time of change, cases of well developed malarial fever appeared on board. This seemed to prove 
conclusively that the fever was brought to the ship by the wind. 



MALARIAL EEYER. 



849 



point, only for one night, nothing more need be feared in that region from 
malaria, until the average temperature shall haye again reached 60° F. 
This law holds in all malarial districts. In these districts, after the 
temperature has fallen below the freezing point, persons may have the 
fever, but it is the result of previous poisoning. Again, the generation 
is less rapid and the poison is less virulent during the day than at night. 
This is the uniform testimony of those who have seen most of, and written 
most on malarial diseases. It is also almost universally conceded that mala- 
rial districts are most pestiferous during months when the atmosphere is hot 
and dry, with little or no wind, especially when this state of atmosphere 
has been preceded by long, heavy rains, and that the virulence of the 
poison is greatly diminished as soon as fresh, strong winds clear the atmos- 
phere. 

The question arises : How does malarial poison gain entrance into the hu- 
man body ? The most reasonable view is that this is effected through the 
respired air. Certain facts seem to show that it maybe introduced through 
the intestitial tract with the food and water. There seems to be scarcely 
a doubt but that it may be taken into the stomach with foul drinking- 
water. When this poison has once been introduced into the circulation, it 
undoubtedly has the power of reproducing itself. From this fact, which 
must be regarded as well established, these who regard this poison as a liv- 
ing organism, claim that these organisms may reproduce themselves in- 
definitely, but this has never yet been demonstrated. 1 

It has also been claimed that certain races are more exempt than others 
from malarial fever, also that there are idiosyncrasies of constitution which 
render certain individuals exempt from diseases of this type, for in dis- 
tricts where these fevers prevail there are persons who never have the 
fever. This exception, both in races and individuals, is due to the greater 
physical power of the individual, which enables him to resist these noxious 
atmospheric influences. In a district where malarial influences prevail, 
the weak and anaemic are the most liable to be attacked, and all those in- 
fluences which tend to lower vitality, and to render feeble the powers of 
resistance, must be regarded as special predisposing causes. A strong man 
may resist for a long time, while the old and children very quickly suc- 
cumb to the influence of the poison. Women are more susceptible than 
men. We can no more account for the fact that one person can take in 
large doses of malarial poison without being affected by it, while another 
is affected by a very small quantity, than we can account for the fact 
that one person can take large quantities of alcoholic stimulants without 
showing any signs of intoxication, while a very small quantity will intox- 
icate another, supposing, in both instances, the individuals to have ap- 
parently an equally vigorous constitution. Some claim that when a person 



1 1880. Recently Crudeli (of Rome) and Klebs of Prague) examined the lower strata of air, the soil, and 
the stagnant water, and in the two former they found a " microscopic fungus," consisting of numerous 
movable shining spores, long and oval, nine micro-millimeters in diameter. This fungus was cultivated 
and when inoculated into animals they all had a regular typical chills and fever with an enlarged spleen. 
They call this the bacillus malaria. Roman physicians now claim that they have found this in the human 
subject. It is said to be always in the blood during the period of invasion. The spleen and the marrow of 
the bones are its favorite seats. 
54 



850 



ACUTE GENERAL DISEASES. 



has been poisoned with malaria, complete recovery never takes place ; others 
that even in the worst cases recovery is possible. My own experience leads 
me to believe that when an ind.ivid.nal has once suffered, from malarial 
poisoning, he is much more susceptible to the poison than one who has 
never been so poisoned. Some unknown physical change has taken place 
which renders him a fit subject for malarial manifestations upon the 
slightest exposure. 

The doctrine of latency of malarial poison in the human body is an in- 
teresting and at the same time a very obscure subject. That there is a 
period of incubation, or rather that a certain time elapses between the ex- 
posure and the development of malarial fever, seems to be settled. For a 
certain period, often a long one, always elapses before new-comers in a 
malarial district have their first attack of the fever ; sometimes the poison 
remains latent until after they have removed from the district. It is on the 
basis of the latency of the malarial poison that the relapses can be ac- 
counted for which occur in those who, having lived in a malarial district, 
remove and remain in a non-malarial one. This reawakening of the mala- 
rial poison may depend upon a variety of causes, such as taking cold, over- 
fatigue, sudden changes of temperature, etc. From my own observation, I 
am convinced that it is impossible to bring one wholly from under the 
influence of the poison while remaining in a malarial district, though he 
may become exempt from its influence if he remains beyond the malarial 
belt. Undoubtedly, an individual may become so acclimated as to resist 
malarial influences, and live for a long time in a malarial district without 
suffering any evil effects from it. There can be no question but that those 
living in such districts suffer less from the acute manifestations of the 
poisoning than new-comers. But those changes which are called chronic 
malarial manifestations are constantly going on in those who are supposed 
to be acclimated. 

Malaria acts like any other poison : after a time the system reaches a cer- 
tain degree of tolerance. This tolerance, or immunity from its manifesta- 
tions, amounts to nothing more than the accommodation of the system to 
its influence. Let the acclimated person, as he is called, be taken sick 
with any active form of disease, such as diphtheria or pneumonia, and it 
usually proves fatal, not that there is anything unusually severe in the 
diphtheria or pneumonia, but death is due to the fact that the system is 
depressed by the malarial poison, and its power of resistance to disease is 
lessened. 

INTERMITTENT FEVER. 

Like typhoid fever, intermittent fever is met with in all parts of the 
world, although the region of its development may be said to be limited 
by 63° north and 57° south latitude. "Within these parallels it is the 
more prevalent nearer the equator. 

Morbid Anatomy. — Its anatomical changes are few. None of those 
changes in the blood which are present in the more severe forms of in- 
fectious diseases are found, those which are present in the pernicious type 
of malarial fever, such as pigmentation and marked diminution in the red 



INTERMITTENT FEVER. 851 



globules are much less prominent. Some disintegration of the haemoglobin 
and corpuscular pigmentation, however, will be developed when the fever 
is distinctly established. But the blood clots imperfectly, and is of an 
abnormally dark color, and if the fever has continued for a long time there 
may be slight diminution in the number of the red globules and a decrease 
in the fibrin-factors ; but these changes, to a great extent, are due to the 
high temperature which attends its paroxysms. 

The only constant pathological lesion of intermittent fever is congestion 
of the internal organs. The spleen and liver are always more or less en- 
larged, but the enlargement is due to simple hyperemia; no structural 
changes occur in these organs until the intermittent paroxysms have been 
often repeated, and the malarial poisoning has been of long duration. 
There is also more or less hyperemia of the kidneys and the mucous mem- 
brane of the intestines, but it is not attended by any signs of gastric or 
intestinal catarrh. As yet no one has been able to prove that any structural 
change takes place either in the nerve tissue or in any other tissue of the 
body ; nor from the structural or functional disturbances that occur during 
the fever has any one been able to find satisfactory answer to the question: 
why is it a paroxysmal and not a continued fever? During a paroxysm of 
the fever the white blood-globules are very rapidly increased in number. 

Etiology. — This subject has just been considered. All agree that simple 
intermittent fever is due to malarial poisoning, and that the poison is in- 
troduced into, the body either through the lungs or through the intestinal 
tract. Whatever tends to depress the mental or physical powers of an in- 
dividual renders him more susceptible to malarial influences, and con- 
sequently these depressing influences must be regarded as predisposing 
causes. Among these may be included 
intemperance, exposure to night air, exces- 
sive fatigue, bad hygiene, and a long list 
of like debilitating causes. 

Symptoms. — This fever is paroxysmal, 
and differs in its types according to the 
period of time which intervenes between 
the paroxysms. The first, and most com- 
mon, is the quotidian type, in which the 
paroxysm occurs every day, and there is 
an interval of twenty-four hours between 
the paroxysms. 

The second is the tertian type, in which 
the paroxysm occurs every third day, with 
an interval of .forty-eight hours between the 
paroxysms. 

The third is the quartan 1 type, in which 
the paroxysm occurs every fourth day, 
with an interval of three days or seventy- 
two hours between the paroxysms. These 
are the regular and more common types. 



Day. 



J 05 
J 04 
/OS 

SVI° 

/eo l 
99' 

93" 



iS 



6. 



6. 



1 



Fig. 172. 

Fever Curve in Quotidian Intermittent. 



1 In 98,237 cases in the U. S. army, ouly 1,757 were quartan. 



852 



ACUTE GENERAL DISEASES. 



Day. 



/05 

/04° 

icrf 

/02 
IOl° 
/CP 

99 
98° 



in 



Fig. 173. 

Fever Curve in Tertian Intermittent. 



Other types exist, which, although irregular, are unquestionably modi, 
fications of those already mentioned. Among these is the double quotidian, 

in which two paroxysms occur daily. Usu- 
ally one paroxysm is severe, the other mild ; 
the severer one generally occurs in the 
morning, the milder in the afternoon or 
evening. There is also double tertian, in 
which a paroxysm occurs daily, but it 
differs from the quotidian as the paroxysms 
that resemble each other occur at intervals 
of forty-eight hours. For instance, the 
paroxysm of to-day is characterized by the 
occurrence of a severe chill and mild fever ; 
to-morrow it is characterized by a short 
chill and severe fever ; the following day 
there occurs the severe chill and mild fever, 
as on the first day. 

A form of intermittent fever is met with 
in which the paroxysm occurs on the 
seventh, fourteenth, twenty-first day, etc., 
with an interval of seven days between the 
paroxysms. The types most frequently met 
with are the quotidian, tertian and quar- 
tan. In the quotidian variety the paroxysm occurs in the morning, in 
the tertian it occurs about noon, while in the quartan it occurs in the 
afternoon or evening. The duration of the 
paroxysm varies with the type of the fever. 
In the quotidian it lasts from eight to ten 
hours, in the tertian it lasts from six to 
eight hours, in the quartan from four to six 
hours. There are many exceptions to these 
rules, but it is a question whether there 
would be any if the disease was permitted 
to run its course without treatment. 

Paroxysms. — A paroxysm of intermit- 
tent fever has three stages —the cold stage, 
the hot stage, and the stage of sweating. 
In most cases these are readily distinguished 
from one another. In the true type of 
intermittent fever regular intervals between 
the paroxysms of fever occur. The phenom- 
ena which usually precede the cold stage 
are pain in the head, a sense of languor, 
and some nausea. 

Cold Stage. — Passage into this stage is 
first marked by a sensation of coldness 
along the back, which soon extends to the extremities, and an uncom 




Fig. 174. 

Fever Curve in Quartan Intermittent. 



INTERMITTENT FEVER. 



853 



fortable sensation of coldness gradually creeps oyer the entire body. The 
skin becomes shrivelled, the finger ends and lips become blue, the face 
is pale, the eyes are sunken, chills rapidly follow each other, the teeth 
begin to chatter, any voluntary motion is attended by trembling, until 
finally, as one chill after another in quick succession passes over the body, 
the teeth chatter so that the noise can be heard some distance from 
the patient, and there is a shaking of the entire body. The surface of 
the body becomes rough, the blood seems to recede from it, and it as- 
sumes the appearance of goose-skin or cutis anserina. The temperature 
of the surface of the body is lower than normal, but if the thermometer 
be placed in the axilla or under the tongue the temperature marks 104° 
or 105° F. The voice of the patient is weak and husky ; the respirations 
are rapid, short and sighing, but the mind remains clear. The urine is 
increased in quantity and paler than normal, and there is frequent desire 
to empty the bladder. Usually these symptoms last from half an hour to 
two or three hours ; the length of time depends upon the severity of the 
case. Children do not have a regular chill ; they merely grow cold, blue 
and livid. 

After the cold stage has continued for a longer or a shorter period, the 
patient begins to have flashes of heat alternating with the chilly sensa- 
tions. Usually these are first felt at the extremities, but they rapidly ex- 
tend over the whole body, and the hot stage is established. 

Hot Stage. — The skin is now no longer shrivelled, but becomes red, 
swollen and turgid, and there is a recession of the blood from the central 
organs to the surface of the body. That the temperature is elevated can- 
not be ascertained simply by laying the hand upon the surface. If, 
however, the thermometer is placed in the axilla, in most cases the tem- 
perature marks 106° or 107° F. Thirst is intense. The uncomfortable sen- 
sation which the patient experienced while passing from the cold to the 
hot stage, has given place to great restlessness, the patient tossing from 
side to side, with face flushed and eyes red and fiery. Sometimes her- 
petic vesicles appear about the mouth. The tongue becomes dry, the caro- 
tids pulsate, the radial pulse becomes firmer and more rapid than in the 
cold stage, and nausea is marked. It may have been present in the cold 
stage, but in the hot stage nausea and vomiting become the prominent 
symptoms. As a rule these symptoms last from half an hour to two hours. 
In exceptional cases they may continue for a much longer time, the ordi- 
nary duration of a paroxysm of a quotidian intermittent being from eight 
to ten hours ; that of a tertian, from six to eight hours ; and that of a 
quartan, from four to six hours. It is possible, especially in those forms 
of malarial fever in which the poisoning is intense, for the hot stage of 
a quotidian to continue twelve hours. 

There is no condition in which, for the time, there is more intense fever 
than in the hot stage of intermittent fever. The urine, which during the 
cold stage was abundant and of a pale color, now becomes highly colored 
and scanty. Not infrequently it is almost suppressed during the hot stage. 
Complete suppression of urine occurs only in the pernicious type of the dis- 



854 



ACUTE GEKERAL DISEASES. 



ease. When the fever has continued for a longer or shorter time, a slight 
moisture appears upon the forehead, which gradually spreads over the en- 
tire body, and the patient becomes bathed in a profuse perspiration. He 
is now in the stveating stage. In children, just before the sweat, coma or 
convulsions may occur. . 

Sweating Stage. — As this stage comes on, restlessness and uneasiness de- 
cline, and a feeling of comfort is experienced as the perspiration makes its 
appearance. The temperature rapidly falls ; the pulse rapidly diminishes 
in frequency and force ; the pulsation of the carotids ceases ; the face as- 
sumes its normal appearance ; the congestion of the conjunctivae disap- 
pears ; and the patient rapidly passes from a high state of fever into 
one in which lie falls asleep, and awakens after a period ranging from one 
to three hours, with a sense of exhaustion. 

Interval. — During the interval between the paroxysms at first the 
patient may feel perfectly well, but if there is a frequent repetition of 
the paroxysms, there will very soon be a marked loss of vitality ; he be- 
comes pale and feeble, and all the symptoms of malarial cachexia are pres- 
ent. There will be more or less of a jaundiced hue to the skin, enlarge- 
ment of the spleen and liver, and pigmentation of the tissues. It is 
true that many paroxysms of simple intermittent may occur before any 
such general disturbance of the health of the patient manifests itself ; 
yet, in the interval between the paroxysms, we cannot call the patient's 
condition one of perfect health. Usually, in the quotidian type, the day 
previous to the development of the first paroxysm, unnoticed by the pa- 
tient, there is a slight rise in temperature, perhaps to 101° F. At the 
same time he experiences a sense of lassitude, and is disinclined to make 
any exertion, either mental or physical. The temperature commences to 
rise in the morning, and by noon it has reached its maximum ; then it be- 
gins to fall, and by evening it may have fallen to nearly its normal stand- 
ard. Thus the course of the temperature is quite characteristic, and may 
be summed up as a rapid ascent, a short and intense stationary period, 
and a critical defervescence constituting the paroxysm, with a perfectly 
normal temperature in the interval. The following day another rise in 
temperature will be noticed ; now the rise does not occur in the morning, 
but after midday, perhaps as late as in the evening. Usually in the quo- 
tidian type of intermittent fever the highest temperature is reached a little 
earlier each day ; if it is reached a little later, the fever is being modified 
or controlled by treatment. 

When the paroxysm comes on a little earlier each day, it is called antici- 
pating, and indicates that the fever is not being controlled ; when it comes 
on later each day it then indicates that the fever is being controlled, and is 
called a postponing intermittent . The types of intermittent fever which 
occur most frequently in temperate climates are the quotidian and the 
tertian. In those who have suffered repeatedly from intermittent fever, 
the disease is liable to run an irregular course, the paroxysms occurring on 
irregular days, and with irregular intervals. In children this fever shows 
certain deviations from the ordinary course. The paroxysms may be 



INTERMITTENT FEVER. 



855 



ushered in by convulsions,- or by a period of stupor. Children rarely have 
the distinct chill ; after a period varying from ten minues to half an hour, 
we have the hot stage of regular intermittent fever coming on, with all its 
attendant phenomena. The intermissions are rarely complete. The child 
loses his appetite and flesh, becomes irritable, and has a pale, waxen look, 
suffers from gastric and intestinal disturbances, and the intermittent very 
soon lapses into the remittent form. 

Differential Diagnosis. — The differential diagnosis of simple intermittent 
fever is never very difficult. There are only two diseases which are liable 
to be mistaken for it, namely, remittent fever, and pycemia. 

It is readily distinguished from remittent fever, for in remittent fever 
there is never a complete intermission, whereas in intermittent there is 
always a period in which there is no fever. A careful thermometrical ob- 
servation for twenty-four hours settles all questions in regard to it. There 
is also a regular development of the paroxysm in intermittent, which does 
not occur in remittent. In remittent, there is usually but one chill, while 
in intermittent a chill precedes each paroxysm of fever. When the chill 
and sweat are absent, but a sense of heat, malaise, headache and lassitude 
come on at pretty regular periods in a malarial district, the thermometer 
showing a pyrexia of 102° to 104° F., the patient is said to have " dumb- 
ague." 

Prognosis. — The prognosis in simple intermittent fever is good. The 
possibility of the development of malarial cachexia must enter into the 
prognosis. When this occurs the case is more than one of simple inter- 
mittent fever ; there is enlarged spleen and liver, with pigmentation of 
the tissues. 

Treatment. — The treatment of intermittent fever is divided into that for 
the paroxysm and that for the interval. 

The treatment for the paroxysm, in most cases, is simply to render the 
patient as comfortable as possible while passing through its various stages. 
At one time it was proposed to tourniquet the limbs, so as to prevent con- 
gestion of internal organs, and thus arrest the paroxysms. Again, it has 
been proposed to apply cold to the surface for the purpose of giving a 
shock to the nervous system, and in that manner to arrest the paroxysm. 
Some propose to cover the surface of the body with sinapisms, in order to 
irritate the cutaneous surface. Some have claimed that if an individual is 
brought fully under the influence of alcohol the regular development of a 
paroxysm can be prevented. It has also been claimed that opium, given 
in full doses at the usual time for the recurrence of the paroxysm, has 
power to prevent it. Experience does not lead me to accept any of these 
statements. It is true that, in some instances, a sudden shock to the 
nervous system may prevent the development of an intermittent paroxysm 
when the paroxysms have become a habit. 

If there is anything in the entire list of means (either remedial or 
hygienic) which has power to prevent the full development of a paroxysm, 
it is opium. When this is administered hypodermically, early in the cold 
stage, it will diminish the severity of the cold and hot stages. Whether. 



856 



ACUTE GENERAL DISEASES. 



in the treatment of the milder forms of intermittent fever the combination 
of opinm with quinine is advisable, is still an unanswered question, though 
it seems to me that in such cases much comfort can be afforded, and the 
patient be much less injuriously affected by the paroxysm if opium be ad- 
ministered in moderate doses. Patients with intermittent fever should be 
kept in bed during the entire paroxysm, however mild it may be. 

During the cold stage, cover them with blankets, surround them with 
bottles of hot water, and let them drink freely of hot water. All these 
means will hasten the hot stage of the disease. 

During the hot stage, the extra clothing and external heat should be 
gradually removed and cold instead of hot drinks should be administered. 
If nausea and vomiting are present in this stage, opium, administered hypo- 
dermically, affords great relief. When the patient reaches the sweating- 
stage, let him alone ; within a few hours he will be entirely relieved and 
in a state of convalescence. 

The treatment of the interval is to prevent the occurrence of another 
paroxysm. A patient should never be allowed to have a second intermit- 
tent paroxysm ; for if the system once becomes accustomed to these parox- 
ysms, they will be repeated upon the slightest provocation. This will be 
found to be the case with those who for a long time have not been sub- 
jected to malarial influence, and yet upon the least nervous excitement or 
fatigue will have a paroxysm. The great remedy at this time is the sul- 
phate of quinine. Skilfully used, it is all-powerful to accomplish this re- 
sult. How and why it arrests the development of these paroxysms is still 
unknown. Our knowledge of its antiperiodic power is purely empirical. 
There is much difference of opinion as to the mode in which it should be 
administered. In commencing the treatment of a case of intermittent 
fever, after the occurrence of the first paroxysm it is always safe to assume 
that the fever is of the quotidian type. At least thirty grains of quinine 
should be administered between the termination of one paroxysm and the 
hour when another is to be expected. The first dose of ten grains should 
be given toward the close of the sweating stage, and twenty grains about 
two hours before the time of the expected paroxysm. If possible, give the 
quinine in solution. If irritability of the stomach causes rejection of the 
quinine, it may be administered hypodermically, or by enema. Three 
grains administered hypodermically has about the same antiperiodic power 
as ten grains administered by the stomach. If one succeeds in preventing 
the occurrence of a second paroxysm much has been accomplished. Hav- 
ing prevented the occurrence of a second paroxysm, it is important that a 
moderate degree of cinchonism should be maintained for a number of days, 
by the daily administration of quinine in moderate doses. About two 
hours before the time of clay at which the first paroxysm occurred, from 
ten to fifteen grains of quinine should be daily administered. 

A patient should visit his physician one month f rom the date of the first 
paroxysm, for although he may not have had a fresh malarial exposure, 
there will be a strong tendency at this time to a repetition of the paroxysm, 
and it is important that at that time he should be again brought fully 



INTERMITTENT FEVER. 



857 



under the influence of quinine. If it is possible for him to remove from a 
malarial district a second paroxysm will almost certainly be prevented. If, 
however, the patient is not seen in his first paroxysm, and if he lives in a 
malarial district, sulphate of quinine, administered in the manner I have 
just recommended, may only prevent for a time the return of the parox- 
ysm, and even complete cinchonism may fail to control it. The case 
should now be carefully examined in order to ascertain if there is not some 
condition present which interferes with the antiperiodic action of the qui- 
nine, such as hepatic or splenic hyperaemia. When careful percussion shows 
that the liver and spleen are increased in size, even after the administra- 
tion of full doses of quinine, the administration of full doses of calomel 
with the quinine will increase the antiperiodic power of the latter, and 
diminish the percussion areas of these organs. 

Occasionally, when full doses of quinine combined with calomel have 
failed to prevent a recurrence of a paroxysm, I have noticed an unusual 
excitement attending its development, and believing from this circumstance 
that owing to individual idiosyncrasies the malarial poison had a more 
than usual irritating effect upon the nervous system, I have accomplished 
the desired result by administering full doses of opium with the quinine. 
In fact, if the patient is of a highly sensitive, nervous organization, I 
never allow a second paroxysm to pass without administering a full dose of 
opium before the time when its return is to be expected. In all those cases 
which are called obstinate, we must ascertain why we fail to control the dis- 
ease by the use of quinine. I rarely have administered arsenic in simple 
intermittent fever. If I fail to control the fever with quinine, after I have 
reduced splenic and hepatic congestion, controlled nervous irritability, and 
increased nutrition by the administration of iron and the moderate use of 
stimulants, I never succeed with arsenic. In some of the chronic forms of 
malarial manifestation, I have found arsenic of great service, but never in 
simple intermittent fever. Salicin, strychnia, piperine, eucalyptus, and 
hydrastia sometimes act antiperiodically when quinine fails. 

Masked Intermittent. — In this connection should be mentioned a 
form of intermittent fever which has been designated as mashed inter- 
mittent fever. For example, to-day a patient has a regular intermittent 
paroxysm, but to-morrow, instead of its recurrence, perhaps he suffers 
from the most intense neuralgia. This neuralgia may have its seat in 
an intercostal or in the sciatic nerve, or, perhaps, more frequently in the 
frontal branch of the ophthalmic division of the trigeminus. Some one 
nerve becomes involved and no other seems to be affected. In some cases, 
an intense hemi crania takes the place of the paroxysm. As a rule, these 
neuralgias have distinct intermissions, and so come to be regarded as masked 
forms of intermittent fever. Instead of a neuralgia, the patient may have 
an attack of asthma, or an attack of indigestion. Diarrhoea, dysentery, 
and sometimes hematuria and apparent suppression of the urine may take 
the place of a distinct intermittent fever paroxysm. Again, a patient may 
have a single well-defined chill, or even two chills, followed by most intense 
hemicrania, and then have no more for a long time ; but sooner or later he 



858 



ACUTE GENERAL DISEASES. 



will have a well-defined intermittent paroxysm which will reveal the real 
nature of the disease. 

REMITTENT FEVER. 



This is a continued fever, with diurnal exacerbations. It is known by 
different names, such as Southern, Western, African, continued, bilious, 
acclimative, and remittent fever. The term remittent fever is the one 
more generally accepted. 

Morbid Anatomy. — The anatomical lesions of remittent fever resemble 
those of intermittent fever ; and the differences are in degree rather than 
in kind. 

Unquestionably, both these types of fever are the result of malarial 
poisoning, and the same diminution of the red globules and the same 
changes in the fibrin factors occur in remittent as in intermittent. Yet 
there are other changes in the blood which are usually present in the 
former, and quite rare in the latter, namely, the presence of free pigment- 
granules. These pigment-granules are met with in some of the pernicious 
forms of intermittent fever ; but in all cases of well-developed remittent 
fever they are present at some time during the progress of the disease. 
This pigmentation is due to haemoglobin which has been liberated from the 
blood-corpuscles within the blood-vessels, and the coloring matter may re- 
main either within the blood-corpuscles, which, after a time, become trans- 
formed into pigment-granules, or remain free in the fluid portion of the 

blood, or infiltrate the adjacent 

m 




cells and tissues. It may be 
transformed into granular or 
crystalline hsematoidin. 

The spleen is not so much 
enlarged in remittent as in 
intermittent fever, and the 
increase in size seems to be of 
a different nature. The enlarge- 
Jsment is evidently the result of 
W congestion, and the organ some 
times presents very nearly the 
same appearance as it presents 
in typhoid fever, except that 
there is more pigmentation. 
There are also structural lesions 
FlG J75 found in the liver, in the 

Section cf the Liver from a case of Remittent Fever, showing stomach and in the intestines, 

A. Centr^of^ml:^ M ^ » ot P»«* « 

B. B. Intralobular capillaries densely pigmented. mitten t fever. The liver is 

C. Hepatic cells, also containing pigment. 

not very much increased in 
size, and is of a bronze hue. The principal change is in color, which 
is uniform throughout its entire substance. This varies in degree in 
different types of the disease, and in different cases of the same type. 



mm 



KEMITTEiTT FEYEK. 



859 



The peculiar color is due to pigmentation of the liver-tissue, and varies 
according to the amount of pigment deposited. Pigmentation may occur 
in other tissues of the body, but not to the same extent as in the liver. On 
a microscopical examination of the liver, pigment is found throughout its 
entire structure — not only in the hepatic cells, but in the nuclei of these 
cells, and in the walls of the blood-vessels. This discoloration is of such 
uniform occurrence that it has been recognized as the characteristic path- 
ological lesion of remittent fever. Consequently, the "bronzed liver" is 
spoken of as the characteristic lesion of this fever. Occasionally this lesion 
occurs in intermittent and pernicious fever, but this is so seldom, and its 
presence is so constant in remittent fever, that if met with at an autopsy 
remittent fever may be suspected. 

The mucous membrane of the stomach is more or less congested, thick- 
ened, and softened. Changes similar to those in typhoid are found in the 
mucous membrane of the intestines ; it is more or less congested, and pre- 
sents very much the apj)earance seen when a moderately severe catarrhal 
inflammation is present. The Peyerian patches are usually enlarged, and 
quite frequently present the shaven beard appearance. In some cases 
there are ulcerations, not, however, as extensive or of the same nature as 
the ulcerative processes of typhoid fever. The mesenteric glands are not 
enlarged, and there is none of that granular infiltration so noticeable in ty- 
phoid fever. 

Etiology. — The great predisposing and exciting cause of this fever is ma- 
larial poisoning. There can be no question but that the same malarial poi- 
son which gives rise to intermittent fever can produce a remittent fever. In 
other words, a remittent can pass into an intermittent fever, and an inter- 
mittent into a remittent fever. While it is possible for this to occur, the 
two diseases do not, as a rule, prevail in the same locality at the same time. 
Endemics of one form may occur and be followed by endemics or sporadic 
cases of the other form. In some localities remittent fever is almost the 
only form of malarial disease, intermittent fever only occasionally occur- 
ring. 

There is probably no form of endemic disease the geographical bounda- 
ries of which are more extensive than those of remittent and intermittent 
fever. In general terms they may be said to encircle the earth parallel with 
the equator, circumscribing a broad belt, limited by 63° north and by 57° 
south latitude. The boundaries of this belt are quite irregular, now ap- 
proaching the line of the tropics, now receding from it. The remittent 
fever which occurs within the temperate portions of this belt is much less 
severe than that which occurs in the tropical regions. From the localities 
in which this fever prevails, it would seem that a higher average tempera- 
ture is required for its development than is required for the development of 
intermittent fever. As already stated, a remittent fever during its con- 
valescence may become an intermittent, and, conversely, an intermittent, 
either from new exposure to malarial influences or to the influence of high 
temperature, may become a remittent. From this fact, the conviction is 
forced upon as that both types of fever are developed from a common poi- 



860 



ACUTE GENERAL DISEASES. 



son. Usually certain atmospheric changes will have taken place to change 
the type of the fever. Intermittent fever may prevail early in the season, 
but as the season advances, and the temperature ranges higher, the fever 
which prevails will assume the remittent type. Those who go from a non- 
malarial district into one where remittent fever is prevailing are likely to 
have it, while the old inhabitants only suffer from the milder form of inter- 
mittent. 

Symptoms. — Its ushering-in symptoms are usually well marked. The 
most constant as well as the most urgent of the premonitory symptoms is 
oppression in the epigastrium. This may be present for forty-eight hours, 
or even a longer time, prior to the development of the fever. There is 
also a certain lassitude, nausea, and loss of appetite ; and with these feel- 
ings uneasiness and perhaps pain in the head and limbs. It does not come 
on gradually, like typhoid fever, but abruptly, usually with a chill. It is 
not difficult to determine when the patient began to be sick. The chill is 
neither so complete nor so long continued as in intermittent fever or pneu- 
monia. During the chill the thermometer will indicate a temperature two 
or three degrees above the normal. With the chill there is a most intense 
headache, and pain in the back and limbs. As a rule the chill is not of so 
long duration as the chill of intermittent, neither does it begin like it, by 
creeping down the back and gradually extending over the body, but there 
is general coldness over the entire surface at the very commencement of 
the chilly sensation. Again, there is not that tremulousness and shaking 
of the body, nor that chattering of the teeth, which are so frequently ex- 
perienced in intermittent fever. Following the chill there is fever, during 
which the temperature rises very rapidly. The fever increases in severity, 
and, within twelve hours from the time of its commencement the tempera- 
ture may reach 105° or 106° F. As soon as the temperature commences to 
rise, the pulse is increased in frequency, and perhaps beats 100 or 120 a 
minute. The face becomes flushed, the eyes are usually suffused, and the 
conjunctivae are somewhat congested. The patient is restless, tossing in 
bed, in the vain search of an easy posture. As the hot stage advances, 
nausea and vomiting are always present, and the sense of oppression in the 
epigastrium increases, and is not relieved by vomiting, which is persistent 
and distressing. 

In the febrile stage of remittent fever the patient suffers from pain in 
the epigastrium, to such an extent that quite commonly it is the only thing 
of which he complains. The epigastric distress is often accompanied by 
the most extreme tenderness upon pressure. The material first vomited 
simply consists of the contents of the stomach, next follows the vomit- 
ing of a greenish matter, and finally, in severe cases, there may be a 
slight amount of black vomit. The quantity of fluid vomited is greater 
than the quantity taken into the stomach. Vomiting of stringy mucus 
tinged with green is always present. Sometimes the patient's stomach 
rejects everything taken into it, and the vomiting is accompanied by intense 
pain in the head. Usually at the commencement of the fever, the bowels 
are constipated. . 



REMITTENT FEYEE. 



861 



The febrile symptoms increase in severity for ten or twelve hours, 
when a slight perspiration appears upon the forehead. In a short time, it 
extends over the entire body, not profuse, but a slight moisture upon the 
surface. With the perspiration there will be a fall of one or two degrees 




Fig. 176. 

Temperature Record in a case of Remittent Fever ending in recovery. 

in temperature, and a fall in the pulse of ten or twenty beats in the minute. 
The thirst will diminish, the vomiting grow less, there may now be ability 
to retain fluids in the stomach, and the patient falls into a quiet, refresh- 
ing sleep, and is relieved from all the severer symptoms of the paroxysm. 
If, however, the thermometer is placed in the axilla, it will indicate fever, 
and although the temperature may show a marked decline, it is still above 
the normal standard. At no time is there a complete interruption ; the 
fever is continuous. This is termed the period of remission. At the same 
hour on the following day all the active febrile symptoms return, the range 
of temperature is higher, the gastric disturbance is more marked, the 
countenance assumes an anxious expression, and all the symptoms are more 
severe. 

This return of the severe febrile symptoms constitutes what is called the 
exacerbation, and the period between the time when the fever abates and 
the development of the exacerbations is called the period of remission. 
Remissions and exacerbations are the characteristic symptoms of a remit- 
tent fever when it is fully developed, at which time a morning remission 
is the rule, though the time of the first paroxysm varies. The morning 
remission is so invariable that it is regarded by many as a diagnostic sign. 
If the exacerbation begins at noon it will usually decline about midnight, 
and the remission will last until about noon the next day. In very severe 
cases there may be a double exacerbation, one at noon, the other at mid- 
night, the remissions being in the evening and morning. The second 
exacerbation is similar to the primary in its attendant phenomena, except 
that it is more severe and of longer duration, ends in a less profuse per- 
spiration, and the remission is not so well marked as the first. On the 
third day at about the same hour, or a little earlier, there is another 



862 



ACUTE GE^EKAL DISEASES. 



exacerbation, which has a st'ill longer duration, is of greater severity, and 
is followed by a more incomplete remission. 

If the disease continues, the remission from day to day becomes less and 
less distinct. By the end of the first week the remission can no longer be 
detected, and the fever becomes continuous, without any marked daily va- 
riation in temperature or pulse. As the remissions become less and less 
distinct, with each returning exacerbation, the tongue becomes more and 
more parched, sordes collect upon the teeth, the countenance becomes dull 
and heavy, distress and pain in the epigastrium continue, and are accom- 
panied by tenderness, although the senses of the patient are so dulled that 
he may scarcely complain of it ; and the vomiting is not so constant, and 
is of a less distressing character ; constipation, which was present at the com- 
mencement of the fever, has now given way to diarrhoea, the discharges usu- 
ally being of a brownish color. With the diarrhoea there is some fulness of 
the abdomen, and some local tympanitis. Hiccough is often obstinate and 
distressing. The pulse is increased in frequency, and will reach 120 or 130 ; 
it is small, thready, and feeble — at the onset of the disease it was full and 
compressible. The patient slips down in bed, picks at the bed-clothes ; 
there is subsultus and difficulty in deglutition, and the tongue is protruded 
with difficulty, as in the severer forms of typhoid fever. The urine is 
scanty, acid, dark colored, but very rarely is it albuminous. It may be 
bloody. The patient passes into a condition closely resembling that of one 
in the third week of typhoid fever, with the exception that there is no erup- 
tion. 

The diarrhoea, abdominal disturbance, and tympanitis, and often the 
tenderness over the ileo-ca3cal region, the typhoid tongue, and the low mut- 
tering delirium, closely ally this stage of remittent fever to typhoid fever. 
After these symptoms have continued a week or ten days, if the case is to 
terminate in recovery, remissions occur and become more and more dis- 
tinct, until finally there is no exacerbation, and the patient passes into a 
state of convalescence. If, however, a fatal termination is to take place, 
the remissions will not recur, but the typhoid symptoms become more 
marked, and the patient finally dies from exhaustion or from complica- 
tions. Of all the symptoms which attend remittent fever, nausea and 
vomiting are the most constant and the most distressing. I have seen pa- 
tients, after the temperature has fallen to its normal standard, suffer for 
weeks from gastric disturbance, attended by more or less jaundice. 

If, in the progress of a remittent fever, the exacerbation occurs a little 
earlier each day, then treatment is not controlling it ; the fever is then said 
to be anticipating, and the disease is almost certainly passing from a dis- 
tinct remittent to a continued remittent. If, on the other hand, the ex- 
acerbation occurs a little later each day, the fever is said to be postponing, 
and it is under control, the remissions become longer, the exacerbations be- 
come shorter and less severe, until the patient reaches complete convales- 
cence. The thermometer will indicate to what extent the disease is being 
controlled. 

Bilious Remittent Fever. — In a certain proportion of cases in all endem- 



REMITTENT FEVER. 



863 



ics of remittent fever, vomiting of " bilious " material, and jaundice are 
prominent symptoms, the skin often becoming so yellow that the patients 
present an appearance similar to that of those suffering from yellow fever ; 
with this yellow discoloration of the skin there is an unusual tenderness on 
pressure over the hepatic region. Under such circumstances this fever 
has been named " bilious remittent " By some of the older writers it has 
been described as an idiopathic fever, distinct from remittent or any other 
form of malarial fever. Medical literature, however, contains no facts in 
support of such a view. The pathology and symptomatology of the fever 
described by writers under the head of bilious remittent fever differ in no 
respect from those of simple remittent, except that the fever is accompa- 
nied by symptoms of more than usual hepatic and gastric disturbance. My 
own experience leads me to regard it as a form of simple remittent, accom- 
panied by a more than usually severe gastro-hepatic catarrh, and that it 
is not entitled to a separate place in the nosology of fevers. 

Infantile Remittent Fever. — It is a matter of every-day experience that 
children are subject to certain gastric and intestinal derangements, which 
are attended by more or less fever, which is very apt to assume a remittent 
type. Such fevers cannot, however, be regarded as specific diseases, for 
they are developed independent of any specific fever poison, and are only 
symptomatic of some local irritation. There is a form of mild typhoid fe- 
ver which is often met with in children, especially in the autumn, which 
has also incorrectly received the name of infantile remittent fever. In 
this class of cases, the usual symptoms of typhoid fever are so modified by 
age that the fever assumes a remittent type. The presence of rose-colored 
spots, and the characteristic typhoid lesion of the intestines, will determine 
the true nature of these fevers. Simple malarial remittent in children does 
not differ from the remittent of adults. Eemittent fever in children is more 
liable to be followed by malarial cachexia than in the adult. 

Differential Diagnosis. — The rules by which a remittent is distinguished 
from an intermittent fever have already been given. 

The differential diagnosis between remittent and typhoid fever is often 
attended with difficulty, if the patient is not seen until the second week of 
the disease, but if he is seen at the very onset of the fever, it is hardly pos- 
sible to confound these two forms of fever. The sudden advent of a remit- 
tent is in marked contrast to the slow development of a typhoid fever. Be- 
sides, they widely differ in the range of temperature during the first week 
of their development. In remittent there is a distinct remission, and there 
can be no doubt as to the type of fever after the first, certainly not after the 
second remission has occurred. Gastric symptoms are much more severe in 
remittent than in typhoid. By these symptoms alone a differential diag- 
nosis can be made. If, however, the fever has been protracted to the third 
week, and the remissions are slight or altogether absent, although many of 
the symptoms of typhoid fever are present, the absence of the rose-colored 
spots, taken in connection with the previous history of the patient, is suf- 
ficient to establish the diagnosis. 

Remittent fever may be distinguished from yellow fever by its high range 



864 



ACUTE GENERAL DISEASES. 



of temperature, by its daily exacerbation and remission, by the presence o: 
pigment in the blood, and by the absence of albumen in the urine, which 
is present in yellow fever. In remittent fever, hemorrhage from the mu- 
cous surfaces, especially from the mucous membrane of the stomach, indeed 
from any source, is of rare occurrence, while in yellow fever it frequently 
occurs from mouth, nose, eyes, ears, bowels, and urinary passages. Death 
often occurs on the third day in yellow fever, but in the severest cases of 
remittent fever not before the seventh day. Yellow fever is portable and 
contagious ; remittent is neither. Kemittent fever may be confounded with 
pyaemia and septicaemia, but their differential diagnosis has already been 
sufficiently considered. 

Prognosis. — The prognosis in simple remittent fever is good. Even cases 
of the severe types of this fever should terminate in recovery, if skilfully 
managed, especially if they are seen in the early stages. Its type varies very 
much according to locality. The remittent fever in New York City is of a 
mild type. In that form which prevails in our Western and Southern 
States a fatal termination is of frequent occurrence. There is a type which 
soon loses its remission, and becomes a pernicious malarial fever, the prog- 
nosis of which is unfavorable. The complications which may render the 
prognosis unfavorable are meningitis, pneumonia, gastritis, enteritis, diar- 
rhoea, dysentery, and splenitis. The prognosis will also be modified by the 
condition of the patient at the time of the attack, and by the character of 
the endemic which is prevailing. 

The symptoms which indicate that recovery is to take j)lace are the fact 
that the exacerbation is delayed or rendered less severe, the early subsidence 
of gastric symptoms and headache, and a decrease in the frequency of the 
pulse, and the appearance of vesicles about the lips. Distinct remissions, 
accompanied by moderately free perspiration, indicate an approaching fa- 
vorable change. On the other hand, if the fever is more continuous than 
paroxysmal, with a pulse becoming daily more feeble and more frequent, if 
there is a tendency to collapse at the close of the exacerbations, and sup- 
pression of urine, with signs of extreme exhaustion, danger is indicated. 
The average duration of this fever is two weeks. 

As this fever varies so greatly in severity at different times and in dif- 
ferent localities, it is impossible to accurately determine its average rate of 
mortality. 

Treatment. — In this disease, we have means at our command by which, 
in the majority of cases, it can be controlled, and by which, in most in- 
stances, its duration may be much shortened. It is hardly necessary to 
refer to such remedial agents as blood-letting, emetics, cathartics and 
diaphoretics, which have all been employed in the treatment of this fever, 
for they have all been supplanted by a single remedy. Experience has 
proved that the poison which causes the fever cannot be removed from the 
system by any of the so-called eliminative methods of treatment. If this 
class of patients are depleted to any extent, the development of those 
typhoid symptoms which are especially to be avoided will be hastened. 
Those living in malarial districts are never up to the normal standard of 



EEMITTEKT FEVER. 



865 



vigor, and, consequently, are in a condition to be affected unfavorably Dy 
any plan of treatment or by any remedial agents which shall enfeeble the 
vital powers. 

The first thing to be done in the successful management of this fever is 
to place the patient under the best possible hygienic surroundings. The 
same care should be exercised in the arrangment of the sick-room as has 
already been proposed in the management of typhoid fever. Those who 
have seen most of remittent fever in its severer form recommend that the 
treatment of each case be commenced by administering a mercurial purge. 
They claim that there is always more or less engorgement of the liver, 
spleen, and mucous membrane of the stomach and intestines, and that, 
so long as these organs remain in this condition, no plan of treatment 
will be successful. However great may be the differences of opinion 
in regard to this, all agree that the sulphate of quinine should be used 
in its treatment. Practitioners differ as to the mode of its administra- 
tion, but all advocate its use. Some maintain that it has greater power 
over the disease when administered in small doses, repeated at short in- 
tervals ; others, that it should be given in one or two large doses during 
the remission, an hour or two before the commencement of the expected 
exacerbations. Others, again, claim that the quinine has its greatest 
power over the fever when administered during the activity of the febrile 
excitement. 1 

From these reports, and from my own experience, I do not hesitate to 
administer quinine at any time during the period of the exacerbation or 
remission. My rule is to give ten or twenty grains at a dose, according 
to the severity of the fever, and repeat it every two hours until cinchonism 
is produced. When cinchonism is reached, although the fever may not 
be controlled, it is well to stop its administration until twenty-four hours 
have elapsed ; by doing this one can better determine the antiperiodic 
power of the drug. If the exacerbations do not disappear, but are de- 
layed and are less severe, the fever is being controlled. If, notwithstand- 
ing this free use of quinine, the exacerbations are more severe and longer 
in duration, and the remissions less frequent, and typhoid symptoms are 
manifesting themselves, stimulants may be demanded. Even large doses 
of stimulants may be required to sustain the patient while he is passing 
through this period of the disease. 2 

Remittent fever is not, like typhoid fever, a disease of days or weeks. 



1 This subject was carefully studied by those engaged in the English Medical Service in India. Under 
the direction of the Surgeon-General in that department quinine was administered at different periods in 
the course of the fever, one surgeon giving quinine at the commencement of the exacerbation, another 
immediately after the exacerbation had passed its height and as the sweating stage was coming on, an- 
other immediately preceding the exacerbation, and still others giving it during 4 the remission. This plan 
was adopted to determine with positiveness when the smallest amount of quinine would have the greatest 
controlling effect over the fever. From the various branches of the department reports were made, 
whence the conclusion was arrived at that quinine, administered during the time of the exacerbation, 
had not only a greater influence in diminishing the severity of the disease, but it also more completely con- 
trolled the fever, and more markedly shortened its duration than when it was administered during the re- 
mission. 

2 Livingstone and other African travellers advise bitter ale as about the best stimulant, and the one best 
borne by the irritable stomach in this fever. 

55 



866 



ACUTE GENERAL DISEASES. 



In its severer forms no time should be lost while waiting for the action of 
cathartics or other remedial agents which are supposed to be of importance, 
but the administration of quinine should be at once commenced. When 
the disease has reached its second or third week, and there is no evi- 
dence that the patient is passing on toward recovery, administer a sec- 
ond time large doses of quinine ; in this way the progress of the 
fever may be arrested. If, after a second cinchonism is produced, 
the fever is not arrested, omit again for a few days the administration 
of quinine ; then repeat the large doses a third time. It is much better 
to proceed in this way than to keep the patient in a continued state 
of cinchonism. It is not necessary to enumerate the long list of drugs 
which at different times have been proposed as specifics in this fever, all 
of which, by common consent, are now regarded as far less reliable than 
quinine. The important thing is to know how and when to administer 
quinine. 

There are certain palliative measures which it is sometimes important 
to employ. If the exacerbations are very intense, the headache very 
severe, and the restlessness or other febrile symptoms are not relieved by 
full doses of quinine, cold may be employed for its antipyretic effect, as 
in typhoid fever. .Full doses of the bromide of potassium promote sleep. 
Frequently, in mild cases, sponging the surface with tepid water is not 
only grateful to the patient, but it has a controlling influence over the 
fever. If vomiting is constant, severe, and exhausting, hypodermics of 
morphine will be found of service. Some advise Fowler's solution to check 
the distressing vomiting. The treatment of this fever is expectant, save 
in the use of quinine. 

CONTINUED MALARIAL FEVER. 

I have included this *f ever in the list of the malarial fevers, although it 
is not altogether malarial in its origin ; malarial poison, however, is es- 
sential to its development. As i 4 -, has many elements in common with 
typhoid, and many which ally it to remittent fever, it has been called 
"typho-malarial." 1 During the late civil war it was called camp and 
Chickahominy fever. 

In its etiological aspect it partakes more of the character of typhus than 
of typhoid. The name typho-malarial fever has been employed by one 
class of observers to indicate the presence of malaria, and the specific poison 
of typhoid fever. By another class the term has been employed to indi- 
cate the presence of malaria and a septic poison. Many doubt the exist- 
ence of such a form of fever, and regard the so-called typhoid element as 
nothing more than a typhoid condition, liable to be developed in con- 
nection with remittent fever, as well as with many other diseases. The 
term typho-malarial is a convenient one for the first class of observers, and 
is one which can be employed by them without confusion ; whereas to the 



1 Wood (Prac. of Med.) calls it entero-miasmatic, and Drake (Dis. of Mississippi Valley) gives it the 
name Remitto-Typhus. 



CONTINUED MA LABIAL FEVER. 



867 



second class of observers it is exceedingly objectionable, and gives rise to 
confusion. 1 

This fever is produced by the combined action of a septic and a malarial 
poison. In some the septic element predominates, and in others the 
malarial. The preponderance of the one or the other will determine with 
a good degree of certainty the course, prognosis, and treatment of each 
individual case. The distinguishing lines, however, between these two 
elements are not always sharply drawn ; both may be modified in their 
manner of development and in their morbid anatomy, by the development 
of intercurrent complications, such as scurvy, pneumonia, etc. 

Morbid Anatomy. — The changes which take place in the constituents of 
the blood are a decrease in the albumen and fibrin-factors, and an increase 
in white blood-globules. In connection with these blood changes there are 
more or less extensive parenchymatous changes in the internal organs simi- 
lar to those met with in other forms of acute infectious diseases. 

The liver is increased in size, and its cut surface presents an appearance 
which closely resembles that known as nutmeg liver. Sometimes it presents 
the peculiar bronzed color of the liver in remittent fever ; at other times it 
very closely resembles the liver of yellow fever. A microscopical examina- 
tion shows free fat and pigment granules, as well as lymphoid, fusiform 
and stellate cells — which are perhaps derived in great measure from the 
spleen ; no pigment is found in the he]3atic cells, but they are stained with 
bile, as is also the inter-lobular tissue. . A . 

In most cases the spleen is enlarged, softened, and of an almost black 
color. The Malpighian bodies are prominent, and present the appearance 
on the torn surface of the spleen of little tumors, varying in size from a 
pin's head to that of a pea. The organ is rarely as much enlarged or soft- 
ened as in typhoid or remittent fevers. It is always the seat of more or less 
pigmentation. The pigment is in the lymphoid cells of the spleen chiefly, 
but it also accumulates about the veins. 

No uniform change will be noticed in the kidneys, except hyperemia, 
which will be most marked in their cortical substance. 

The lungs are the seat of more or less extensive hypostatic congestion. 
Splenization of the lungs is not frequent. 

The heart is pale and flabby. Its muscular fibres are the seat of granular 
or vitreous degeneration similar to that which takes place in the heart in 
typhoid fever. Exsanguinated clots more or less firm may be found in its 
cavities, but they have nothing peculiar about them. They closely re- 
semble those found in persons who have died from failure of heart power. 
They are rarely, if ever, the direct cause of death. 

The intestinal changes, when present, resemble those of typhoid fever. 

While, therefore, no pathological lesions which can be regarded as char- 
acteristic of this type of fever are found, and while the lesions very closely 
resemble those of typhoid fever on the one hand, and remittent fever on 

1847 Wood stated that "remittent or bilious fever, as it was then popularly called, was sometimes 
of a low adynamic character, from co-operation of a typhoid epidemic influence with miasmata.' 1 Forty 
years ago the term gastric fever was given to that variety of marsh fever where the stomach was deranged 
and irritable from the onset. 



868 



ACUTE GENERAL DISEASES. 



the other, still its clinical differences are sufficient to distinguish it from 
both, and to stamp it as a distinct type of fever. 

Etiology. — It is difficult to determine the true etiology of this fever. 
That malarial poison is necessary for its development there can be no 
question. It is equally certain that some other poison besides malaria is in 
operation whenever it prevails. Its infection does not follow the laws of 
development governing the specific cause of typhoid fever, for it is in no way 
connected with the excrements of one suffering from the fever. There are a 
few facts connected with its development which are now well established : 

First. It is met with only in malarial districts. 

Second. In the majority of instances, when this fever has prevailed, its 
development has been preceded or attended by marked and easily recog- 
nized anti-hygienic conditions, such as overcrowding, bad sewerage, and 
other conditions favorable to the development of septic poison. 

Third. That it is a non-contagious disease, and is never propagated from 
the affected to the healthy, either directly by personal contagion, or indi- 
rectly by morbid excretions. 

Fourth. In its morbid anatomy and symptomatology it is a combination 
of malarial and typhoid fever. The special symptoms and lesions of one 
or the other of these fevers stamps its character. In large cities in which 
malarial diseases are prevalent, sewer gases seem to furnish the element 
which is so essential for its development. The history of disease in New 
York city during the past few years furnishes striking examples of the 
combination of these two poisons in developing a type of fever which must 
be classed under the head of continued fever. 

Symptoms. — It is difficult to present a typical picture of this fever. To 
give even an outline of its symptoms which shall be approximately true of 
all, or even the majority of cases, is impossible. Its clinical history varies 
as the malarial or septic element predominates. Besides, there is a large 
number of cases in which neither of these elements predominates, for the 
patient almost insensibly passes from a malarial into a typhoid condition. 
There are also certain anti-hygienic conditions which may be present, 
which give to the fever an unusual and peculiar type. For example, when 
those conditions exist which favor the development of scurvy, as the patient 
enters upon the second week of the fever, the scorbutic phenomena will 
become prominent. At times the dysenteric element may be engrafted on 
this fever, and greatly modify its course, and lead to a train of symptoms 
and morbid changes which closely ally it to epidemic dysentery. The 
course of this fever may also be greatly modified by certain local complica- 
tions which are especially liable to occur during the second or third week. 
The presence of any of these conditions will greatly change its clinical his- 
tory, but the phenomena which attend its early development will always be 
sufficient to determine its true character. 

In considering the symptoms in detail, that class of cases in which the 
malarial element is predominant will first be described. This type of fever 
is usually ushered in by a distinct chill. 1 In some instances no premonitory 



1 In Gibb 1 s account of a malignant epidemic in Nicaragua, Central America, none of the cases began 
with a chill. 



CONTINUED MALARIAL FEVER. 



869 



symptoms are present ; in others the chill is preceded by wandering pains 
in the limbs and back, headache, loss of appetite, and a feeling of great 
exhaustion. In a large proportion of cases in the early stage, the counte- 
nance has a peculiar waxy, clay-colored or yellowish tinge. The chill varies 
in duration from half an hour to an hour, and in character closely resem- 
bles the chill of simple remittent fever. It is immediately followed by 





f. 


2. 


3. 


4. 


5. 


6. 


7. 


8. 


9. 


10. 


II. 


12. 


13. 


14. 


15. 


Id 


17. 


18. 


19. 


20. i 


I 2'Z. 


106° 
105" 


in 




m. 


c- 




e. 




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m. 


















e m 


Tf 




104" 
103* 
102° 
101° 
100° 










































































































































































09° 

-2£ 























































































Fig. 177. 

Temperature Record in a case of Continued Malarial Fever, Remittent type. 



active febrile symptoms, the temperature rising in a few hours to 103° or 
104° F. The pulse reaches 100, and is full and forcible. The excretions 
are all checked, and there is mental disturbance and sometimes delirium. 

When once established, the fever pursues a variable course. At its onset, 
and for the first few days, its phenomena often closely resemble those of 
simple remittent fever, though the remissions are never so well defined, and 
there is at the very onset of the fever an amount of intestinal disturbance 
which is rarely present in simple remittent. The existence of abdominal 
tenderness, especially in the right iliac fossa, is a strong point in its 
diagnosis. As the temperature rises, nausea, vomiting, and epigastric 
tenderness are present in a greater or less degree. These gastric symp- 
toms bear a close resemblance to those which attend the development of 
remittent fever, while the intestinal and abdominal symptoms are similar 
to those of typhoid. Diarrhoea may precede the chill ; in most cases it is 
present during some portion of the fever. At first the tongue presents a 
pale, flabby appearance, with a smooth surface ; soon it becomes covered 
with a white or yellowish-white coating ; later it becomes red, and the 
coating becomes brownish ; in severe cases it may suddenly become clean, 
red and shining, and sordes may collect upon the teeth and lips. 

In those cases in which a scorbutic element exists, the tongue is enlarged, 
pale, and flabby, its surface smooth and covered with a white fur, which is 
thickest on its edges, the gums are swollen and present the characteristic 
appearance of scurvy ; the skin is covered with petechias and irregular dis- 
coloration s, and mental and bodily prostration is early marked. 



870 



ACUTE GENEKAL DISEASES. 



In those cases in which a dysenteric element is present, as the fever de- 
velops, the dysenteric symptoms become prominent, the discharges from 
the bowels are blood-stained and watery. The tongue soon becomes dry and 
brown, and the patient shows signs of extreme exhaustion, with a few of 
the gastric symptoms which are usually so ivell marked in the early period 
of the fever. Throughout the whole course of the disease there is a marked 
tendency to periodicity, the exacerbations usually assuming a tertian type. 1 
In fatal cases, as the patient reaches the second or third week the symptoms 
are very like those of fatal typhoid fever ; the prostration becomes more and 
more complete, the pulse reaches 130 or 140, is feeble, compressible and 
irregular, the skin is hot and cold in patches, the patient gradually passes 
into a state of stupor and coma, involuntary evacuations take place, there 
is subsultus, deafness, a blackened and rigid tongue, and death ensues. In 
cases that recover, symptoms of amendment may be noticed between the 
tenth and twentieth days. The tongue begins to become clean, the abdom- 
inal symptoms subside, the pulse becomes less frequent and fuller, the dis- 
turbance of the nervous system disappears, the appetite gradually returns, 
and the patient enters upon a tedious convalescence, which is attended by 
more or less diarrhoea, mental stupor, cardiac irritability, and a slow return 
of mental and physical vigor. 

The train of symptoms thus briefly sketched may be greatly modified by 
a variety of complications. Not infrequently pulmonary complications 
develop during its second week, and so change its phenomena that the fever 
element may be overlooked and the pulmonary element alone engages the 
attention of the physician. Suppurative inflammation of the cervical and 
inguinal glands sometimes complicates it, and leads one to the mistake of 
regarding it as a purely suppurative fever. Enlargement and suppura- 
tion of one or both parotids are not uncommon events. Again, scurvy 
under certain anti-hygienic conditions may so modify its phenomena as to 
lead one to regard it as an entirely new type of fever. The scorbutic ele- 
ment in this class of cases is developed in connection with the malarial 
exposure. 

The prominent symptoms present in the septic type of this fever, such as 
lassitude, headache, pains in the back and limbs, resemble those of typi- 
cal typhoid fever ; either a distinct chill or a complete intermittent or 
remittent paroxysm ushers in the febrile symptoms. The rise in. tempera- 
ture following the ushering-in chill has no typical range ; in some cases 
the rise is gradual, not reaching its maximum before the middle of the 
second week ; in other cases the rise is sudden, reaching 104° or 105° F. 
within twenty-four hours after the occurrence of the chill. In typhoid 
fever during the first week, there are indistinct forenoon remissions and 
afternoon exacerbations, but in this fever the remissions are well-marked, 
especially on every second or third day, causing the fever to assume a more 
or less distinct tertian or quartan type. One of its earliest symptoms is 



1 As the disease progresses the exacerbations become shorter ; the remissions longer, and at times a 
normal or even a subnormal temperature may be reached, temporarily, as the adynamic condition becomes 
pronounced. 



CONTINUED MALARIAL FEVER. 871 

well-marked hepatic tenderness ; with the hepatic tenderness there is en- 
largement of the spleen, which, as the fever progresses, reaches a much 
larger size than is ordinarily met with in typhoid fever. During the first 
week the pulse is full and rarely more than 100, but during the second and 



Day: 


1 


. 2 


3. 


4, 


5. 


6 


7. 


8. 


9. 


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II. 


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16. 


17. 


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20. 


21. 


22. 


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98° 





























































































































































































































♦Sponge Bath. 

Fig. 178. 

Temperature Record in a case of Continued Malarial Fever. Septic variety. 

third weeks it is small and compressible, and in severe cases ranges from 
110 to 130 per minute. 

The appearance of the tongue varies with the period of the fever. At 
first it is swollen, with red projecting papillae, and has a light white coat- 
ing. As the typhoid condition becomes more marked its appearance 
changes ; it becomes dry and brown, and frequently the brown coating 
cracks and fissures are formed in the mucous membrane underneath. 
Should the tongue become moist and begin to clean, it is an indication 
that convalescence is being established. The coating is removed in two 
ways, either gradually from the edges to the centre, or it is thrown off in 
flakes. In the latter case, after the removal of the coating, the tongue as- 
sumes a beefy red appearance, and after a short time may again become 
brown and dry. Under such circumstances there will be a renewal of the 
fever-symptoms. After the fever has continued a few days the surface be- 
comes dry and harsh, and the skin assumes a dingy hue, which is quite char- 
acteristic ; sometimes there is a well-marked jaundice. The urine gradually 
diminishes in quantity and deepens in color until convalescence com- 
mences, when it increases in quantity. It is rarely albuminous. 

Diarrhoea may occur at any period. It is not usually excessive until the 
second or third week. There is nothing characteristic about the discharges. 
They are usually of an exceedingly fetid odor, watery and dark-colored ; in 
the later stages of the disease they sometimes contain blood. In some in- 
stances the character of the stools is termed bilious and an 'excessive he- 
patic secretion is then indicated ; at other times they are of dark clay 
color, showing a deficiency of the biliary secretion. With the diarrhoea 
there is usually more or less abdominal tenderness, especially in the right 



872 



ACUTE GENERAL DISEASES. 



iliac region ; but tympanitis is rarely well-marked. In many cases there 
is retraction of the abdomen. 

As already stated, headache is very constant in the early period of the 
fever. It often precedes the nshering-in chill. As the fever progresses it 
gives place to a delirium, which is never violent, but which is muttering 
in character, and is attended by restlessness and insomnia, or by drowsi- 
ness, subsultus, picking at the bed-clothes, and great nervous prostration. 
If delirium is not present, or after it has disappeared during convales- 
cence, there is great lack of mental vigor and a tendency to apathy. 
The other nervous phenomena, which are usually present in any con- 
dition when marked . typhoid symptoms exist, are not prominent in this 
fever. 

The subsequent phenomena which may attend its development will vary 
with the intensity of the fever and the resisting power of the patient. 
Epistaxis is not uncommon ; bronchitis is a frequent complication. In 
fatal cases, at the close of the second or during the third week, symptoms 
of extreme prostration come on, the patient gradually passes into a state of 
stupor, which lapses into one of coma, and death ensues. In cases that are 
to recover, usually by the end of the second week the tongue begins to 
clean, the gastric and intestinal symptoms, with the exception of the diar- 
rhoea, begin to subside, the pulse becomes slower, the nervous disturbances 
disappear, the appetite returns, and the patient enters on a convalescence 
which is usually protracted. Its phenomena may be modified by certain 
anti-hygienic surroundings, to which those suffering with this fever may 
have been subjected prior to, and during, its development. Thus, when it 
prevails among those who have suffered privations, been badly fed, badly 
clothed, overcrowded in badly ventilated apartments, or surrounded by de- 
composing animal and vegetable substances, although the fever is attended 
by the same general phenomena, there are certain variations which ally 
it to relapsing fever. Prominent among these are neuralgic and arthritic 
pains in various parts of the body, especially in the back and limbs ; hem- 
orrhagic tendencies marked by bleedings from the gums and mucous sur- 
faces ; and not infrequently large ecchymoses occur in various parts of the 
body. 

In this class of cases the fever is of a low type from the commencement, 
with quotidian exacerbations and remissions. Diarrhoea usually precedes 
the development of the febrile symptoms. Frequently during the second 
week a muttering delirium comes on, accompanied by drowsiness and a 
tendency to stupor. Despondency, indisposition to make any exertion, 
and a state of utter indifference as to the future are frequently met with 
during the entire period of the fever ; in fact, mental and bodily prostra- 
tion is more marked here than in any other fever. In fatal cases death may 
be the result of hemorrhage from the mucous surfaces, or from exhaustion. 
In cases that recover, convalescence comes on late, and is slow and tedious. 
Diarrhoea frequently follows the subsidence of the fever, and leads to a 
fatal result. 

Differential Diagnosis. — The affections with which continued malarial 



CONTINUED MALARIAL FEVER. 



873 



fever is likely to be confounded, are typhoid, remittent, relapsing, typhus, 
and yellow fever. 

The advent of continued malarial fever is usually marked by a distinct 
chill, while typhoid comes on insidiously and is attended not by a dis- 
tinct chill, but by a chilly sensation. The rise of temperature in con- 
tinued fever is sudden and follows no typical range, while in typhoid 
the typical range of temperature during the first week is diagnostic of 
the fever. In typhoid fever, on the sixth or eighth day, rose-colored 
spots appear ; in the other, although an eruption may be present, it has 
none of the characteristics of the typhoid eruption, is not rose-colored, 
does not disappear on pressure, and remains visible throughout the whole 
course of the fever. Besides the absence of these characteristic symptoms 
of typhoid fever, there is, in continued malarial fever, a distinct periodi- 
city in the febrile action, a certain icteroid hue of the skin, hepatic tender- 
ness, and great gastric disturbance, conjoined with which the appearance 
of the tongue, the character of the diarrhoea, and the non-infectious 
character of the stools will serve as important aids in the differential 
diagnosis of these two forms of fever. If, upon microscopical examina- 
tion of the blood, free pigment is found, the diagnosis of continued mala- 
rial fever is established. 

The malarial type resembles remittent fever in its ushering-in symptoms. 
In both cases there is a chill followed by fever, attended by one or more 
distinct exacerbations and remissions. The early appearance of the enteric 
symptoms, attended by other well-marked typhoid phenomena by the end 
of the second week, establishes the diagnosis, and as the fever progresses 
the typhoid condition becomes more and more apparent. Besides, remit- 
tent fever yields more promptly to quinine. 

Severe cases which are complicated by scorbutic tendencies marked by 
petechias and great prostration of the vital powers may be confounded with 
typhus fever ; yet the severity of the attack, the higher range of tempera- 
ture, the greater frequency of the pulse, the dusky countenance, the ab- 
sence of diarrhoea and all other abdominal symptoms in typhus fever, ren- 
der it easy to make the differential diagnosis between the two types of 
fever. Besides, typhus fever has a characteristic eruption, is only propa- 
gated by contagion, and, if it prevails, does so epidemically. 

Occasionally yelloiv fever has been confounded with continued malarial 
fever. The range of temperature is lower in yelloiu fever, and on the third 
or fourth day it falls suddenly, and there is a more or less complete remis- 
sion. The circum orbital pain, the appearance of the eye, the pulse rarely 
ranging over 110, the peculiar color of the skin, the character of the mat. 
ter vomited, the absence of diarrhoea, and the shorter duration of the dis- 
ease, will enable one to make the diagnosis of yellow fever. The urine is 
rarely albuminous in continued fever ; nearly always so in yellow. Again, 
yellow fever usually prevails epidemical^, and is confined to certain locali- 
ties and certain seasons of the year. It is a portable disease, and the 
yellow fever poison may be conveyed from an infected to a non-infected 
district by means of clothing or merchandise, while the poison of contin- 



874 



ACUTE GENERAL DISEASES. 



ued fever is of endemic origin, and cannot be carried beyond the infected 
district. 1 

Prognosis. — The ratio of mortality in continued malarial fever varies 
greatly in the different regions in which it occurs, and as the malarial 
or septic element predominates. The hygienic surroundings of the patient 
and the range of atmospheric temperature will also very greatly influence 
the prognosis. Statistics of this fever in different localities and in differ- 
ent years give the ratio of mortality from eight to ten per cent. The 
septic type is more fatal than the malarial. Great caution should be exer- 
cised in prognosticating the result of any case, for the mildest cases some- 
times suddenly assume a severe type and terminate fatally, while very severe 
and apparently hopeless cases unexpectedly improve, and recovery takes place. 

The average duration of those cases which terminate in recovery is from 
three to four weeks. The period of convalescence is prolonged ; three or 
four weeks often elapse before the patient is completely restored to health. 
A fatal relapse may occur at any period during convalescence. 

Its most frequent complication is inflammation of the respiratory organs, 
the development of which is marked by those symptoms which usually 
attend the development of the different acute pulmonary affections. In 
the majority of instances the signs of bronchitis are not present until the 
fever is well established. The bronchitis resists treatment, and does not dis- 
appear until convalescence is fully established. When pneumonia occurs it 
is catarrhal in character, and few of the strongly marked rational symptoms 
of ordinary pneumonia are present. The physical signs, however, will al- 
ways enable one to determine the presence of pulmonary complications, and 
any great irregularity in temperature during the course of the fever should 
be an indication for a careful physical examination of the chest. 

It is sometimes difficult to distinguish between the cerebral symptoms 
of this fever and those symptoms which attend meningeal complications, 
but the meningeal complications are of so very rare occurrence that it is 
safe to assume they are not present until some of the diagnostic symptoms 
of meningitis occur. Serious abdominal complications, such as intestinal 
perforation, peritonitis, and hemorrhage are rare, but when they do occur 
their advent is marked by such urgent symptoms that one loses sight of 
the ordinary symptoms of the fever. It is hardly necessary to refer to 
those modifications in the clinical history of this fever which follow the 
development of abscesses, bed-sores, gangrene, etc. The occurrence of any 
of these complications will very materially influence the prognosis in any 
given case. Capillary bronchitis and pneumonia are especially dangerous 
when they develop during the third week of the fever. Anti-hygienic sur- 
roundings, such as overcrowding and improper food, materially affect the 
prognosis. If continued malarial fever prevail among those who are 
crowded into badly-ventilated apartments, who from filth and improper 
nutrition have septic and scorbutic tendencies, the ratio of mortality is 
much greater than among those who are free from such complicating 
influences. 



1 The points of differential diagnosis between this disease and relapsing fever are considered under the 
head of relapsing fever. 



CONTINUED MALARIAL EEVER. 



875 



The symptoms which may be regarded as indicating an unfavorable ter- 
mination are a continued high temperature, showing little or no tendency 
to remission ; a very frequent, feeble, fluttering pulse ; continued hic- 
cough ; profuse diarrhoea, the discharges at times being involuntary and 
containing mucus, pus, and blood ; a dry, red, cracked, and fissured 
tongue ; great drowsiness, with a tendency to stupor and coma ; and the 
appearance of petechial spots on the surface of the body, attended by fre- 
quent hemorrhages from the lips, gums, and tongue. In a severe case, 
the occurrence of any of these phenomena renders the prognosis more 
unfavorable. 

The character of the prevailing fever will also greatly influence the prog- 
nosis in any given case. If the type of the prevailing fever is mild, or if 
comparatively few deaths have occurred, though the symptoms in a given 
case may appear unfavorable, yet recovery is probable. If, on the other 
hand, the type is severe, and many deaths have occurred, cases apparently 
mild will suddenly become severe, and the prognosis becomes unfavorable. 
As already stated, the hygienic surroundings and the previous habits of the 
patient very greatly influence the prognosis. "With drunkards, and those en- 
ervated by vicious habits, a mild type of this fever will probably prove fatal. 

Treatment. — No plan can be presented which will be applicable to all 
cases. 

The first question which meets us is : Cannot the development of this 
fever be prevented ? It has been stated that its development was princi- 
pally due to three causes — namely, malarial poison, overcrowding, and 
improper diet. In a large proportion of instances it is possible to do away 
with the last two causes. The overcrowding and the faulty diet may be 
prevented, and thus the septic poison which gives to this fever its "ty- 
phoid" type may be destroyed, or its development prevented. The strict 
observance of hygienic laws in the localities where this fever prevails has, 
in some instances, entirely changed the type of the disease. Even after 
the fever symptoms have been well developed, the removal of patients from 
anti-hygienic surroundings has frequently been attended by the most satis- 
factory results. When isolated cases of this fever are met with in localities 
apparently free from such sources of infection, a careful search should be 
instituted in order to find the source of the infection. Defective sewerage 
and faulty drainage have been found to be fruitful sources of infection. 

There are no specifics. In those cases in which the malarial symptoms 
predominate, the administration of quinine will in many instances arrest 
its progress or shorten its duration ; but in those cases in which the septic 
element predominates, while quinine may act as an antipyretic, it has little 
power to arrest its progress or to shorten its duration, but it will, in many 
instances, render the course of the fever milder. Warburg's tincture in 
many cases will have a controlling power over the fever when quinine fails. 

It has been claimed by some that arsenic has a specific influence over the 
fever, and that it exercises a peculiar and most beneficial effect upon the 
intestinal lesions. There is little doubt but that arsenic, like quinine, acts 
beneficially in many cases of the malarial type of this fever ; but unques- 
tionably this beneficial effect is due to its acknowledged power over malarial 



876 



ACUTE GENERAL DISEASES. 



affections, and not to any specific influence which it has over the fever. As 
an antiperiodic it is inferior to quinine. Eucalyptus does not act as bene- 
ficially in continued malarial fever as in the simpler forms of malarial fever. 

It is of importance to remember that this class of patients do not bear 
well the prolonged application of cold to the surface, either by means of 
the cold bath or the cold pack. The danger resulting from the injudicious 
use of cold baths is greater in this than in any other infectious disease. 

The rules for the administration of stimulants are the same as those 
given for their administration in typhoid fever. The effects of the first 
few doses should be carefully watched. They should never be given indis- 
criminately, for there is greater danger of over-stimulating in this than in 
any other fever. Their use is indicated whenever signs of heart-failure 
are present, such as a feeble pulse and an indistinct first sound of the 
heart. The use of stimulants is not necessarily contra-indicated when 
delirium is present. Frequently after their administration the delirium 
will pass away, and only when it is decidedly increased by their use should 
they be abandoned. 

The state of the bowels, skin and kidneys demands the closest attention. 
If, early in the disease, the bowels are constipated, a calomel purge com- 
bined with ten or fifteen grains of quinine will often be followed by marked 
benefit. In any stage of the disease brisk purgation should be avoided. 
If diarrhoea is present, it should not be interfered with unless it becomes 
exhausting ; then it should be checked by small doses of opium combined 
with astringents. Symptoms referable to disturbance of the nervous system 
sometime require special treatment. If there is extreme restlessness, mus- 
cular twitchings, or active delirium, opium may be administered in full 
doses. The effect of the first dose must be carefully watched. If sleep 
soon follows its administration, and the delirium gradually subsides with- 
out any aggravation of the other symptoms, its use may be continued ; if, 
instead of producing sleep, the patient becomes more wakeful, and the de- 
lirium is increased and more active, and the other symptoms are greatly 
aggravated, its use must be immediately abandoned. Under these circum- 
stances chloral maybe tried with great care. 1 Quain advises gr, xv.-xx. of 
bromide of potassium under similar conditions. 

Some claim that spirits of turpentine in the treatment of this form of 
fever has almost a specific power, while others regard it useful only as a 
stimulant. My own experience leads me to employ it only as a stimulant 
during the second and third week of the disease, when there is great pros- 
tration and marked typhoid symptoms. It may be given as an emulsion in 
doses of twenty drops every two hours. The diet best suited to patients 
with this fever is milk administered in the same way as was proposed in 
the case of typhoid fever patients. Special complications occurring during 
the non-septic variety must be met with such remedies as the condition of 
the patient and the peculiar complications may require. 



i Wood recommends Hoffman's anodyne and spts. seth. nitroei for restlessness ; and musk, asafoetida 
camphor, and similar drugs for the hiccough. 



PERNICIOUS MALARIAL FEVER. 



877 



PERiaCIOUS MALAEIAL FEVER. 

This form of fever has received other names, at different times and in 
different localities. It has been called congestive fever, ardent fever, tropical 
typhoid fever, and pernicious fever. The latter name seems most appro- 
priate, and at the present time is generally adopted. 

It is true that in the majority of cases there is more or less congestion of 
the internal organs, and sometimes the patient is overwhelmed by these con- 
gestions, hut in a large number of cases no such congestions exist, and undei 
such circumstances the designation pernicious is to be preferred. In its 
severe and dangerous form it may be remittent or intermittent in character, 
and may assume any of the types of periodical fever, but the quotidian and 
tertian types are the most common. Sometimes its pernicious character is 
clearly marked at the onset of the fever, during the first paroxysm ; at 
other times it comes on insidiously, and its pernicious character is not 
suspected until after the occurrence of two or three paroxysms. 

There are several well-marked and distinct varieties of pernicious fever — 
the most common and most important of which are the comatose, the delir- 
ious, the algid, and the gastro-enteric. It is the locality in which perni- 
cious fever prevails that gives the fever its distinctive peculiarity. Perni- 
cious fever not infrequently appears as an epidemic ; sporadic cases are met 
with in those regions where simple intermittent and remittent fevers 
prevail. 

Morbid Anatomy. — Its anatomical lesions are similar in kind to those of 
intermittent and remittent fevers, but they differ very much in degree. For 
instance, the pigmentation is more abundant. The abundance of the pig- 
ment, and the extent of the pigmentation will vary with the severity of 
the fever. The other changes in the different organs and tissues of the body 
are very similar in character to those described in connection with inter- 
mittent and remittent fever. The post-mortem appearances in pernicious 
fever vary with the intensity of the malarial infection and the peculiar 
atmospheric conditions under which the fever is developed. In some in- 
stances there will be evidences of intense engorgement of the blood-vessels of 
the brain, and the entire brain substance will be more or less thoroughly 
pigmented. In others, minute blood-extravasations will be found scattered 
here and there throughout the substance of organs. Small blood-extravasa- 
tions into the spinal cord, accompanied by more or less pigmentation, are 
very apt during life to be attended by tetanic spasms. In persons dying 
of pernicious fever after the third attack, I have found all the organs of the 
body pigmented. Sometimes there is intense engorgement of the liver, that 
is, the most marked post-mortem changes will be found in that organ, and 
the amount of pigmentation present will correspond with the intensity of 
the congestion. With intense engorgement of the organ there are usually 
blood-extravasations. 

Occasionally, infarctions occur in the spleen, and around each there will 
be a mass of pulpy material. The spleen is more invariably found softened 



878 



ACUTE GENERAL DISEASES. 



thau in any other fever. In connection with this softening, which is very 
extensive and similar to that found in typhoid fever, the organ rapidly be- 
coming a soft, pulpy, bloody mass, it is also enlarged even beyond what it is 
in typhoid fever and is darker in color than normal. It is unnecessary to 
describe in detail the enlargement of the capillary vessels which occurs as a 
necessary result of this intense engorgement. Sometimes the kidneys and 
the lungs are the seat of intense hyperemia, as the result of which the 
functions of these organs are more or less extensively interfered with. 
Hemorrhagic infarctions in the lungs are not infrequent. A low form of 
pneumonia is sometimes present. The heart is pale and flabby. 

Etiology, — The exciting and predisposing causes of pernicious fever differ 
from those of the simpler forms of malarial fever only in degree, not in 
kind, but a higher range of temperature is requisite for the development of 
pernicious fever. It prevails only in those localities where the average 
range of temperature, for a time, reaches 65° F. 

Symptoms. — Pernicious fever may commence abruptly ; generally the pre- 
monitory symptoms which mark its development do not differ from those 
which mark the development of intermittent and remittent fever. In most 
varieties the attack commences with a chill, which is usually severe and 
prolonged. The attack may commence with distinct intermittent parox- 
ysms of the quotidian type, but rarely more than two of these intermittent 
paroxysms will occur before it assumes the pernicious type ; or a remittent 
fever with a distinct exacerbation and remission may go on for four or five 
days before its pernicious character will be developed. The milder form 
either gradually passes from a simple intermittent into a pernicious fever 
by a progressive increase in the severity of the paroxysm, or a single parox- 
ysm of not unusual severity is suddenly followed by a pernicious one ; a 
fatal result rarely occurs until the third paroxysm is passed. Again, a dis- 
tinct chill may be followed by a condition that will at once be recognized as 
one of the varieties of pernicious fever. The ushering-in symptoms will 
always vary with the type of disease which is about to be developed. I shall 
not describe the phenomena that attend all these different varieties, but 
only those most commonly met with. 

As the varieties in type of this fever are as numerous as the localities in 
which they occur, and as the type in any locality may change with every 
succeeding year — that is, the type of one year may be very unlike that of 
the preceding or following year — it is very difficult even to classify its dif- 
ferent forms. The slight variations which are met with in the pathologi- 
cal lesions of the different varieties arc still more difficult of description 
and classification. For instance, there is one variety which is character- 
ized by a tendency to coma, called the comatose variety ; another is charac- 
terized by a tendency to a peculiar form of delirium, termed the delirious 
variety ; still another is characterized by a marble-like coldness of the sur- 
face, called the algid variety ; again, we have one which is characterized 
by vomiting and purging, or choleraic symptoms, termed the g astro -enteric 
variety ; then one in which there is acute jaundice, termed the icteric 
variety ; then one in which there are profuse hemorrhages, termed the 



PERNICIOUS MALARIAL FEVER. 



879 



hemorrhagic variety ; and still another in which there is profuse diaph- 
oresis, termed the colliquative variety. 

Comatose Variety. — A patient has a distinct paroxysm of one of the sim- 
pler forms of malarial fever (intermittent or remittent), with no special 
phenomena attending it, except that he has had a more than usually severe 
headache ; with this there has been perhaps vertigo, stammering and in- 
distinctness in the speech, an inability to talk with freedom, and a more 
than usual tremulousness during the hot stage. From this condition he 
passes as usual into the hot stage of an intermittent, or rapidly into an ex- 
acerbation of remittent, then into a state of stupor and unconsciousness, 
and finally lies upon his back, with a flushed face, congested conjunctivae, 
dilated pupils, slow, deep, stertorous respiration, and perhaps a very slow 
pulse, or, if slow at first, it may soon become frequent. The axillary tem- 
peratures range from 105° to 107° F. The 
patient is now partially unconscious ; he is 
apparently paralyzed ; the urine is retained 
in the bladder, and the bowels move invol- 
untarily. If the pulse is slow, it is full 
and hard. The respiration becomes more 
and more stertorous, and unconsciousness 
more and more complete. Usually a moist- 
ure makes its appearance within twelve 
hours from the commencement of the first 
paroxysm, and the patient awakes to con- 
sciousness perspiring profusely. The head- 
ache and giddiness pass off, and if the fever 
which preceded it was remittent, there may 
be a well-marked remission ; if it was an 
intermittent, there may be a distinct inter- 
mission. With the next remittent exacer- 
bation or during the hot stage of an inter- 
mittent, the pain in the head, giddiness, 
unconsciousness, and all the symptoms al- 
ready described will return with greater in- 
tensity than before. With the second at- 
tack the patient may pass into a fatal coma. 

In this variety patients sometimes pass 
into a condition of apparent death, 
which may last for hours. Some are, nevertheless, perfectly conscious, see- 
ing and hearing everything which occurs around them, although unable to 
move or utter a sound ; others are unconscious. Even though the strong- 
est counter-irritants are applied to the surface, there is no sign of life, 
until, at the beginning of the sweating stage, the patient comes to con- 
sciousness. If a patient survives the second paroxysm, quite probably he 
will die during the third. With each successive paroxysm the prognosis 
becomes more and more unfavorable ; patients sometimes lie in a comatose 
condition for days, and finally die apparently from cerebral congestion. 




Fig. 179. 

Temperature Record in a cast 
cious Fever. 

{Comatose variety.) 



of Perni. 



880 



ACUTE GENEKAL DISEASES. 



Delirious Variety. — In this variety, the patient, after passing into the 
hot stage of an intermittent or into the exacerbation of a remittent, becomes 
delirious. Mild delirium is not uncommon during the progress of an inter- 
mittent or a remittent fever, but the delirium now referred to is of a more 
active character. If delirium is developed during the exacerbation of a re- 
mittent or during the hot stage of an intermittent, which has been preceded 
by severe headache, dizziness, ringing in the ears, and great restlessness, 
one may be quite certain that he has to deal with a case of pernicious fever, 
especially if it is prevailing in the locality. In this variety of pernicious 
fever there will also be more or less headache during the interval, and per- 
haps other peculiar cerebral phenomena. The delirium which appears is 
always violent in character ; perhaps the patient will require restraint ; he 
may be disposed to jump out of the window, or in some way to do injury 
to himself or those around him. During the paroxysm of delirium the 
face becomes flushed, the eyes brilliant, the conjunctivas injected, the 
pupils dilated, and the patient is constantly crying, singing, and trying to 
escape. In those who are extremely anaemic the countenance assumes a 
pale, sunken aspect. The pulse is full and hard, and the carotids beat 
violently, the temperature often reaches 107° or 108° F. This delirious 
state may continue for hours. Suddenly the patient passes from it into a 
condition of collapse, or gradually sinks into a coma from which he never 
wakens. During the whole period the axillary temperature rarely falls be- 
low 105° F. 

In favorable cases the delirium gradually becomes milder, a profuse per- 
spiration comes on, and the patient falls into a prolonged sleep, from which 
he awakens conscious, though weak and exhausted, with headache and 
vertigo, but without the slightest recollection of what has passed. These 
attacks of delirium may be repeated three or four times before a fatal ter- 
mination is reached, but so much danger attends them, that a second attack 
should never be allowed to occur if it can be prevented. 

In this variety of pernicious fever, other nervous phenomena may accom- 
pany or take the place of the delirium, such as epileptiform convulsions, 
tetantic spasms, etc. The tetanic spasms sometimes resemble the phe- 
nomena of hydrophobia. That form of tetanus w T hich occurs in various 
malarial districts, and is sometimes called sporadic tetanus, I believe 
will be found to have many things in common with this type of pernicious 
fever. 

Gastro-Entenc Variety. — In this variety the patient, after he has passed 
into the hot stage of an intermittent, or the exacerbation of a remittent, 
is seized w T ith almost incessant vomiting and purging. The vomiting and 
purging are peculiar, altogether unlike that which is sometimes present in 
the simpler forms of malarial fever. There is blood-stained material, both 
in the matter vomited and in that discharged from the bowels. In some 
instances, the discharges may be so reddened as to look like beef-brine or 
the washings of raw meat ; sometimes the proportion of blood is so great 
as to cause the discharges to have the appearance of clear blood. In some 
endemics the discharges assume the appearance of rice-water, having no 



PERNICIOUS MALARIAL FEVER. 881 



odor, and similar in appearance to those of Asiatic cholera. The patient 
has no abdominal pain or tenderness, but has a sense of weight and burning 
in the stomach, accompanied with cramps in the calves of the legs, cold- 
ness and blueness of the surface, with a small, almost imperceptible pulse, 
sunken eyes, and the <tf facies"of cholera. So closely do these patients 
resemble in appearance those of Asiatic cholera that this disease has fre- 
quently been mistaken for it. During the attack the thirst is most in- 
tense. The respiration is peculiar ; it consists of a double inspiration, 
followed by a double sighing expiration. The restlessness is very great, 
the patient is constantly tossing from one side to the other ; sometimes, an 
hour or two before death, he suddenly springs up and walks across the room. 

The usual length of the fatal paroxysm is from three to six hours. 
Patients die in a state of collapse. After the vomiting and diarrhoea have 
assumed the characteristic appearances already described, very few patients 
recover. As death approaches, the pulse becomes more frequent, feeble, 
irregular, and fluttering in character. The respiration is more and more 
prolonged and sighing, the skin cold and shrivelled, and covered with a 
cold, clammy perspiration. It frequently happens when all these symp- 
toms are present that the patient cannot be convinced that he is seriously 
ill, and wishes to get out of bed and go out of doors. 

Algid Variety. — This variety is characterized by coldness of the surface 
of the body, while the rectal temperature may range from 104° to 107° E. 
The attack begins with a chill of not un- 
usual severity or duration, but soon after 
the patient enters into the hot stage of the 
paroxysm, or, during the exacerbation of a 
remittent, the surface of the body begins 
to grow cold, while at the same time he 
complains of a sensation of burning and 
intense thirst. A cold perspiration soon 
covers the surface. The pulse becomes 
slower and slower, falters, and disappears at 
the wrist. Alternately the extremities and 
face become cold ; only the abdomen re- 
tains its normal temperature. The surface 
has a cold, marble-like feel, and the tem- 
perature in the axilla may fall to 88° or 
84° F. In the comatose and delirious 
varieties the temperature rises higher than 
normal, and may reach 106° or 107° F., but 
in this variety it sometimes falls two or 
three degrees below the normal. The 
tongue becomes white, moist, and cold; the 
breath is cold, and the voice feeble and in- 
distinct. The action of the heart is feeble, 
often perceptible only on auscultation. The 
mouth is clean, and the patient seems to himself to be in a comfortable 
50 



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Fig. 180. 

Temperature Record in a case of Per- 
nicious Fever. 
{Algid variety.) 



882 



ACUTE GENERAL DISEASES. 



condition, except that he feels exhausted and is sensible of great internal 
heat. The mind is clear. The expression of the countenance is that of 
death. 

This variety is very insidious in its progress. To one not familiar with 
it, the calm which follows the febrile excitement will be mistaken for relief, 
perhaps attributed to some plan of treatment pursued, or to some remedial 
agent which has been employed. If a patient in one of these paroxysms is 
to pass on to recovery, the pulse gradually returns in the wrist, and the sur- 
face regains its normal feel and temperature. As the warmth returns to the 
surface, the patient passes on to convalescence in the same manner as pa- 
tients recover from a comatose or delirious paroxysm. An algid pernicious 
paroxysm is rarely preceded by a distinct intermission, and it rarely has any 
appreciable remission. Once established, it marches steadily on to a fatal 
issue, unless arrested by treatment. 

There is another variety which will occasionally be met with, in which a 
profuse perspiration, called a " colliquative stveat," comes on at the end of 
the fever stage and continues through the succeeding intermission, accom- 
panied by great prostration, feeble heart action, and labored respiration. 
Upon the second or third return of this sweat the patient sinks and dies, 
apparently from exhaustion. Again, severe hemorrhages from the stomach, 
bowels, or kidneys may occur during the sweating stage of a pernicious par- 
ox}^sm and endanger the life of the patient from sudden syncope. 

A mild form of hsematuria sometimes occurs independent of a pernicious 
paroxysm in chronic malarial poisoning. 

Icteric Variety. — This is always endemic, confined to certain localities, 
and occurring in them whenever any form of pernicious fever prevails. It 
begins with a violent, long-continued chill, during which jaundice shows 
itself. The jaundice gradually deepens, and extends over the. whole body. 
Intense nausea accompanies its development, with a copious vomiting of 
bile, and a bilious diarrhoea. The patient suffers with a most intense head- 
ache, pain in the region of the spleen and over the kidneys, and a feeling of 
numbness in the limbs. The pulse is small, frequent, and hard. The urine 
is dark'colored. As the hot stage comes on, the pulse becomes fuller and 
more frequent, the respiration is labored, the skin very hot, the tempera- 
ture reaching 106° or 107° F., and the thirst is most intense. This stage 
lasts three or four hours, and often terminates in death. If the patient 
passes into the sweating stage, recovery usually takes place. During the 
intermission the mind is clear, but the jaundice continues. Unless the 
disease is controlled by treatment, each succeeding paroxysm becomes 
more and more severe. 

This variety is incorrectly called pernicious bilious remittent fever. If 
the attack is mild, there is only a slight staining of the skin, but in that 
form in which there is an apparent arrest of the functions of the liver, the 
patient may die deeply jaundiced within two or three days after the first 
discoloration appears. The mild form of so-called bilious remittent fever, 
in which the febrile movement is constant, is very different from the form 
under discussion, and is better classed under the head of simple remit- 



PERNICIOUS MALARIAL FEVER. 



883 



tent. All these different varieties depend on the same blood-poisoning, 
differing in its manifestations according to its intensity and the predispos- 
ing atmospheric or septic conditions which may exist in the localities where 
they are developed. 

Differential Diagnosis. — The diagnosis of pernicious fever is sometimes 
very difficult. In determining whether a given case is, or is not, one of 
pernicious fever, the first inquiry will be in regard to the character of the 
prevailing fever. If pernicious fever is prevailing in the locality, a diagno- 
sis will easily be made ; if, however, the first case in the locality falls under 
observation, probably great difficulty will be experienced in making a diag- 
nosis, and this difficulty, to a certain extent, will vary with the type of the 
fever. If, for example, a case belongs to that class in which there is a 
tendency to coma, delirium, etc., it may be confounded with some form of 
cerebral disease. This form of pernicious fever has been mistaken for cere- 
bral apoplexy, meningitis, and acute urcemia. 

As a rule, it is not difficult to draw the line between apoplexy and perni- 
cious fever of the comatose or delirious variety. The constant and promi- 
nent symptom of apoplexy is hemiplegia, which is of rare occurrence in per- 
nicious fever. It may occur, but if it does, it is developed slowly. Nei- 
ther coma nor hemiplegia is ever reached suddenly in pernicious fever. Eise 
in temperature, rapid pulse, and all the phenomena of intense febrile ex- 
citement are present before the occurrence of either. On the other hand, 
in apoplexy the hemiplegia is of sudden development, attended by a slow 
pulse, irregular contracted pupils ; or, perhaps, one pupil is dilated and 
the other contracted, and its occurrence is preceded by a sudden loss of con- 
sciousness, and not attended or preceded by high febrile excitement. 

As regards pernicious fever and meningitis, although in both diseases 
the patient reaches a condition of coma, yet in meningitis days elapse be- 
fore the coma is reached, and during those days there has been pain in 
the head, photophobia, and delirium, extending over a considerable period 
of time ; whereas, in pernicious fever the patient reaches his condition of 
coma within twelve hours. Besides, in pernicious fever there will be a 
history, not only of the prevailing type of malarial disease, which will in- 
dicate its character, but the attack of coma or delirium will be preceded 
by a distinct malarial paroxysm — perhaps two of these paroxysms ; then 
the patient will pass rapidly into a state of coma. In meningitis the fever 
rarely ranges above 102° or 103°, the face is pale, the abdomen retracted, 
and the pulse is tense and wiry — all markedly contrasting with delirious 
pernicious fever. 

The gastro-enteric and cold or algid varieties of pernicious fever closely 
resemble cholera. They may be distinguished from it by the character of 
the primary discharges. There may be a time in this type of pernicious 
fever when the discharges will very closely resemble those of cholera ; but 
they will always have been preceded by one or two bloody discharges. In 
cholera there is albumen in the urine, the occurrence of which is com- 
paratively rare in pernicious fever. In cholera there are the peculiar sur- 
roundings of the patient, the prevalence of cholera in the locality, etc. 



884' 



ACUTE GENEEAL DISEASES. 



When the endemic is at its height it is almost impossible to make a differ- 
ential diagnosis between the two diseases from the clinical history of the 
cases ; but, when we take the early history of the endemic, at which time 
the cases at their commencement were marked by distinct intermittent or 
remittent paroxysms, the true character of the disease is very readily de- 
termined. If in any given case there is still a question whether it is or is 
not one of pernicious fever, it may be determind with positiveness by a 
microscopical examination of the blood, which will be found to contain 
free pigment. 

The icteric variety of pernicious fever which often, in many of its phe- 
nomena, so closely resembles yellow fever, maybe distinguished from it 
not only by the history of its development, but by the fact that when it 
prevails as an endemic, those are seized with the fever who have been long- 
est under the influence of malarial poison, whereas new-comers are not 
usually attacked ; in yellow fever districts new-comers are almost certain 
to contract the disease. The symptoms in icteroid pernicious fever tend 
to become typhoid and adynamic, while in yellow fever the symptoms are 
active and there is little tendency to a typhoid condition. Then the jaun- 
dice of yellow fever appears late in the disease, while the jaundice of this 
form of pernicious fever comes on early, even before the chill passes away. 
Again, bloody urine is frequently present in this type of pernicious fever, 
while in yellow fever hematuria rarely occurs without the accompanying 
evidences of nephritic inflammation. The presence of free pigment in the 
blood will aid in settling the question of diagnosis in difficult cases. 

Prognosis. — In all varieties of pernicious fever the prognosis is unfavor- 
able, unless it can be controlled before the occurrence of the second parox- 
ysm. The prognosis will depend in a great degree upon the character of 
the prevailing endemic or epidemic, as also upon the stage of the epidemic, 
for the ratio of mortality is always greater during the earlier period of an 
epidemic than during its decline. All agree that the prognosis is better in 
every variety of pernicious fever if there are distinct intermissions, however 
short may be their duration. If the paroxysm does not last more than 
twelve hours, and terminates in a distinct remission, the prognosis is far 
better than when one paroxysm follows another without any distinct re- 
mission. Unquestionably the most favorable cases are those of the tertian 
type. Those varieties in which the cases most frequently terminate fatally 
are the gastro-enteric and the algid ; those in which recovery is most 
likely to occur are the comatose and delirious. 

The prognosis is also much influenced by the age and condition of the 
patient and by the presence or absence of complications. The mortality 
is greatest among the very young and very old, and among the intemperate. 
Patients with, pernicious fever may die suddenly during a paroxysm, or the 
paroxysms may be prolonged and run into each other, and the patient may 
finally pass into a typhoid or collapsed condition. If the second or third 
paroxysm is not attended by signs of intense visceral congestion, if it de- 
clines with profuse warm sweats, if it has been preceded by distinct inter- 
vals, if the urine is free, and the appetite early returns, a speedy recovery 



PERNICIOUS MALARIAL FEVER. 885 

is at hand. On the other hand, if the second or third paroxysm is pro- 
tracted and accompanied by great anxiety and restlessness, with active de- 
lirium and a tendency to coma, with coldness of the surface ; if there is 
intense pain in the epigastrium, with tingling of the surface, and scanty 
and high-colored urine ; if there is profuse vomiting and purging, bleeding 
at the nose, and cold, colliquative sweats ; if the pulse becomes small and 
feeble, or the radial pulse is imperceptible, the danger is very great, and a 
fatal issue is almost certain. Sometimes severe and fatal dysentery comes 
on at the end of a paroxysm ; at other times, as the paroxysm subsides, 
the fever assumes a typhoid type, and, after a period of continued fever 
ranging from ten to twelve days, it terminates fatally. 

Treatment. — The expectant plan of treatment cannot be practised in the 
treatment of pernicious fevers. The alarming symptoms crowd upon one 
another with great rapidity, and it is only by prompt and vigorous measures 
that in the severe forms of the disease the patient can be rescued from im- 
pending death. The issue of life or death often hangs upon a single hour. 
Some have proposed, before administering the only specific which we 
possess capable of controlling this disease, to produce free purgation by the 
administration of cathartics; others to bleed and freely vomit the patients. 
If the case is one of the gastro-enteric variety, emetics and purgatives are 
certainly very plainly contraindicated. It is now a well established fact 
that in no variety of pernicious fever do patients bear depletion. In India, 
where the most severe types of this fever prevail, the English surgeons are 
very positive in their testimony upon this point. All forms of depletion 
have been abandoned by them. Although stimulating enemata and friction 
to the surface may act as aids in the management of the algid and delirious 
varieties, they must not be relied upon as having any controlling influence 
over the disease. 

Those who have had the most extended opportunities for testing the dif- 
ferent remedies and plans of treatment which have been employed in the 
management of this fever are united in the opinion that quinine and opium 
are the only agents which can be relied upon for controlling its different 
varieties. In fact, the hypodermic use of these drugs has inaugurated a 
new era in its treatment, for in a large proportion of the severer forms it is 
impossible to get the full effect of either of these remedies by the ordinary 
methods of their administration, the usual avenues for their introduction 
being closed. 1 

Whatever solution may be used, administer from five to seven grains of 

1 The solution of quinine commonly employed by the English surgeons for this purpose is made by 
adding one hundred and fifty grains of quinine and fifty drops of dilute hydrochloric acid to four ounces 
of water, and then evaporating the solution to two ounces. Of this, thirty drops may be administered at 
each injection. Some add carbolic acid to a solution of quinine in dilute sulphuric acid ; the carbolic 
acid is added to prevent abscess at. the point where the injection is introduced. 
The formula for this solution is as follows : 



Quiniae disulphatis SF- 

Acidi sulphuric, dil fll v. 

Acidi carbolici.... ^ ij. 

Aquae destillat 1 *• 

M. 



Thirty minims is the quantity usually administered at each hypodermic injection. 



886 



ACUTE GENERAL DISEASES. 



quinine every hour until the paroxysm has passed away, then continue its 
use in the three-grain doses every four hours. With the first hypodermic 
of quinine administer one-fourth of a grain of morphia. The morphine 
should be administered with each dose of quinine until the patient is 
brought fully under its influence, without regard to the stage of the 
paroxysm. 1 

During the past few years a remedy known as " Warburg s Tincture 
has been quite extensively employed in the treatment of pernicious and- 
other forms of malarial fever. 2 Each half ounce of this tincture contains 
seven and a half grains of quinine. It is recommended to give half an 
ounce of this tincture at the onset of the paroxysm ; if this does not con- 
trol it, the same quantity must be repeated in four hours. If it cannot be 
retained by the stomach, it may be administered in capsules, i\ every 



» I have recently used the following : 

Quiniae sulphatis 2 i. 

Acidi hydrobrom 2 l \ • 

Aquae destillat 3 vl * 

M. 

Thirty minims may be administered at each injection. 

The bimuriate of quinine with urea, made by Messrs. McKesson and Bobbins, Phila., is highly recom, 
tended for hypodermic injection, as it is very soluble, and abscesses seldom or never follow its use. 
Formula : 

Bimuriate Quinia and Urea 3 1. 

Aq. Destillatse, ad f 

M. f. sol. 

Two minims contain one grain of the salt. 

a Formula, Warburg 's Tincture : 
Ead. Rhei 
P. Aloe Soc. 

Rad. Angelica Officinalis, aa 

Rad. Helenii 
Crocus Hispan. 
Sem. Foeniculi 

Cretse Preparat., aa. , 

Rad. Gentian 
Rad. Zedoar 
P. Cubeb 
G. Myrrhse 
G. Camphor 

Boletus Laricis, aa 

Confect. Damocratis* 

Q.uiniae Sulph 

Sp. Vini Rect 

Aqua? Purae 

Macerate, in a water bath, twelve hours, express and filter 



5* 



liv. 

3 Ixxxij. 
Oxx. 
Oxij. 



* Conf ectio Damocratis : 

Cinnamon fourteen grams. 

Myrrh eleven \ " 

White Agaric, Spikenard, Ginger, Spanish Saffron, Treacle, Mustard Seed, Frankin- 
cense, and Chian Turpentine, each ten " 

Camel's Hay, Costus Arabacus, Zeodary, Indian Leaf, Mace, French Lavender, Long 
Pepper, Seeds of Harwort, Juice of the Rape of Cistus, Strained Storax, Opponax, 

Strained Galbanum, Balsam of Gilead, Oil of Nutmeg, Russian Castor, each eight " 

Water Germunder, Balsam-Tree Fruit, Cubeb, 'White Pepper, Seeds of Carrot of 

Crete, Poley Mont, Strained Bdellium, each seven " 

Gentian Root, Celtic Hard, Leaves of Dittany of Crete, Red Rose, Seeds of Mace- 
donian Parsley, Sweet Fennel Seed, Seeds of Lesser Cardamom, Gum Arabic, 

Opium, of each Jive ** 

Sweet Flag, "Wild Valerian, Anise Seed, Sagapernum, each three 

Spigrul, St. John's Wort, Juice of Acacia, Catechu, Dried Bellies of Skunks, each. . . . two and one-half u 

Clarified Honey. 915 « 

The roots, etc., to be finely powdered, and the whole mixed thoroughly. 



DENGUE FEVER. 



887 



twenty-four hours. 1 It is claimed that the tincture is retained by the stom- 
ach when all other remedies are rejected. Prof. Maclean says that he has 
seen the most hopeless cases — those manifesting a degree of severity which 
seemed to preclude the possibility of recovery — commence to convalesce as 
soon as the patient was brought under the influence of this remedy. 2 No 
special rules can be laid down in regard to the administration of stimulants 
in pernicious fever ; the condition of the patient must be the guide. 
They are only of service as means to aid in carrying a patient over a dan- 
gerous period. Their continued use in large quantities is strongly objected 
to bv those who have had the most extensive experience in the management 
of this fever. Do not wait for the action of a calomel purge. Do not resort 
to any depleting measures. However mild the paroxysm, no time should be 
lost ; bring the patient as rapidly as possible under the influence of quinine 
and opium, or, if Warburg's tincture is used, administer it in full doses as 
early as possible, and continue its administration until convalescence is 
fully establish edo 

DENGUE EEVEK. 

Dengite* hreah-'bone, or dandy fever first appeared after the landing of a 
cargo of slaves from Africa, hence its earliest name was African Fever. It 
is neither an intermittent, a remittent, nor a pernicious fever. It is an 
acute disease which appears as an epidemic in hot climates. It is charac- 
terized by a febrile excitement remitting in its character, and is accom- 
panied by more or less intense arthritic pains, attended by the develop- 
ment of a papillary eruption resembling that of measles. 

Morbid Anatomy. — The morbid anatomy of this variety of fever does not 
differ essentially from that of the severer types of malarial fever, except that 
a cutaneous eruption commences on the palms of the hands and extends 
rapidly over the entire body. In most cases, arthritic changes of a rheu- 
matic character are present ; usually the external lymphatic glands are 
somewhat enlarged. This disease seems to be an exanthematous malarial 
fever, with a rheumatic or neuralgic element. 

Etiology. — Dengue or break-bone fever prevails epidemically in malarial 
districts ; it may occur as a sporadic disease. Its infection has been carried 
in clothing from one seaport to another. 4 Some claim that the disease de- 
pends upon a specific contagion ; but its contagious character has not been 
established. Its prevalence is not arrested by cold weather. The intensity 

1 The tincture may be evaporated nearly to dryness, and put up in capsules containing from one to two 
drams each. 

2 Prof. Maclean's rules for its administration are as follows :—" One-half ounce (half of a bottle) is 
given alone, without dilution, after the bowels have been evacuated by any convenient purgative, all fluids 
being withheld ; in three hours the other half of the bottle is administered in the same way. Soon after- 
ward, particularly in hot climates, profuse, but seldom exhausting, perspiration is produced ; this has a 
strong aromatic odor, which I have often detected about the patient and his room on the following day. 
With this there is a rapid decline of temperature, immediate abatement of frontal headache— in a word, 
complete defervescence, and it seldom happens that a second bottle is required. If so, the dose may be 
repeated as above. In very adynamic cases, if the sweating threatens to prove exhausting, nourishment 
in the shape of beef-tea, with the addition of Liebig's extract and some wine or brandy of good quality, 
may be required.'" 

3 El dengue means in Spanish, affectation, a dandified manner. 

4 Dengue seems to have a specific poison ; and the disease is in some degree infectious. Some regard ii 
as more highly contagious than even the exanthematous fevers. 



888 



ACUTE GENERAL DISEASES. 



of the malarial poison unquestionably has some influence in increasing or 
lessening the severity of this fever. In districts slightly malarial its type 
is usually mild ; but in districts strongly malarial its type is severe. It at- 
tacks all classes and all ages, rich and poor, black and white, the very 
young and the very old. Occasionally it has occurred as the precursor of 
yellow fever. In 1780 it was epidemic in Philadelphia. In 1827 a very 
extended epidemic of this fever prevailed in the West Indies ; during the 
prevalence of this epidemic, the specific poison of the disease was trans- 
ported in clothing and merchandise to many neighboring seaports. In 
our Southern States, in 1880, it prevailed as an epidemic. One attack 
does not protect against a second. 

Symptoms. — The period of incubation is estimated at from three to five 
days. Its initiatory symptoms are sudden and well pronounced, and its de- 
velopment is very rapid. In the majority of cases, the earliest symptoms 
are headache, photophobia, great restlessness, chilliness alternating with 
flashes of heat, and pain in the back, limbs and joints ; the small joints 

swell, and there is soreness and stiff- 
ness of the muscles. The skin be- 
comes hot and dry, and in some in- 
stances the temperature reaches 107° 
or 108° F. The pulse is rapid, rang- 
ing from 120 to 140 beats per minute. 
The face is flushed and the eyes red 
and watery. Thomas says that in 
children it often begins with a con- 
vulsion. 1 

After the fever has continued about 
twelve hours, the pains in the joints 
and back become intense, and shoot 
down the sciatic nerve. Nausea, 
vomiting, and pain in the epigastrium 
are usually prominent symptoms. 
Early in the fever the lymphatic 

Temperature Record in a severe case of Dengue S laTlds beCOme Solved 5 tlie in S ui " 

Fever - nal are first affected, then those in 

the axilla and neck ; they increase very rapidly in size, and become ex- 
ceedingly tender. The testicles, or rather, the epididymes, enlarge, and 
the swelling continues until the subsidence of the other symptoms. The 
active febrile excitement continues from twelve hours to three or four days, 
when it subsides, leaving the patient in an exceedingly feeble and prostrate 
condition. Sometimes the fever abates suddenly, with critical symptoms, 
as in relapsing fever, such as profuse sweats, diarrhoea, or epistaxis. Pro- 
fuse diarrhoea may usher in the disease. The patient after being in a pas- 
sive condition for two or three days, passes into the period of remissicn. 
The pains now become less, the glandular swellings diminish, there is less 
febrile excitement, but the fever does not entirely subside. 

i Dengue. J. G. Thomas, M.D., Savannah, 1881. 



Dag: 



■ f. 


2. 


3. 


4. 


5, 


6. 


7, 


6. 


9. 






m 


e. 








■ 








e. 

n 


m. 


<z. 


m 

f- 


e. 


m 


I-. 




f 










— 








1 


































v 


















\ 






























\ 


L 





DENGUE EEVEK. 



889 



After two or three days a second fever paroxysm occurs. About the 
same period intervenes between the first and second paroxysm as between 
the first and second paroxysm in relapsing fever. The second paroxysm 
of fever is more intense than the first, the pain in the joints is more severe, 
and finally, when the fever has reached its maximum, and the pain is most 
intense (usually on the fifth or sixth day), an eruption makes its appear- 
ance. It first appears upon the palms of the hands, then upon the neck 
soon it extends downward and is seen upon the chest, and finally spreads 
over the entire body. Usually it is papillary in character and very closely 
resembles the eruption of measles. As soon as the eruption is developed, 
the febrile symptoms subside and the patient goes on to convalescence. A 
second and terminal rash usually appears in crops after defervescence. It 
is miliary, or may resemble herpes or urticaria. Dengue without fever is 
where the joint and febrile symptoms are absent, but the rash (both ini- 
tial and secondary) is present. This is common in children. The intense 
arthritic pains accompanying the papillary eruption, and the glandular 
swellings are the characteristic symptoms of this type of fever. As the 
second paroxysm of fever subsides, the patient is left with stiifness and 
soreness of the joints, which sometimes do not pass away for weeks. 

Occasionally the disease assumes a typhoid type, the tongue becomes 
covered with a dark brown coating, the gums become red and spongy, the 
pulse slow and feeble, and the surface is covered with a cold sweat. As 
soon as the second eruption appears, the patient is generally free from 
fever, and passes on to a rapid and complete convalescence. During its 
active period there is a peculiar tendency to syncope. In very severe cases 
the pain in the testicles will continue after the subsidence of the fever, and 
a serous effusion will take place into the tunica vaginalis. The joints will 
remain painful and flabby. There will be extreme nervousness and anxi- 
ety. The heart's action will be intermittent, and the lymphatic glands 
which have been enlarged form indurated tumors which very rarely sup- 
purate. 

The duration of this fever varies with the period of remission. Its aver- 
age duration is about eight days. In those epidemics where there is an ab- 
sence of articular pains, the mucous membranes of the mouth and throat 
are involved. In some epidemics the fever has occurred five or six times in 
the same individual. 

The course of the disease may be divided into periods. First, that of 
febrile exacerbation lasting two or three days, then an intermission of 
two or three days, then a second febrile exacerbation which lasts two or 
three days, then convalescence. Its average duration is from three to eight 
days. 

Differential Diagnosis. — This fever may be confounded with rheumatism, 
or with remittent fever. In some of its phenomena it closely resembles 
relapsing fever. 

It may be distinguished from remittent fever by the persistency of the 
rheumatic and neuralgic pains, by the cutaneous eruption, and by the 
length of the remission. 



890 



ACUTE GENERAL DISEASES. 



It may be distinguished from rheumatism, as it prevails epidemically, 
and a period of febrile excitement precedes the arthritic phenomena. 

It may be distinguished from relapsiag fever by the eruption and by the 
character of the remissions. 

Prognosis. — The prognosis is always favorable, although the symptoms 
which attend its development may be alarmingly severe. The prognosis 
'is only unfavorable when it occurs in the very aged or in feeble infants. 1 

Treatment. — This fever always runs a definite course, and its treatment 
is the symptomatic treatment of fever, combined with well-recognized 
anti-rheumatic remedies. It is claimed that emetics and free purgation 
diminish its severity. A favorite combination is ipecacuanha, calomel, and 
colchicum — which is to be administered every night in cathartic doses. 
Calomel should never be administered alone, nor in combination with other 
drugs, if its specific effect is likely to be produced. The administration 
of colchicum with spirits of nitre and nitrate of jootash, in such proportion 
that profuse diaphoresis may be produced, in connection with effervescing 
draughts, will usually afford relief from the pain in the head and limbs. 
Should the arthritic pains persist, opium may be administered in sufficient 
quantity to afford relief. Salicylate of soda or salol are of great benefit 
where arthritic pains are severe. 

During the remission the bowels should be kept freely opened with sa- 
lines, and quinine combined with an alkali should be given at stated inter- 
vals. Narcotics may be given in small doses to produce sleep, should the 
patient be wakeful. By the employment of these measures a return of 
fever may be prevented and the arthritic pains will gradually subside. 
If this plan is pursued, should the fever return, it will be mild in char- 
acter, attended by little constitutional disturbance. The weakness and 
exhaustion which attend convalescence may be combated by the free use of 
wine or malt liquors. 

The diet should be most nutritious. Nourishment should be admin- 
istered at stated intervals, during the night as well as during the day. The 
lymphatic enlargement, especially in the inguinal region, should be treated 
locally with iodine. Citrate of iron and quinine will be found of great 
service during convalescence. If a single joint remains swollen and tender 
for a considerable period after the subsidence of the fever, the occasional 
application of a blister is recommended. 

In some epidemics, relapses after an interval of two or three weeks 
have been of frequent occurrence. They run a milder course than the 
primary fever. The relapses more closely resemble an attack of articu- 
lar rheumatism than the primary fever. Quinine is said to furnish great 
protection against a relapse. 



1 Among sequela* Thomas records heart affections, but does not say what these are ; though he says they 
are not the same as in rheumatism. Peripheral paralysis of the forearm may occur. Catarrh of the fauces, 
trachea or oesophagus is mentioned as a sequela. 



CHRONIC MALARIAL INFECTION. 



891 



CHRONIC MALARIAL INFECTION. 

Malarial cachexia, or chronic malarial infection, may be a sequela of any 
form of acute malarial disease. It may be developed in those who have 
never suffered from any form of malarial fever, but who have resided for 
some time in a malarial district. One who has had repeated attacks of 
intermittent or remittent fever, or has simply lived for some time in a mala- 
rial district and has become exceedingly anaemic, with an enlarged spleen 
and enlarged liver, may be regarded as in a condition of chronic malarial 
cachexia. 

Morbid Anatomy. — The morbid anatomy of chronic malarial infection 
does not differ from that of the severer types of malarial fever, except in 
the more advanced stages of the tissue-changes. Thus the spleen is often 
ten or twelve times its normal size, tough, firm and resistant. Its surface 
is uneven, its capsule thickened and more or less adherent to the adja- 
cent organs. Its substance is rich in pigment matter, and presents the 
minute changes, either of simple hyperplasia or amyloid degeneration. 
Similar tissue-changes take place in the liver and kidneys. In some in- 
stances the muscular tissue of the heart undergoes fatty or amyloid de- 
generative changes. (Edema of the subcutaneous cellular tissue, and an 
accumulation of fluid in the serous cavities, are common attendants of 
chronic malarial cachexia. 

Etiology. — It may be the result of prolonged exposure in a district only 
slightly malarial, or of a short exposure in a district strongly malarial. 

Symptoms. — Those who are the subjects of chronic malarial infection 
complain of vertigo, ringing in the ears, loss of memory, disturbances of 
sight, loss of appetite, nausea, dyspeptic symptoms, and pain and oppres- 
sion in the epigastrium. The bowels are rarely constipated ; diarrhoea is 
often present in the morning. The sleep is disturbed ; it may be profound, 
but it is unrefreshing. The patient awakes in the morning with a con- 
fused feeling about the head and a general feeling of discomfort. Some 
complain of pains in the back and loins and along the sciatic nerve ; others 
of pain and tenderness in the joints and stiffness of the muscles of the limbs 
and back ; they become easily fatigued on exertion, have shortness of 
breath and palpitation of the heart. 

The nervous system seems to suffer most severely. One of the most com- 
mon nervous manifestations is lo?il anaesthesia, which usually shows it- 
self upon the outer surface of the thighs. Itching, burning, and a sense 
of formication, tingling, or numbness are very common symptoms. Not 
infrequently numbness of the arms and fingers and tickling and burning 
of the feet are complained of, and a patient will fear that he is about to 
have an attack of paralysis. 

Hemiplegia sometimes occurs. I remember one case in which there 
was complete loss of power of the right arm and leg, yet no facial paraly- 



892 



ACUTE GENERAL DISEASES. 



sis. This patient had never had a paroxysm of malarial fever, and for that 
reason the possibility of malarial infection lmd been excluded. 

Chronic malarial infection may be unattended by any nervous manifesta- 
tions. This form shows itself in catarrhal inflammations affecting the 
mucous membrane of the stomach, intestines and bronchial tubes. Pa- 
tients have a form of bronchitis which is really a chronic malarial affection. 
A gastro-enteritis, in which there is marked interference with digestion, 
may be developed. If this is treated with the ordinary remedies for dys- 
pepsia, no good result is accomplished, while a few doses of quinine will 
relieve the patient and establish the diagnosis. The chronic intestinal 
catarrh which results from chronic malarial infection may give rise to a 
troublesome diarrhoea which will assume all the characteristics of chronic 
diarrhoea. As already stated, anaemia is a very common result, and pal- 
pitation of the heart is a very frequent and sometimes distressing accom- 
paniment of such anaemia. It often gives rise to temporary attacks of 
melancholia and hypochondriasis. Persons imagine they have disease of 
the heart, kidney, or spine, etc. 

Another nervous manifestation of chronic malarial infection is neuralgia. 
Certain nerve-trunks or their roots seem to be directly involved, while the 
nerve-centre connected with the affected nerve- trunks escapes. The first 
branch of the fifth nerve is most liable to be affected. This neuralgia fol- 
lows a periodic course. Persons over forty are most liable to be affected by 
it. Usually the nerve-trunks first affected are the ones involved in suc- 
cessive attacks ; thus if a certain intercostal nerve is the seat of the primary 
neuralgic paroxysm, at each subsequent attack this particular nerve will be 
the seat of the neuralgia. 

In some instances chronic malarial infection manifests itself by hemor- 
rhages from the mucous surfaces, such as epistaxis, haematemesis, hema- 
turia, etc. The most troublesome cases of menorrhagia (occurring inde- 
pendent of a mechanical cause) often recover after the administration of 
large doses of quinine, when all the remedies ordinarily employed in such 
cases have failed to produce the desired result. 

Differential Diagnosis. — The first question that now arises is : How can we 
decide whether the manifestations are malarial or non-malarial ? In the 
majority of cases there will be some enlargement of the spleen. There is 
not necessarily any rise in temperature. The manifestations will be more 
or less paroxysmal. If the patient has localized anaesthesia or hyper- 
aesthesia, it will be found to be more severe at some particular hour in the 
morning or evening. If the patient has lost power over one portion of the 
body, he will find that the loss of power ij more marked at a certain period 
of the day. The patient may not observe this periodic tendency, and it is 
frequently elicited only after careful examination and close questioning 
by the physician. In the severer cases of chronic malarial infection, 
when there is hemiplegia or some structural change affecting the mu- 
cous membrane of the stomach, intestines, bronchial tubes, etc., there are 
also evidences of pigmentation of the tissues. Free pigment is frequently 
found in the blood. 



CHROKIC MALARIAL IKFECTIOK. 



893 



The diagnosis of chronic malarial infection, to a certain extent, depends 
upon the circumstances which attend its development. If the individual 
has repeatedly suffered from malarial paroxysms, or if he has resided for 
some time in a malarial district without having had a distinct malarial 
paroxysm, and although the peculiar malarial cachexia which is so charac- 
teristic of malarial poisoning is not present, yet it is always well to carefully 
consider the question of malarial infection. 

While the manifestations of chronic malarial poisoning are legion — and 
in many instances they very closely simulate the phenomena of other dis- 
eases — still, with a history of possible malarial exposure, and after exclud- 
ing all other conditions, we determine that the patient is suffering from 
some form of blood poisoning, and then the nature of the poisoning is 
readily determined. In very doubtful cases one may confirm an uncertain 
diagnosis by treatment. 

Prognosis. — The prognosis in chronic malarial infection depends upon 
the severity of its manifestations, and the degree of enlargement of the 
spleen and liver. When the symptoms are mild and the spleen is but 
slightly enlarged, and when neither ascites nor oedema of the lower ex- 
tremities is present, the prognosis is generally good. If the patient is very 
anaemic, the spleen very greatly enlarged, and the area of hepatic dulness 
very much increased, the prognosis is unfavorable. When distinct tumors 
can be detected in the spleen and liver, they indicate an exceedingly grave 
form of malarial infection ; if the tumors are large, they can rarely be re- 
duced, if the individual in whom these tumors are found removes from 
a malarial district, a long time may elapse before they very much interfere 
with his health and comfort. 

The possibility of a patient being able to take up his permanent residence 
in a non-malarious region must be taken into consideration before a prognosis 
is given in any case. So long as such a patient is under malarial influences, 
however slight, the progress of the disease cannot be permanently arrested; 
and when the manifestations of the graver forms of malarial infection are 
present, there is little prospect that the disease can be temporarily relieved 
while he remains in a malarial district. 

Treatment. — The first and most important thing to be accomplished in 
the treatment of chronic malarial infection is the removal of the individual 
from a malarious district to a high, warm, mountainous region. It is of 
the greatest importance that all exposure to wet and cold, and the damp air of 
the evenings and nights, should be avoided; the sleeping apartments must be 
dry and airy, and flannel should be worn next to the skin. So long as the 
thermometer shows even a slight febrile movement, quinine must be given 
in full doses. If anaemia is present, iron must be combined with the qui- 
nine, and administered immediately before or after taking food. In those 
cases in which the spleen and liver are very much enlarged, when no febrile 
excitement is present, iodide of iron combined ivith cod-liver oil will be found 
of great service. 

It is claimed by some that muriate of ammonia has a very beneficial effect 
in this class of cases, but my own experience does not lead me to favor it. 



894 



ACUTE GENERAL DISEASES. 



One-half an ounce of "Warburg's tincture taken daily for ten days, two hours 
before breakfast in the morning, is often efficacious when quinine fails. If 
the bowels are constipated, aloes or rhubarb should be given in connection 
with some of the saline mineral waters. 

In those cases in which the measures already referred to fail to produce 
any improvement or afford any permanent relief, arsenic may be resorted 
to, but the effects of the drug must be carefully watched, and on the ap- 
pearance of oedema Or of gastric disturbance, it must be promptly discon- 
tinued. It must be borne in mind that the use of all these therapeutic 
agents is not sufficient; proper attention must be paid to hygienic measures. 

The neuralgias which are such frequent manifestations of this infection 
are best treated by combining a full dose of opium with large doses of qui- 
nine. If paralysis is a manifestation of the malarial poisoning, strychnine, 
iron and quinine may be combined in its treatment, in connection with 
cold douches and friction to the paralyzed limbs. A most nutritious diet 
and a liberal use of good wine are indicated in all cases. The daily use of 
brandy in small quantities is often of great service. 

In regard to the use of quinine in this class of cases, I am convinced that 
its indiscriminate use does harm. After fairly testing its effects, if no relief 
is obtained, it should be discontinued for a time, or at least until the bene- 
ficial effect of a removal from a malarial district is tried, or until, by the 
use of mild cathartics and daily administration of cod-liver oil and iron, the 
patient is in a condition to be benefited by it. Quinine seems to have no 
effect upon many who suffer from the severe manifestations of this infection, 
so long as they remain in a malarial district, but as soon as they remove to 
a non-malarial district it acts promptly. It is of the greatest importance 
that one should be familiar with the condition in which quinine is indicated 
in the treatment of this class of affections. Avoid depressing remedies in 
all forms of chronic malarial infection : drastic cathartics, exhausting 
diaphoretics, and other depressing remedies must not be used. They do 
greai: harm by exhausting the already enfeebled vital powers. Especially 
is this true in regard to the free use of mercurials, which are so commonly 
resorted to in this affection. Unquestionably, an occasional cathartic 
dose of calomel is of service, but the administration of small doses repeated 
after short intervals to produce its constitutional effects, will always be fol- 
lowed by the more serious manifestations of the malarial infection. 

The exhausted system of this class of patients needs rest, concentrated 
nutrition, and the influence of a change of climate. 



SECTION V. 



CHEONIC GENEEAL DISEASES. 



1. Eheumatism. 

2. Gout. 

3. Lithaemia. 

4. Diabetes. 

5. Anaemia. 

6. Chlorosis. 

7. Progressive Pernicious Anaemia. 

8. Leucocythasmia. 

9. Pseudo-Leukaemia. 
10. Addison's Disease. 



16. Scrofula. 

17. Eickets. 



18. Alcoholism. 

19. Trichinosis. 

20. Syphilis. 



11. Ammonaemia, 

12. Haemophilia. 



15. Myxcedema. 



13. Scurvy. 

14. Purpura. 



EHEUMATISM. 



Eheumatism is a term still vaguely used to cover all inflammatory and 
painful affections of the fibrous tissues about the joints and in the muscles 
which depend upon some constitutional morbid state. There are five dis- 
tinct varieties : — 

1. Acute Articular Eheumatism, or Eheumatic Fever. 

2. Sub-acute Articular Eheumatism. 

3. Chronic Articular Eheumatism. 

4. Arthritis Deformans. 

5. Muscular Rheumatism, "Myalgia." 



Acute articular rheumatism, or rheumatic fever, is the most acute man- 
ifestation of the morbid constitutional state. 

Morbid Anatomy. — The blood when drawn from the vessels coagulates 
rapidly, the fibrin which can be derived from it is in excess of the normal ; 
sometimes it reaches ten per cent., and it is readily separated from the other 
constituents. The number of red discs is diminished and the serum is al- 
kaline. 

The joints are the chief points of attack ; yet in many cases where they 
have been greatly enlarged and excruciatingly painful during life, no change 
has been detected after death. The synovial membrane is usually injected ; 
the capillaries are dilated, and the reddening is best marked where the mem- 
brane joins the cartilage. The cells of the synovial fringes multiply; the 
epithelial cells are enlarged and often surrounded by fat. The lymphatics 
of the synovial adventitia are enlarged ; and the cartilage-cells proliferate 
and the fundamental substance segments. Sometimes the articular carti- 



ACUTE AETICTJLAE EHEUMATISM. 



896 



CHRONIC GENERAL DISEASES. 



lages are cedematous. Small hemorrhages may occur in, or a thin fibrinous 
exudation may cover, the synovial membrane. The ends of the bones have 
been found abnormally vascular in a few cases. Inflammatory oedema of 
the peri-articular tissues is very common. 1 The fluid in the joint-cavity 
may be normal, or it may be increased in amount and slightly turbid. Eloc- 
culi of lymph are sometimes seen floating in it ; and at times it contains an 
abnormal number of cell elements. These elements often undergo fatty 
change, and may resemble Gluge's corpuscles. The color of the fluid varies ; 
its reaction is alkaline. Albumen and fibrin are found in abundance. Urate 
of soda is never found. If the temperature has been high, the liver and 
other internal organs may show cloudy swelling, or parenchymatous de- 
generation. 

Etiology. — Acute rheumatism may be regarded as a constitutional dis- 
ease, — " a specific inflammation of joint structures attended with fever." 
Some claim that there is an excess of sulphur in the blood of rheumatic 
patients ; others regard the disease as due to a change in the normal rela- 
tions of the salts. Another view is that lactic acid — -the normal product of 
nutritive changes in the tissues — accumulates in the blood in excess on 
account of a change in the blood salts, consequent upon some change in 
the albumen. 2 It is a disease of temperate climates, occurring mostly 
between December and March. In common with gout, diabetes, and arte- 
rial sclerosis, its etiology is very closely connected with disturbances of the 
hepatic function. 

There is an hereditary tendency in about thirty per cent, of cases. It 
attacks persons between fifteen and thirty oftener than those of any other 
age. In old age it is exceedingly rare. 3 It is most frequently met with in 
those exposed to wet and cold, as cabmen, laborers, and maid-servants. It 
attacks men oftener than it does women. Insufficiency, or a poor quality 
of food, and prolonged residence in a damp atmosphere or dwelling predis- 
pose to it. 

Any impairment of the general health from defective nutrition renders 
one more liable to a rheumatic attack. Erysipelas, dysentery, scarlatina 
and gonorrhoea are named among its exciting causes. Pregnancy is said 
to have caused rheumatic arthritis, and prolonged lactation may induce it. 
Scrofula, phthisis, and cancerous affections so often precede rheumatism 
that a connection between them cannot be denied. The exciting causes in 
one predisposed to it are exposure of the unprotected surface to sudden 
changes of temperature, to wit : cold and suddenly checking perspira- 
tion. 

Symptoms. — In many instances dyspeptic symptoms precede a rheumatic 
attack, which usually comes on suddenly at night. A distinct febrile 
movement may precede the articular symptoms for twenty-four or forty- 
eight hours. Uneasiness and restlessness, a vague feeling of malaise, or 

1 Garrod states that the only change found in some cases is a lax state of the ligaments and opacity of 
the cartilages. 

2 Richardson's experiments consisted in injection of lactic acid into the peritoneal cavity of a cat. The 
next day peri- and endocarditis were developed. Canstatt regards the articular affection as the result of a 
disturbance of innervation, consequent upon peripheral irritation set up by a chill. 

8 Diseases of Old Age.— Charcot and Loomis. N. Y., 1831, pp. 150, 151. 



ACUTE ARTICULAR RHEUMATISM. 



897 



slight and indefinite pain in the joints that are to be affected, may also 
precede its development. In all cases there is aching pain and stiffness in 
some one of the larger joints, which rapidly increase in severity, accom- 
panied by a rise in temperature proportional to the rapidity of the develop- 
ment of the articular symptoms and the number of joints involved. The 
temperature commonly ranges from 102° to 103° F. ; but it occasionally 




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Fig. 182. Fig. 183. 

Temperature Record in a mild case of Acute Ten-perature Record from the eighth day in a 

Rheumatism. fatal case of Acute Rheumatism. 

rises to 105° F., and 109° and 110° F. have been reached before death in 
severe cases. There are distinctly marked exacerbations and remissions, 
the minimum temperature being nocturnal The pulse is full, bounding 
and compressible, as a rule keeping pace with the temperature ; it often 
reaches 120 per minute independent of the fever, seemingly on account of 
the severe pain. 

The joints attacked become red, swollen, and so tender that the weight of 
the bed-clothes cannot be borne, nor can the patient bear the shaking of 
the bed by the footsteps of attendants. Fluctuation can soon be made out 
in those joints whose situation permits examination. Muscular cramps 
usually accompany the joint symptoms. The face is flushed and the body 
is bathed in a copious, sour smelling, and acid sweat, especially about the 
affected joints. Sudamina are common. The saliva is said to become 
acid, and inflammatory fluids poured out into serous cavities during rheu- 
matic fever have been found distinctly acid in reaction. There is great 
anxiety and restlessness, but the sufferer dares not move, so agonizing is 
the pain in the joint. 

The urinary secretion is diminished, its color being darker than normal. 
On cooling it deposits a brick-dust sediment of urates. Its specific gravity 
varies from 1.025 to 1.030. Urea and coloring matter are in excess, while 
57 \ • ". 



898 



CHROXIC GENERAL DISEASES. 



the chlorides are diminished. Sulphates and albumen are not* infrequently 
found. Uric acid is increased. 1 The tongue is covered with a thick 
creamy fur. There is anorexia and great thirst, the bowels are usually 
constipated and the fasces are dry. 

The large joints are usually involved first. The joint involvement is 
remarkably symmetrical : thus one ankle joint swells, and as soon as this 
subsides its fellow is immediately attacked, and the affection travels rapidly 
from one joint to another in a symmetrical course. There is little oedema, 
pitting or cuticular desquamation after the acute symptoms have subsided, 
except in the very weak and feeble. As a rule, one joint remains swollen 
for three or four days, while others are being successively involved. By 
the seventh or eighth day half a dozen articulations may be involved. The 
hip-, finger- and toe-joints, the spinal articulations, and the symphysis 
pubis are rarely involved. Not infrequently sudamina, herpes urticaria, 
and miliaria accompany the articular symptoms. 

There is usually little mental disturbance ; but when the temperature 
reaches 105° F. there is often great restlessness, insomnia, and a mild wan- 
dering delirium. I regard this delirium (when not occurring in drunk- 
ards) as indicative of extensive blood changes and a sign of great danger. 
One of the characteristics of rheumatic fever is the intense anaemia devel- 
oped in a few days after its onset, even when no antiphlogistic remedies 
have been employed. Auscultation of the heart reveals "blowing" haemic 
murmurs, even when no cardiac complications exist. The articular symp- 
toms often subside suddenly, and cardiac or cerebral symptoms as suddenly 
make their appearance. Cerebral symptoms are always attended by high 
temperature. The cerebral and cardiac phenomena are not due to a metas- 
tasis in the strict sense of the term, nor yet are they complications. There 
is some bond of connection between these cerebral and heart lesions and 
the joint affections, — the exact nature of the connection is not known. The 
fibrous tissue of the heart is as liable to be involved as the joints ; and in 
many young subjects the heart involvement precedes that of the joints. 

Differential Diagnosis. — The connection between gout and rheumatism is 
considered under the head of gout. 

Pycemia may be mistaken for rheumatic fever ; but the recurring chills, 
sickly, sioeet breath, slow development, jaundiced skin, previous history, 
and finally the presence of infarctions, multiple abscesses and thrombi are 
sufficient to distinguish pyaemia from rheumatic fever. Suppurative syno- 
vitis may occur in pyaemia, but not in acute rheumatism. 

iVim-rheumatic arthritis is to be distinguished by its persistence in one 
joint, by the absence of the characteristic sweats, by the graver local and 
more trivial constitutional symptoms, and by the absence of cardiac com- 
plications. 

Prognosis. — Apart from the complications, acute polyarticular rheumatism 
is not a fatal disease ; three per cent, is its average death rate. The disease 
lasts from three to four days in one joint ; the whole duration of the fever 
and attendant arthritis is from three weeks to thirty days. The rule is that 



] Parkes and Garrod, respectively, found thirteen and eleven and one-half grains in a quart of urine. 



ACUTE ARTICULAR RHEUMATISM. 



899 



no crippling of the joints follows the acute attack. If the course of the dis- 
ease is prolonged, complications are usually present ; in many cases its course 
is erratic in that just as convalescence is apparently established all the acute 
symptoms reappear. It runs no cyclical course, — there is no definite limit 
to its duration ; patients may recover in two or three days or a week, or it 
may persist for a month or longer ; generally the milder the attack the 
shorter its duration. I have seen six or seven weeks elapse before the joints 
have returned to their normal state ; in such cases all the joints become 
involved in succession and the articular phenomena are persistent. The 
more robust the individual the sooner is convalescence established. Some- 
times the fever subsides and the joint affections persist. 

The frequent occurrence of endo- and pericarditis leaves little doubt as to 
their intimate connection with the rheumatism. The younger the subject 
the more liable are the cardiac affections to occur. Statistics are most di- 
verse on this point ; some say five, others seventy-five per cent, of all cases 
of rheumatic fever are accompanied by cardiac inflammations. Another, 
graver, sequel is ulcerative endocarditis. The worst legacy acute rheuma- 
tism leaves is a crippled valvular apparatus in the heart. 1 Endarteritis, 
pleurisy, pneumonia, cerebral and spinal meningitis, laryngitis, bronchitis 
and peritonitis are its principal complications. A strange sequel of rheu- 
matic fever is chorea. 

Instead of complete recovery, acute rheumatism may become subacute 
or chronic. Muscular rheumatism frequently follows an attack of acute 
articular rheumatism. 

Treatment. — The hygienic surroundings of rheumatic patients should be 
very carefully attended to. The temperature of the apartment should range 
from 68° to 70° F. ; all draughts should be avoided, and the patient should 
be clothed in flannel and covered with flannel sheets. The diet should be 
milk and seltzer- water. If this is not well borne, concentrated food, other 
than animal, can be given. Animal food and alcoholic stimulants are con- 
traindicated during the active period of the disease. As soon as the fever 
declines, nutritious and easily digested animal food may be freely given. 

Only a few of the many external applications which have been made to 
the affected joints will be referred to. Cold by the means of ice-bags to 
the joints has been strongly recommended. Friction, with chloroform or 
opium in glycerine combined with alkalies and the tincture of aconite is a 
favorite plan with some. "Hot-packs" by means of flannel compresses 
wrung out in water as hot as the patient can bear, or bathing the joints in 
warm laudanum and then covering them with oiled silk is always grateful 
to the patient. Wunderlich and Niemeyer advocate, respectively, ethyl 
chloride and ether to be rubbed over the affected joints. The " blister 
plan," which consists in surrounding all the affected joints with fly blisters, 
temporarily relieves the pain, but the rheumatic attack is not shortened, 
nor do they afford any permanent benefit. My experience leads me to the 

1 Two cases of acute rheumatism were recently (July 31st, 1882) reported by Mayer in " Henoch's Klinik," 
where peculiar and significant complications were observed. The patients were children ; and both had 
little tumors develop about the joints (malleoli, elbow, etc.). that on section, after death, proved to be con- 
nective-tissue neoplasms which had a tendency to necrobiosis or to osseous-like change. 



900 



CHRONIC GENERAL DISEASES. 



opinion that if the affected joints are protected from changes of tempera- 
ture by cotton batting and oiled silk, all is accomplished that can be by 
local applications. 

Internal Medication. — Innumerable remedies have been brought to the 
notice of the profession as specifics in the treatment of rheumatism, yet it 
is still the most unmanageable of all diseases. Garrod is of the opinion 
that colored water is about as potent as anything. He claims that rheu- 
matic fever is a " self -limiting disease/' sometimes running a long, some- 
times a short course. Bleeding, mercury, and antimony and mercury are 
no longer employed. Some advocate the use of iodide of potassium ; some t 
colchicum, some veratria, some guaiacum, and some quinine. Garrod's 
" quino-alkaline " plan, which combines quinine with the alkaline treat- 
ment, is a favorite method with many. It is claimed that the so-called 
alkaline treatment shortens its duration and diminishes the frequency of 
cardiac complications. It consists in the administration of the soda salts 
in from 3v to 3x daily until the urine becomes alkaline. 

My experience inclines me to the opinion that while alkalies in the early 
stages relieve the pain in the joints, they do not shorten the duration of 
acute rheumatism, and if long continued they do positive harm. 1 The 
tincture of the chloride of iron, in one-half drachm doses, is especially ser- 
viceable as soon as the temperature reaches 100° F. Within the past few 
years salicin, salicylate of soda, and salicylic acid have been very exten- 
sively employed. It is claimed that immediate relief follows the adminis- 
tration of the salicylates — that the temperature falls, that the pain and 
swelling of the joints subside, and that the duration of severe attacks has 
been limited to thirty-six or forty-eight hours. But it causes great depres- 
sion of the heart, increases the liability to cardiac complications, causes 
irritability of the stomach, and places the patient in a weak and debilitated 
state ; for the past few years I have seldom employed it, for my experience 
shows that while in some cases it may relieve the urgent symptoms of the 
disease in two or three days, relapses are almost certain to follow, and the 
duration of the disease is not shortened, and I have seen very serious toxic 
effects follow its use. Salol is to be preferred to salicylic acid. Benzoic 
acid and benzoate of soda are claimed by some to act mere efficiently than 
salicylic acid and to be less harmful. I have not seen any good results fol- 
low their use. 

During the past few years I have obtained the most satisfactory results 
in the use of antipyrine during the acute stage of articular rheumatism. 
I have come to employ it almost to the exclusion of all other remedies for 
the relief of the arthritic pains, and in many cases it has seemed markedly 
to shorten the duration of the disease. The treatment of the various com- 
plications is considered under their appropriate heads. 



1 Gull, Sutton and Lebert found marked diminution in the duration of rheumatism from steady admin- 
istration of lemon juice. 



CHRONIC ARTICULAR RHEUMATISM. 



901 



SUB- ACUTE RHEUMATISM. 

Sub-acute rheumatism is usually a sequela of acute, or occurs in one who 
has at some time had an acute attack ; it is attended by slight if any fever ; 
the pain in the joints is not severe, except on motion ; and the swelling and 
redness are not excessive, and are limited to one or two joints, usually the 
large ones. There is no tendency to disorganization or permanent crip- 
pling of the affected joints ; and although it may last six or seven weeks, 
or three or four months, the joints usually return to their normal condi- 
tion. The blood changes are the same as in acute. The articular symp- 
toms are less metastatic than in acute ; anaemia is always well-marked, and 
cardiac complications are not infrequent. 1 The treatment is a milk diet, 
iron and cod-liver oil, and a warm climate, and heat to the affected joints. 
The so-called anti-rheumatics have failed in my hands to relieve or cure. 

CHRONIC ARTICULAR RHEUMATISM. 

Chronic articular rheumatism usually involves only a few joints ; it oc- 
curs most frequently in those who have had rheumatic fever in early life. 
Although it may be of long duration it rarely induces extensive changes in 
the joints. 

Morbid Anatomy. — The parts affected are the fibrous tissue around the 
joints, the fibrous envelopes of the nerves, the aponeurotic sheaths of the 
muscles, the fasciae, and the periosteum. The synovial membrane is thick- 
ened, the fringe-like processes are hypertrophied and very vascular, and 
the synovial fluid becomes turbid and cloudy. The ligaments are thick- 
ened, the cartilages relaxed, shaggy, and sometimes in a state of fatty de- 
generation. The more protracted the disease the greater the thickening of 
the peri-articular structures, and the thicker and scantier will be the fluid 
in the joint. The fibrous tissue developed about the joints causes more or 
less stiffness and loss of motion, but not ankylosis. 

Etiology. — It is a disease of adult and advanced life, occurring oftenest 
in those whose hygienic surroundings are bad, and who are exposed to wet, 
cold, or sudden changes of temperature. A residence in dark and damp 
dwellings predisposes to it. Previous attacks of acute articular rheuma- 
tism develop a tendency to chronic rheumatism. It is often hereditary, and 
then there may be no appreciable exciting cause to its development. Both 
sexes are equally liable. 

Symptoms. — There is aching and constant pain in some one or more of 
the larger joints, usually the knee or ankle, but sometimes those of the 
upper extremities. The affected joints are tender and slightly swollen, and 
their movements are constrained. No fever is present. The aching and 
deep-seated pains are often worse at night. When it is the result of expos- 
ure, heat will give a grateful sense of relief ; when a rheumatic diathesis 
exists, the heat of the warm bed-clothes increases the pain, and relief is 

1 Barwell, who calls this disease "Sub-acute Rheumatic Synovitis," says it may lead to hydrops artieuli. 
—Diseases of the Joints, 1881, p. 138, et seg. 



902 



CHRONIC GENERAL DISEASES. 



often obtained by exposure of the joint to dry cold. Old people with rheu- 
matic joints are great "weather prophets," often being able to foretell the 
coming of a storm. After rest, motion gives great pain, but use renders 
the joint temporarily more supple and less painful. The pains undergo 
exacerbations and remissions, and the disease may continue for years with- 
out causing much deformity or great crippling of the joints. The muscles 
near the joint usually undergo more or less atrophy, and as a result the af- 
fected joints appear larger than they really are. 

Palpation may reveal fluctuation in the joint, and auscultation gives a 
rough, grating crepitus during motion. 

Differential Diagnosis. — Chronic articular rheumatism may be distin- 
guished from arthritis deformans by the absence of deformity of the af- 
fected joints, the history of previous acute rheumatic attacks, the large 
joints being mainly involved, the partial or complete recovery during warm 
weather, and its return on exposure to wet and cold ; arthritis deformans 
is a steadily progressive disease, one joint after another being involved and 
never recovered from. 

Prognosis. — There is little chance of complete recovery after middle life ; 
it is only possible in those cases treated at the onset under favorable 
hygienic conditions. In long-standing cases, wasting of the muscles may 
lead to great crippling of the joint. Muscular rheumatism is a frequent 
accompaniment of articular. Chronic rheumatism never affects the dura- 
tion of life, except as it may deprive the patient of exercise and sleep, and 
thus interfere with nutrition. 

Treatment. — This form of rheumatism is benefited mostly by local treat- 
ment, such as blisters, iodine, belladonna, aconite, opium, and chloroform 
liniments, veratrum ointment, etc., etc. Most rheumatic patients have 
their favorite prescriptions for local use, which they claim afford them 
almost instant relief. If there is but little pain in the joints, ammonia 
and turpentine liniments are of service. Thick flannels should always be 
worn about the joints. Some advocate, for both pain and stiffness, spong- 
ing the joints with hot water. The Galvanic or Faradic current will tem- 
porarily reduce the swelling and pain, and sometimes improves the mobility 
of the joint. Local or general baths form an essential part in the treat- 
ment of this form of rheumatism. Hot air, or vapor baths are not so 
efficacious as hot water. Many of the hot saline springs for bathing have 
acquired a great reputation in the treatment of this form of rheumatism, 
cures being effected in cases that had resisted all other methods of treat- 
ment. 1 Massage and rubbing are always beneficial ; and undoubtedly 
much of the good that is claimed for certain liniments is due to the rub- 
bing and manipulation of the joints during their application. 

Internally, tonics should be employed, such as iron, quinine, strychnine, 
etc. Cod-liver oil is the most useful of all internal remedies, and should 
be administered continually. All the means for improving the general 
health of the patient should be carefully considered, and if possible he 



1 Those which I have found most efficacious in this country are the Hot Springs of Arkansas, the Vir« 
ginia Hot Springs, and the Richfield Springs in New York State. 



ARTHRITIS DEFORMANS. 



903 



should reside in a dry, warm climate. Colchicum, arsenic, iodide of po- 
tassium, and guaiacum have gained reputation in its treatment, as have 
also the turpentine and cajeput oils combined with sulphur ; but 1 have 
been unable to find sufficient proofs of their beneficial effects to strongly 
recommend their use. Becently, Kawson advises guarana, and Heller 
liquor ammom'i. 1 

The diet must be highly nutritious and absolutely non-stimulating : I 
am convinced that errors in diet and " fits of indigestion" prolong, and 
are powerful to develop this disease. Exercise is important, and if pos- 
sible a sea voyage in a warm climate should be taken. 

ARTHRITIS DEFORMANS. 

(Rheumatoid Arthritis.) 

Arthritis deformans is a chronic inflammation of the synovial capsule, 
the ligaments and tissues of the joint, unattended by suppuration and with 
little fluid accumulation in the articular cavity. 

Morbid Anatomy, — The synovial membrane and articular cartilages are 
first involved. The fringes of the former are increased in number, and 
are very vascular : they are called "the destructive vegetations" of the 
synovial membrane. The central portion of the articular cartilages be- 
comes roughened or villous, gets gradually worn down, and finally disap- 
pears, and the bones thus laid bare undergo eburnation. The ivory-like 
surfaces are striated, the striae running in the direction of the articular 
movements. 2 "While the central portion of the cartilage is disappearing, 
its margin forms nodular irregular outgrowths. The synovial fringes take 
part in the hypertrophic processes, and form pyriform excrescences, which, 
after a time, become converted into fibrous tissue. These outgrowths in 
some cases blend with the osseous structure of the epiphysis, and in others 
become detached and are free. Lateral expansion of the joint surfaces 
with enlargement of the ends of the bones takes place and leads to de- 
formity, dislocation, and immobility. All the joints may, in course, be 
involved, especially those of the hands and feet. The thickened ligaments 
sometimes undergo partial cartilaginous, osseous, or fatty degeneration. 

The tendons are sometimes thinned and ossified. The fluid in the joint 
cavity is thick, turbid and yellow, and alkaline in reaction. There are no 
blood changes ; no urates are found in the joints. The adjacent muscles 
undergo atrophy. 

Etiology. — This disease is regarded by some as a peculiar form of chronic 
rheumatism, while others regard it as an essentially different disease. It 
mav occur at any age ; but the tendency to it increases with advancing 
years. Women are more liable to it than men. The smaller joints are 
most often involved in women ; the larger in men. It is very rare in dry, 
hot climates. Damp dwellings, poor food, and mental depression are 

1 Wien. Med. Presse, Uec, 1875. 

s Charcot calls eburnation a " sclerosis of bone, accompanied by vascularization of the deep parts." 



904 



CHRONIC GENERAL DISEASES. 



powerful predisposing causes. Thin people suffer oftener than the cor* 
pulent. It is met with oftenest in the poorer classes. 1 

Symptoms. — The symptoms of arthritis deformans are all referable to 
the changes which occur in the joints. It may come on insidiously, neu- 
ralgic pains sometimes preceding stiffness and deformity. As the soft 
parts atrophy, the joints stand out distorted and rigid from the flabby mus- 
cular surroundings. There are usually no severe inflammatory symptoms, 
the joints are only slightly tender to pressure, but motion always gives 
pain. Months and years may elapse before the articular changes are 
completed ; but once started, they are progressive, until the joint is anky- 
losed or deformed. 2 The immobility of the joints depends upon the 
osteophytes or fibro-cartilaginous transformation of the synovial mem- 
brane or fibrous union of the surfaces of the bared bone. 

In some cases the disease begins with all the signs of rheumatic fever, 

with inflammatory symptoms of a mild 
type. No cardiac signs are present, 
and no excess of uric acid can be 
found in the blood. The acute symp- 
toms gradually subside, leaving the 
joint irreparably crippled. The small 
joints are usually first involved. The 
metacarpophalangeal articulations of 
the index and middle fingers are 
usually first attacked. In forty-five 
cases, the smaller joints of the hands 
and feet alone were involved in twenty- 
five ; the great toe in four ; the hands 
and feet with a large joint in seven ; 
the large joint first, then the fingers in 
nine. After a time large joints, the 
temporo-maxillary articulation, or the 
articular processes of the vertebrae, 
especially the cervical, become involved. 
The hip, shoulder, elbow, knee, and 
hands are its favorite sites. In many 
joints abnormal mobility is developed, 
i. e., the hip may slip up and down in 
its socket. Subluxations are common, 
in the fingers especially. 
Deformity from Articular Rheumatism. Early in the disease a friction crepi- 

tus is heard as the articular surfaces 
are rubbed upon each other, which becomes coarser as the disease ad- 
vances. There are painful spasms of the muscles in the affected limb, 
more marked at night and just before a storm. When the disease is local- 

1 Charcot advocates a nervous origin, especially when it begins in the smaller joints. Barwell regards 
:t as due to colitis, originating in " some constitutional cachexia," which, in some of its tendencies, re- 
sembles the rheumatic diathesis. 

2 Remak believes that the painful swellings on either side of the joint are " neurotic nodes.' 1 '' 




Fig. 184. 



AKTHRITIS DEFORMANS. 



905 



ized in the hip joint, it has been called "morbus coxae senilis." In such 
cases the limb is shortened and the patient limps. The greatest variety of 
deformity takes place in the hands of those who have been long the sub- 
jects of this disease. The constitutional disturbance is never commensur- 
ate with the local signs. The skin becomes dry and harsh ; there is great 
acidity of the stomach, cold extremities and a condition of extreme anae- 
mia. 1 

Differential Diagnosis. — Arthritis deformans may be mistaken for chronic 
articular rheumatism without deformity, and chronic gout. 

Gout is hereditary, and occurs more in males. Arthritis deformans is 
rarely hereditary, and occurs oftenest in females. Attacks of gout are 
periodic, and the small joints are found involved. Arthritis is progressive, 
and the large joints are generally first attacked. Kidney complications are 
common in gout and rare in arthritis. Chalk-stones develop in the joints in 
gout and are never present in arthritis. Uric acid is always in excess in 
gout, and never in arthritis ; deformities and ankyloses are less marked and 
extensive in gout than in arthritis. 

Prognosis. — Arthritis deformans never destroys life, and is never recovered 
from ; patients with this disease may attain very old age. The greater 
the number of joints involved the more deplorable will become the condi- 
tion of the patient. There is rarely complete ankylosis. When false joints 
form there is a possibility that such patients may walk or move about with 
comfort. 2 

Treatment. — Treatment of this disease is very unsatisfactory ; for the 
most part we must trust to local measures for relief, and to such constitu- 
tional measures as shall improve the general health. Quinine, iron, cod- 
liver oil, arsenic and strychnia are indicated. The diet should be nutritious 
and easily digestible. Alcoholic stimulants, if they improve nutrition, 
are of service. Change of climate and habits of life is often followed by 
an arrest in its progress. Flannels should always be worn next the skin. 
Mineral waters and warm saline baths, either artificial or natural, often 
temporarily arrest its progress and relieve the pain in the joints. The 
preparations of iodine and the acute rheumatism and gout remedies have 
seemed to me to do more harm than good. Local frictions with iodine, 
mercury, and iodoform sometimes relieve. If the pain is so severe as to 
prevent sleep, it must be relieved by anodynes. Great care must be exer- 
cised in their use that the patient does not become addicted to them. The 
constant or Faradic current may be cautiously tried ; in many cases it is of 
great benefit. 3 The parts should be moved as much as possible if the joints 
are not painful. In the so-called acute attacks rest is necessary ; and then 
leeches and blisters to the joints are indicated. 

1 The only vrinary change is diminution in the amount of phosphoric acid by nearly fifty per cent.— 
(Drac/imann.) 

2 Charcot describes numerous cases complicated by asthma, megrim, cystitis, and such skin diseases as 
eczema, nummular psoriasis, lichen, and arthritic prurigo ; but these complications are the result of the 
long confinement and inability to excercise, rather than necessary sequelae. 

* Retnak and Althaus. 



906 



CHEOKIC GENERAL DISEASES. 



MUSCULAR RHEUMATISM, 

{Myalgia,) 

Muscular rheumatism is a rheumatic affection of the voluntary muscles, 
the fasciae, periosteum, and other fibrous structures, accompanied by pain 
and tenderness, but by no other evidences of inflammation. It has been 
named according to its seat, torticollis (wry-neck), cephalalgia, pleurodynia, 
lumbago, etc., etc. 1 

Morbid Anatomy. — The negative results of autopsies lead to the conclu- 
sion that there are no constant anatomical lesions, except those due to 
transient hyperemia, or to scanty serous exudations into the muscles. In 
a few cases there is evidence of inflammation of the fibrous sheath of the 
muscles and of muscle-degeneration. Thickenings and adhesions of the 
neurilemma of the nerves supplying muscles that have long been subject 
to chronic rheumatism have been found. 

Etiology. — Muscular rheumatism is not uncommon in the children of 
the gouty or rheumatic. It is often intimately associated with articular 
rheumatism, which sometimes precedes, sometimes follows it. Exposures 
to cold and damp draughts are often the exciting causes of an attack, es- 
pecially after the muscles have been over-fatigued. Sudden straining of 
a muscle may induce it. It often seems to have a malarial origin. It may 
come on suddenly in a rheumatic or gouty subject without any appreciable 
exciting cause. 

Symptoms.— An attack usually comes on suddenly with severe, deep-seated 
pain in the group of muscles affected. The pain is of a stretching or tearing 
character, increased by movement or pressure ; it is always more severe at 
night, and remits or disappears during the day. It may be migrating or 
remain fixed in certain muscles or fasciae. It is usually acute when the 
muscle is in action, and dull when the parts are at rest. Certain positions 
mitigate the pain. In many instances it will wholly disappear in a few mo- 
ments, and the sufferer, who perhaps has been for hours enduring excrucia- 
ting cramp-like pain, feels a sudden sense of relief. Such attacks are fol- 
lowed by lassitude. 

Lumbago, pleurodynia, and ivry-nech are the most common forms. 

Lumbago, or rheumatism of the muscles on either side of the lumbar 
spine, usually is the result of straining the lumbar muscles, or sitting on 
the damp ground, or is excited by a current of air across the back. The 
patient is unable to bend backward or forward ; if the pain comes on while 
he is in a sitting posture, he is compelled to walk with the body bent at 
the hips. Lumbago comes on very suddenly, and the pains are more in- 
tense than in any other form. 

Intercostal rheumatism, or pleurodynia, is attended by many of the symp- 
toms of acute pleurisy. There is pain in the side, which is increased by 



1 These different varieties are grouped by some in the list of the symptoms of chronic rheumatism; 
others regard them as neuralgias. 



MUSCULAR RHEUMATISM. 



907 



every respiratory movement ; the sufferer leans to the affected side. Cough- 
ing, sneezing and defecation render the pain more intense. 

In ivry-neck the muscles on one side of the nape of the neck are involved. 
The patient holds his head toward the muscles that are affected, so as to 
relax them, and, in attempting to turn his head, turns his whole body like 
a pivot. 

If the frontal, occipital, or temporal muscles are involved, it is termed 
rheumatic cephalalgia. 

If the abdominal muscles are involved, it is termed abdominal rheuma- 
tism. In all cases there is pain and rigidity of the muscles or groups of 
muscles involved, accompanied by a fixed position. There is no fever or 
constitutional symptoms. 

Differential Diagnosis. — Lumbago may be mistaken for renal colic. 

In renal colic there is no tenderness on either side of the lumbar spine, 
which is always present in lumbago. The position of the patient is not 
fixed as in lumbago. In renal colic the pain radiates along the ureter, to 
the end of the penis, and is often accompanied by retraction of the testicle 
on the affected side. The urine is diminished during, and copious and 
bloody after, the attack. 

An examination per vaginam will decide between uterine disease and 
lumbago. 

Lumbago may be distinguished from disease of the spine by the fact that 
in the latter affection pressure on the ends of the spines will produce pain, 
while lateral pressure gives negative results ; in rheumatism of the muscles 
the reverse is the case. 

Pleurodynia may be mistaken for pleurisy and intercostal neuralgia. 
Pleurisy is accompanied by fever, increased pulse-rate, cough and — on 
physical examination — by physical signs of pleurisy. None of these condi- 
tions are present in pleurodynia. In intercostal neuralgia there are three 
(diagnostic) points of tenderness : at the exit of the nerve from the spine ; 
at its termination near the sternum: and midway between these points, while 
there is no tenderness over the muscles. In pleurodynia these points of 
tenderness are absent, and the intercostal muscles are tender. 

Abdominal rheumatism may be mistaken for peritonitis ; but in perito- 
nitis there will be fever, increased pulse-rate, and Avell -marked constitu- 
tional symptoms which are absent in abdominal rheumatism. In the lat- 
ter, deep, firm pressure affords relief. 

Trichinosis is accompanied by symptoms that resemble those of muscular 
rheumatism ; but the history of the case, the oedema of the feet, and a 
microscopical examination of a portion of the muscle, will decide the diag- 
nosis. 

Prognosis. — No danger attends this form of rheumatism. An acute at- 
tack may last a few hours or days. If it become chronic, the muscular 
pains may last for months. Wry-neck is the mildest and lumbago the se- 
verest variety. One attack generally favors the occurrence of a second. 

Treatment. — In the young, if there is an hereditary tendency to rheuma- 
tism, cod-liver oil acts as a prophylactic. At the commencement of an at- 



908 



CHKO^IC GENEKAL DISEASES. 



tack a hot-air or Turkish bath will be of service. Guaiacum, sulphur and 
arsenic are the favorite drugs in chronic cases. Quinine is almost a specific 
in the malarial form. In vigorous persons subject to muscular rheumatism 
the surface should be warmly covered with flannel, and the individual should 
accustom himself to a morning rub-down with a dry, coarse towel after 
a cold sponging. The bromides are useful in some cases. 

In lumbago hot anodyne fomentations and anodyne liniments will often 
give relief if vigorously applied. Hypodermics of morphia may be given 
for temporary relief. These patients should remain quiet in the position 
that gives them most relief. 

In intercostal neuralgia, cupping, blisters, and hot poultices will often 
relieve. But in severe cases hypodermics of morphia must be resorted 
to. 

In ivry-neck, the cervical region should be swathed in warm flannel. 
Gentle traction likewise aids in this. The constant and Faradic currents 
may be passed alternately through the affected muscle. Showering with 
water as hot as can be borne is very efficacious in some cases. Acupunc- 
ture affords relief in many instances. Veratria and aconite are often used 
in ointments. Manipulation by a skilled " rubber " is one of the most 
efficient means of local treatment. If anaemia is present chalybeate waters 
and tonics are indicated. 

GOUT. 

Gout is a constitutional disease of mal-nutrition, characterized by an 
excess of uric acid in the blood and the deposit of urates in the cartilages 
and fibrous structures of joints and throughout the body. The constitu- 
tional condition is generally described as the " gouty diathesis/'' — lithasmia ; 
and the term gout is applied only to the phenomena, which may be either 
acute or chronic, attendant upon the elimination of the urates and their 
deposition in the joints. 1 

Morbid Anatomy.— The primary changes, so far as we are able to appre- 
ciate them, are in the blood and consist in an excess of uric acid. 2 In just 
what way the nutritive processes are at fault, and whether the urates found 
in the blood are there as the result of an excess or a deficiency of activity, 
are points as yet undetermined. In acute gout this excess occurs only just 
previous to, and during the paroxysm, when the proportion of urates may 
reach 1 in 20,000 or even 1 in 6,000, and the corpuscular elements remain 
unchanged, but in chronic gout it is permanent though in much smaller ra- 
tio, and is accompanied by anaemia. Traces of oxalic acid are occasionally 
found in the blood, and there is always decrease of alkalinity and increase 
of the fibrin-factors. 

Although the blood change is the essential one, the articular are the 
more manifest and characteristic, and consist in the deposit of the urates in 

1 It has received the names of podagra, chiragra, ironagra and arthritis according as it affects the foot, 
hand, knee, or several joints. 

3 The precise combination in which uric acid occurs in the blood is undetermined. It is probably 
*ither as the acid or neutral urate of soda. 



GOUT. 



909 




the joints with the attendant inflammatory and ulcerative processes. The 
primary deposit occurs in the cartilage capsule and cells at the point of 
least vitality and most remote from vascular supply, and gradually in sub- 
sequent attacks invades the cartilage, periosteum, synovial fringes, and 
fibrous tissues of and about the joint, 
where it is found between the connec- 
tive-tissue fibres. This deposit con- 
sists principally of the urate of soda 
in the form of minute needle-shaped 
crystals, but to the unaided eye ap- 
pears amorphous ; chloride of sodium, 
urates of lime, magnesia or ammonia, 
hippuric acid and phosphate or car- 
bonate of lime are present in small 
proportion. In the earlier stages the 
articular surfaces are slightly granular 
in appearance, with a thin amorphous 
incrustation. But as the acute attacks 
are repeated, or in the later stages of 
chronic gout, the incrustation in- 
creases, the surfaces are decidedly 
roughened : gradually erosions occur 
from epithelial degeneration and attri- 
tion, and all the adjacent structures 
are infiltrated and covered with a thick 
deposit of urates. The articular 
changes may go on to entire destruc- 
tion of the cartilages and articular surfaces, while the extra-articular de- 
posits form large concretions or tophi. These may induce ulcerative and 
suppurative processes until they finally protrude through the skin, are dis- 
charged from abscesses, or produce fibrous and osseous ankylosis. The 
veins about the joint become dilated,, varicosed, and filled with thrombi 
which may at any time cause embolism= All these changes are gradual in 
their development, but each attack of gout, even the first, leaves its per- 
manent mark in the affected joint. Aside from the acute attack, inflam- 
matory processes of a low grade are eventually engendered by the irritation 
of the deposits, and molecular changes enter as an element in the destruc- 
tive processes, or the inflammation may result in the production of ecchon- 
drosis. 

The small joints of the body are most frequent! v affected, and of these 
the metatarso-phalanseal articulation of the great toe is so unquestionably 
first as to render it the classical seat of acute gout. In order of frequency 
after this are the joints of the fingers, knee, elbow, hip. and shoulder. 
Other joints are but rarely affected. But all the cartilages and fibrous 
tissues throughout the bodv as well as those of the joints may be the seat 
of gouty manifestations. Tophi are frequently found in the cartilages of 
the ear, nose, or eyelids, and are then of the highest clinical significance. 



Fig. 185. 
Section of a Goutv CartiJaee. 



.1. Artie la 
B. Normal 
C Crystal* 
D. Dense dt 



''soda in the stroma, 
ates. x 300. 



910 



CHROMIC GENERAL DISEASES. 



iff hi^P: % ' : : 




1:1 



They may be present also in the larynx, sclerotic, tendons of the hands, 
and even on the spinal dura or outer coat of the arterial sheaths. 

The most important visceral lesions are found in the kidney, and consist 
in a similar deposit of urates and subsequent cirrhotic changes. The 
primary deposits here are probably in the tubules and their epithelium, 
and the interstitial deposits and fibrous changes are secondary. The 

kidney presents a granular appearance, 
and on section the fine striae of urates 
may be seen throughout the tubular 
structures. More abundant deposits 
may aggregate in the pelvis as calculi 
and incite pyelitis. The heart is event- 
ually hypertrophied and may present 
signs of fatty degeneration, while the 
arteries present varying stages of athe- 
roma from the primary fibroid changes 
to distinct calcareous deposits. Fibroid 
and cirrhotic changes also occur in the 
liver and stomach, and finally uric acid 
is present in both the normal and patho- 
logical fluids found in the body. 

Etiology. — The exact nature of those 
changes which result in the gouty 
diathesis is still undetermined, but cer- 
tain etiological relations are quite clearly 
established. Gout is pre-eminently a 
disease of middle life, and although it can be developed in any constitution, 
heredity can be traced in fully sixty per cent, of cases, and almost in- 
variably so when it is present in children or early adult life. 

Clinical experience proves that the direct exciting cause is the product 
of the following factors in varying proportions. — First. An excess of nitro- 
genized material in the system from over-eating and the use of alcohol. 
Excess as applied to eating is a relative term, and in certain constitutions 
an amount of food, which in others would be very moderate, may so exceed 
the demands of the system as to be the cause of gout. Of alcoholic 
beverages the sweet wines and malt liquors are considered more gouty than 
spirits. 

Second. Deficient or suddenly arrested oxidation. Lack of exercise and 
its consequent abundant supply of oxygen are the most frequent causes 
of such deficiency of oxidation, but it is also probable that the con- 
stitutional and hereditary tendency exerts a powerful influence over the 
assimilative function, and that impaired nervous energy may be the ulti- 
mate cause of defective oxidation. 

Third. Failure in the excretive power of the kidney. Such failure may 
result either from deficiency of the eliminative power of the renal epithe- 
lium or mechanically from obstruction of the tubules by deposits of urates, 
and is the prime factor in producing the acute gouty attack. In a system 



Fig. 186. 

Vertical Section of a Malpighian Pyramid in 
Gouty Nephritis. 

The stria?, consisting of urates, follow the general 
course of the tubules. Much ' of the deposit has 
been washed out of the specimen in hardening. 

x 30. 



GOUT. 



911 



already laden with urates, a few glasses of wine, a fit of dyspepsia, ex- 
posure, severe mental effort, or a fit of anger may be sufficient to bring on 
an attack of gout. 

Symptoms. — Gout maybe either acute or chronic, and appear as "regu- 
lar" in the joints, or as irregular, misplaced, retrocedent or anomalous 
gout in the non-articular structures and the internal organs. 

In most cases of acute gout premonitory symptoms precede the first 
paroxsym ; there will be a history of occasional pains in one or both great toe- 
joints, a feeling of malaise with sleeplessness, constipation, dyspepsia, and 
perhaps pain in the side, a dry, hot skin, scaly eruptions and scanty urine. 
Sometimes an attack is preceded by a peculiar sense of well-being, even ex- 
citation ; at others by great anxiety, irritability, and depression of spirits. 
Asthmatic symptoms often precede the outbreak of an attack. Usually 
between midnight and four or five in the morning the individual wakes 
with a burning, throbbing pain in the ball of the great toe, which the 
slightest pressure greatly intensifies. 

The affected joint becomes red, swollen, hot and shining ; the veins are 
distended, and it resembles a joint about to suppurate. There is some fe- 
brile movement which varies in intensity with the number of joints affected. 
The temperature may in a severe attack reach 105° F. The pulse is full 
and bounding but compressible. As the fever comes on the pain in the af- 
fected joint is so great that the patient cannot move it; he becomes restless, 
tossing for hours, until finally, in a profuse perspiration, he falls asleep. In 
a few hours he awakes refreshed and comparatively free from pain ; but the 
affected joint is swollen, tense, and vividly red. He continues comfortable 
during the day, but about the same hour the next night there is a recurrence 
of the local pain and the fever, which is followed by another remission the 
following morning. 

These nocturnal exacerbations and morning remissions continue with 
about the same severity for two or three days, then the maximum of pain 
is reached. At the end of a week they have gradually subsided ; the af- 
fected joint remains tender and swollen for a week or two longer. This 
swelling is due to oedema, and pits on pressure, and as it disappears des- 
quamation occurs. Following the attack, there is a feeling of well being 
which has led to the popular belief that an attack of gout is beneficial. 

There is usually marked digestive derangement during an attack, with 
anorexia, a thickly furred tongue, and constipation. The urine is scanty, 
high colored, and contains less uric acid than normal, depositing on cool- 
ing a copious sediment. The bladder is irritable, and there is a scald- 
ing sensation on urination. Intense cramps in the muscles adjacent to 
the affected joint may occur. Occasionally during the first attack both 
great toe joints are involved ; and instead of disappearing at the end of a 
week, successive outbreaks occur in the other joints. 

An individual may have only a single attack ; but usually a second su- 
pervenes within a year. Gradually the attacks approach each other, and 
are more prolonged though less severe, until a condition of chronic gout is 
reached. In the second and third attacks the joint formerly involved, or 



912 



CHRONIC GENERAL DISEASES. 



its fellow of the opposite side, presents the same phenomena as in the 
primary attack. 

Although all gout is strictly speaking chronic, by chronic gout is 
understood those gouty manifestations which are developed as the parox- 
ysms coalesce, and the patient is scarcely ever free from some gouty mani- 
festation. Tophi form around the 
affected parts, and the joints be- 
come so distorted or crippled that 
walking becomes difficult. Grad- 
ually the health deteriorates, and 
feebleness and a gouty cachexia be- 
come marked and visceral derange- 
ments become prominent. When 
chronic gout follows acute, the ar- 
ticular phenomena are always prom- 
inent. But when, as not infre- 
quently happens, gout is chronic 
from, the onset, tophi form early 
without acute inflammatory symp- 
toms, and the visceral affections are 
prominent. In chronic gout the 
urine is greater in amount, lighter 
in color, of lower specific gravity, 
and contains less uric acid than nor- 
mal. In a few cases casts and al- 
bumen make their appearance. 
Misplaced gout — gout that has re- 
troceded from a joint to an inter- 
nal organ, also called visceral, masked, internal and metastatic gout— 
may attack any organ and result in a long series of functional disturb- 
ances. 

The sequelae and complications of gout are numerous. Those referable 
to the nervous system are vertigo, neuralgia, headache, stupor, convulsions, 
delirium, apoplexy and lunacy. 1 Those referable to the vascular system are 
arterial degeneration, angina pectoris, cardiac palpitation, and valvular dis- 
ease. Those referable to the lungs are asthma, which alternates very 
often with the articular phenomena of gout, and bronchitis, which some 
regard as the commonest manifestation of gout, after arthritis. Eefer- 
able to the digestive tract is a long list of gastro-intestinal catarrhs, cir- 
rhoses of the liver, jaundice, and cirrhotic kidney. 

Differential Diagnosis. — Grout is generally easy of diagnosis. It may, 
however, be mistaken for rheumatism. 

Gout attacks the small and rheumatism the large joints. A rheumatic 
attack is of longer duration than a gouty paroxysm, and has no perio- 
dicity. In gout the fever is slight, 102° to 103° F., and is in inverse ratio 
to the number and size of the joints involved ; in rheumatism there is usu- 

1 These are regarded by some observers as evidences of cerebral gout.— Garrod, Todd, Trousseau. 




Fig. 187. 
Deformity from Gout. 



GOUT. 



913 



ally a higher range of temperature. Cutaneous affections are common in 
gout and rare in rheumatism. The heart is frequently involved in acute 
rheumatism, and rarely in gout. The gouty attack coming on at night in 
the great toe joint is in marked contrast to the onset of rheumatic fever. 
Acute articular rheumatism is a disease of early adult life, while gout is 
rare before thirty-five. In gout there is a history of high living, or an 
hereditary predisposition ; in rheumatism there will be a history of expos- 
ure or exhaustion. In gout there is an excess of uric acid in the blood ; 
this is never the case in rheumatism. When we are enabled by the mi- 
croscope to see uric acid crystals derived from serum of a patient with an 
arthritis, the diagnosis of gout is established. Tophi never form in rheu- 
matism, but are always present late in gout. 

The joint affection of pycemia may be mistaken for gout ; but the history, 
in connection with the constitutional signs of pyaemia, will remove all doubt. 

Prognosis. — Gout rarely kills, but complete recovery from it is also rare. 
Death is generally the result of visceral complications or of the cachexia 
induced by blood changes. The prognosis is less favorable in hereditary 
gout, and in those who persist in high living and the use of alcoholic bev- 
erages, and when the larger articulations are affected. The appearance of 
albumen in the urine, and total absence of uric acid from the secretions 
are grave symptoms. The prognosis is exceedingly unfavorable when there 
is great crippling of the joints accompanied by an extensive cachectic con- 
dition. Concerning the doctrine of antagonisms, it has been proved that 
gout does not exclude cancerous or phthisical developments. 

Treatment. — The treatment of gout will be considered under four heads : 
(1) General hygiene ; (2) Dietetics ; (3) External, and (4) Internal treat- 
ment. 

I. Gouty subjects should take systematic exercise in the open air, espe- 
cially horseback-riding. A country residence is to be preferred to the city ; 
and a warm, dry climate at a moderately high elevation is preferable to a 
severely cold one. They should always be clad warmly in flannel, and 
should avoid sudden and violent physical exertion, severe mental strain, and 
all unnecessary exposure to vicissitudes of temperature. They should retire 
and rise early, sleeping in a large, well-ventilated apartment without drafts. 

II. Dietetics. — Simple, nutritious food should be taken at stated inter- 
vals and in small quantities. Starving will not cure gout. As vegetables 
may be taken more freely than animal food, all pastry, eggs, tea and 
coffee, and alcohol should be avoided, and great care should be taken not 
to overload the stomach. Game and highly seasoned food, cheese, dried 
meats, tomatoes, and strawberries are to be avoided. Vegetables that con- 
tain the least starch, such as cabbage and the salads, are to be preferred. 
The principal articles of diet should be beef, mutton, and chicken, bread, 
milk, and fruits. Some patients, however, bear albuminoids badly, and 
find relief from their rheumatic symptoms on a farinaceous diet. Alkaline 
mineral waters, seltzer, vichy, lithia, etc., may be taken with and after 
meals. When stimulants must be given on account of the enfeebled diges- 
tion, light wines, whiskey, or gin will be found least objectionable. 

58 



914 



CHROMIC GENERAL DISEASES. 



III. External Treatment. — The affected limbs should be kept raised above 
the level of the body during an acute attack, and wrapped in flannel or 
cotton batting. Cold applications and leeches to the affected joints do 
harm. When the pain is intense opium may be applied to the joint, or 
morphine may be injected near it. Tepid alkaline washes and horse-chest- 
nut oil are strongly advocated by many. 1 Vapor and Turkish baths are 
often of the greatest service and should be taken weekly during the inter- 
vals between the paroxysms. 

IV. Internal Treatment. — Colchicum and the alkalies are our chief 
remedies during the paroxysm. For thirteen centuries colchicum has 
been used in this disease ; it relieves the symptoms, but how we do not 
know. Its efficacy has been attributed at various times to the elimination 
of uric acid, its sedative action on the circulation, its purgative and nar- 
cotic powers. My rule is to give one of the following pills 2 every three 
hours until the specific purgative action of the colchicum is obtained ; or 
five drops of the fluid acet. ext.- of colchicum in alkaline water may be 
given every two hours. The maximum dose of the latter should be given 
at the end of the attack ; small doses only are admissible at the commence- 
ment. When marked cerebral, circulatory, or gastro-enteric phenomena 
occur, colchicum is to be discontinued. Carbonate of potash, Kochelle 
salts, and the urate or citrate of lithia, are important adjuvants to the 
colchicum treatment. 3 Chloral, sulfonal, opium, and hyoscyamus may be 
given during the acute attack, to relieve the pain and restlessness of the 
patient. Common ash leaves, cinchona and gentian, the sulphate of qui- 
nine, and the iodide of potassium with tr. guaiac. ammo, have been exten- 
sively used in the treatment of gout, not only during the paroxysm, but during 
the interval. The benefit derived by gouty patients at the different springs 
which are so highly recommended seem to me to be due to the change of 
air and scene and to the dietetic restrictions more than to the bathing. A 
restricted diet, exercise in the open air, and a Turkish bath once or twice 
a week have succeeded with me as well as a residence at some spring. 

In chronic gout, tonics (iron, arsenic, etc.) are usually demanded. The 
inhalation of oxygen has been advocated as a remedy for the impoverished 
blood condition. Chemically active remedies — ammonia phosphate and 
benzoic acid — have not proved as useful clinically as theoretically. It 
should be remarked that the excessive use of mineral waters is contra- 
indicated in those who are advanced in years, in individuals whose kid- 
neys no longer have the power of elimination, and in those with whom 
alkalies disagree on account of some peculiar idiosyncrasy. 

1 Charcot spe.iks highly of atropine and blisters as topical remedies. 



2 R Pulv. ipecac. gr. i. 

Ext. colchi. acet gr. i. 

Hydrarg. protochlor. (calomel) gr. i. 

Ext. aloes fl gr. i. 

Ext. nuc. vomic gr. 



3 Strieker caused the tophi to disappear by giving 1% grains of lithia carbonate and 3>£ grains of sooe 
bicarbonate in 16 ounces of carbonic acid water a day.— Virchouu's Archiv., vol. xxxv. 



LITHiEMIA. 



915 



LITH^EMIA. 

Lithaemia strictly implies an excess of uric acid in the blood — an excess 
which at a certain point becomes gout. The term is often employed, 
however, to cover a general diathesis in which disturbances in the retro- 
grade changes produce a persistent increase of uric acid without marked 
tendency to its accumulation, the renal excretion being proportionately 
increased. The condition being purely a functional one, it has of itself no 
morbid anatomy. Its pathology is also somewhat obscure, although it is 
now generally accepted that the primary defect is in the liver. It is impos- 
sible to make any exact distinction between this arrest of the retrograde 
elements at the uric acid stage and the excessive formation of both urea 
and uric acid in gout. The former, however, appears to be the condition 
present in cases of an inherited lithaemic diathesis, while the latter is devel- 
oped either by excess of consumption of nitrogenized element or lack of 
oxygenating power. The one is inherited and the other acquired. In the 
one the lithaemic condition and its consequences are present, despite the 
most careful dieting ; in the other they are avoided or removed by proper 
diet and exercise. For the lithaemic diathesis we must assume, therefore, an 
inability on the part of the cell to produce oxidation, even when the neces- 
sary elements are furnished. This diathesis is so closely connected w T ith the 
fibroid diathesis as to make it impossible to say in just what degree the arte- 
rial and other scleroses, so invariably present, are the result of the lithaemia. 

Whatever the etiological relation, arterial changes are the more frequent 
and serious accompaniments of the lithaemic state, even in those chronic 
forms which do not pass into distinct gout. Derangements of the gastro- 
intestinal functions, cutaneous eruptions, and innumerable evidences of 
nervous disturbance, as asthma, cardiac palpitation, neuralgias, headache, 
etc., are also present in all distinct cases. 

Etiology. — An inherited defect of constitution is the primary and prin- 
cipal cause in patients who have never been given to excesses in eating or 
drinking. The acquired form depends upon a decrease in the ratio between 
the amount of food consumed and available oxygen for its oxidation. This 
may be induced by excesses in eating and drinking, or by a sedentary life, 
causing deficient respiration. Indulgence in stimulants and narcotics, sex- 
ual excess, or any form of nervous strain, may so affect the vital functions 
through the nervous system as to develop a latent lithaemic diathesis, or to 
exaggerate to serious proportions a moderate lithaemic condition. 

Symptoms. — The primary disturbances in the lithaemic diathesis are with 
the gastro-intestinal tract, and include all the forms of acute and chronic 
indigestion. Acidity of the stomach with gaseous eructations are charac- 
teristic symptoms. The evidences of intestinal indigestion are less marked. 
The flatus, which such patients pass rather abundantly, even when there is 
neither diarrhoea nor constipation, gives evidence, by its odor, of the con- 
dition of the intestinal contents. Haemorrhoids are usually present. Diar- 
rhoea may alternate with constipation, but the bowels are often perfectly 
regular. The tongue is often free from coating, but the breath is quite 



916 



CHRONIC GENERAL DISEASES. 



constantly offensive. In extreme conditions the skin becomes dry and 
scaly, or even covered with a persistent eczematons eruption, the hair is 
dry and wiry, the nails brittle, and the perspiration strong and offensive. 
Irregular or weak cardiac action is one of the earliest evidences of the 
effects upon the nervous system. Palpitation is prominent, but appears to 
depend upon no fixed cause. Frequent after eating, it also appears with- 
out cause, while the patient is quiet or even in bed. It is equally perverse 
in its continuance and disappearance as in its advent, lasting sometimes 
five minutes, or, again, several hours. Such hearts are also often easily 
excited to a rapid but regular action by slight exertion. Respiration is 
not affected by these turns of cardiac palpitation. The other nervous 
symptoms include all forms of neuralgias, headache, nausea, dizziness, 
vertigo, somnolence when erect, and wakefulness when recumbent, with 
all the mental irritability, anxiety, and depression which can be crowded 
into a sane man. This melancholia appears to depend more upon the 
gastro-intestinal condition than the lithaemia, although it is not absent 
when digestion is apparently perfect. On physical examination the liver 
may be found congested and slightly enlarged. The urine is high-colored 
and contains an excess of uric acid in combination, and often an excess of 
urea and phosphates. Oxalate of lime crystals are frequently abundant. 
On listening to the heart early, little is learned ; but as the condition pro- 
gresses, evidences of increased arterial tension will be found long before 
the radial pulse gives any sign of arterial changes. 

These patients remain in thisconditionfor yearsat times, but sooner or later 
the arterial or renal changes become prominent, and they pass on to chronic 
gout, contracted kidney, or arterial fibrosis, with their attendant dangers. 

Treatment. — The indications for treatment are : first, a reduction of the 
nitrogenized elements of the food to a minimum ; second, the stimulation 
of oxygenation by a full supply of oxygen and an increase of the circu- 
lation ; third, an increase in hepatic function ; and, fourth, the removal of 
the excess of uric acid. It is generally stated that such patients should be 
put upon a meat diet, and all starches and fats withheld, because these lat- 
ter undergo fermentation in the stomach. When gastric digestion is slow 
or imperfect, the presence of both albuminoid and starchy foods will be 
followed by fermentation, when either class alone will be fully digested. 
The general rule, therefore, is to give to such patients only one class of 
foods. If albuminoids are best borne, let them be used alone, and vice 
versa. When gastric digestion is weak, the starches are better borne ; but 
when intestinal digestion is most at fault, the albuminoids are to be pre- 
ferred. Physiologically a diet free from flesh meat is to be advised, and clini- 
cally it will be found to be the better in the larger proportion of cases. 

Oxidation is best improved by regular but persistent exercise in the open 
air. When this is impossible, patients must come as near to it as possible. 
Muscular exercise is the best stimulant to nutritive changes in the tissues, 
but passive exercise, cold and salt baths, frictions, etc., are not to be neglected. 

As stimulants to hepatic activity, nitric or nitrohydrochloric acid is at 
times of value. Mercurials, podophyllin, and other cholagogues, may 
also be employed. Other medication is directed to the indigestion, and 



DIABETES MELLITUS. 



917 



has already been considered. This indication will have been largely ful- 
filled by the active exercise already advised. 

For the removal of the excess of nric acid in the blood no remedy has 
yet been suggested which excels the salts of lithia. The carbonate or 
citrate should be taken constantly in moderate amounts. They may be 
made palatable if given in cold carbonic water, or the lithia waters may 
be used. Large amounts of water not only dissolve the uric acid, but assist 
the kidneys in its removal, rendering it less irritating. 

DIABETES MELLITUS. 

The term diabetes mellitus is applied to a constitutional disorder arising 
from malassimilation, in which the first appreciable change is the presence 
of sugar in the blood. When the proportion of saccharine matter reaches 
three parts in one thousand, it appears in the urine, producing the symp- 
tom which has given the name to the disease. 1 It has at various times 
been regarded as a disease of the kidney, alimentary canal, liver, and 
nervous system, but its exact pathogeny has never been determined. 

Physiological experiments and clinical facts, however, tend to show that 
the abnormal condition may be the result of either of these pathological 
processes or of their united action : 

First. — Excessive activity in the glycogenic function of the liver or in 
the primary assimilative processes may so overload the blood with sugar as 
to cause it to appear in the urine. Whether this hyperactivity is the re- 
sult of active hyperemia simply, or arises from disturbed nervous supply 
is uncertain. The occasional appearance of diabetes following the use of 
stimulants, and its very general occurrence as a result of irritation of the 
vaso-motor areas in the floor of the fourth ventricle, would seem to indicate 
that hyperemia, either from local or central irritation, is an important 
factor, but what nervous influence is primarily at fault in producing this 
mysteriously perverted functional activity is undetermined. 

Second. — The secondary assimilation may fail to dispose of the sugar pro- 
duced, and the kidneys are again called upon to eliminate it from the 
blood. Until physiology can speak with more definiteness than to say that 
sugar is disposed of in the system "either by oxidation or, as seems more 
probable, in other ways," 2 it is useless to speculate as to what organ or 
functions are at fault in this form of diabetes. 

Morbid Anatomy. — The only characteristic lesion is the presence of sugar 
in the blood in varying proportions, up to nine or ten parts in a thousand, 
and secondarily in all the organs, secretions and excretions. It is most 
abundant in the urine. Glycogen, acetone and kreatin are generally pres- 
ent in the organs and fluids, and the blood contains more fat than nor- 
mally. The parenchymatous changes in the viscera are principally degen- 
erative, the result of the blood change. The liver is usually hypersemic, 
with possibly some fatty degeneration. The lungs are nearly always tuber- 
culous, with points of catarrhal pneumonia, or possibly of gangrene, at- 
tended by pleurisy. The heart is soft and flabby, and, like the other mus- 

1 Synonyms : Glycosuria, Glucosuria, Mellituria, GlycohEemia. 

2 Foster's Phys., 25 Am. Ed., 18S1, p. 537. 



918 



CHRONIC GENERAL DISEASES. 



cles, pale and dry. The spleen is hypercemic, kypertrophied and firm. 
Aside from hyperemia, the kidneys often present the usual changes of 
chronic parenchymatous nephritis (large white kidney), possibly the result 
of the excessive work thrown upon them. Softening, cirrhosis, and 
tumors may be present in the brain, and when they involve the fourth 
ventricle become of interest from an etiological standpoint. Emaciation 
becomes marked early, and in protracted cases may be extreme. The 
skin, which is harsh and dry, is generally the seat of furuncles, carbuncles, 
bed-sores, and gangrene. 

Etiology. — Diabetes is a disease of early adult life, and is met with more 
frequently in males than in females. In some cases it appears to be heredi- 
tary. It is a well-established fact that mechanical irritation of a certain area 
of the medulla — an area corresponding very closely with the vaso-motor 
area in the fourth ventricle — invariably produces glycosuria, and clinical 
facts prove with a great degree of certainty that diabetes is frequently the re- 
sult of lesions producing similar irritation. Such irritation may result from 
general shock or concussion, cerebral hemorrhage, softening, cirrhosis, ab- 
scess or tumors, also from excessive mental labor, shock, grief, and possibly 
from the excessive use of cerebral stimulants. Blows upon the epigastrium 
are included in its list of causes. Pregnancy, impaired digestion, and im- 
moderate use of sugar, new wine, and alcohol have also been named as causes. 

Symptoms. — Although diabetes may be acute, and result fatally within 
two or three weeks from the time the increased flow of urine is first noticed, 
it usually comes on insidiously. The patient notices that for some time he 
has been passing more urine than usual, and has been unusually thirsty. 
While his appetite has been good, and he has taken more food than he is ac- 
customed to, he is losing flesh and strength ; and there is an abnormal dry- 
ness of the mouth, throat and skin, with intolerable itching, followed by des- 
quamation. His sleep is disturbed by a frequent desire to empty the bladder. 

As the disease advances he becomes listless and debilitated, and there is 
decrease or abolition of sexual desire ; in women the menses are often sup- 
pressed. The tongue is red or coated, and nearly always thicker than nor- 
mal ; the gums are pale, retracted, and bleed easily, and the teeth become 
carious. There are nausea, vomiting, and well-marked dyspeptic symptoms, 
with constipation, and most patients complain of a constant sinking feeling 
at the epigastrium. In many instances the breath has a heavy, sweet odor, 
and the taste is perverted. Attacks of profuse diarrhoea, lasting for a 
day, occur in advanced cases, and may. precede an unexpected fatal issue. 
Headache, often amounting to intense hemicrania, is common. There is de- 
rangement of the special senses, especially of sight (soft cataract and amblyo- 
pia) ; dulness of mind, irritability and restlessness, melancholia and hypochon- 
dria. The temperature, pulse-rate, and respirations are below the normal. 

In some cases the classical course of the disease will be varied from ; there 
will be little thirst or loss of appetite and no emaciation ; the patient may 
even gain in flesh. 1 In diabetes from "over-production" the quantity of 



1 Frank describes a "diabetes decipiens" in which the amount of urine passed is not above the nor- 
mal while a large amount of sugar is present. Quincke relates some very interesting cases of diabetes 
where delirium, stupor and coma have appeared before death.— Berlin. Klin. Woch. No. 1, 18S0. 



DIABETES MELLITUS. 



919 



nrine passed is greater than in the other form, the skin affections are more 
severe and frequent, the patient does not emaciate, but loss of sexual desire 
comes earlier. In the variety due to defective assimilation, the emaciation, 
anaemia, loss of strength and flesh, and palpitation, vertigo, and dyspnoea are 
early and marked signs, while the nervous phenomena are not prominent. 

The Urine. — Yery rarely the amount of urine passed is but little increased; 
generally, however, it very rapidly rises to twenty, thirty, fifty or more pints 
in twenty-four hours. The calls to urinate become very frequent both by 
day and night, and the genitals are inflamed and excoriated. The urine is 
acid, of a light straw color, with possibly a faint green tint, clear, without 
sediment, and of a slightly aromatic odor and a sweet taste. The specific 
gravity varies from 1.030 to 1.070 with an average of 1.040, and the propor- 
tion of sugar from a trace to 50 to 100 or more parts in a thousand. In 
rare cases, a low specific gravity of 1.008 or 1.010 is recorded, but a specific 
gravity of 1.030, when the quantity of urine passed is normal or increased, 
should always lead to an examination for sugar. Urea is always present in 
increased amount, and uric and hippuric acid, kreatinin, sulphuric and 
phosphoric acids, acetone, alcohol, and albumen are frequently found. In 
certain cases where the patient continues to fail, although the quantity of 
sugar lessens, inosite appears in the urine, and continues to increase as the 
sugar lessens. It may amount to two or three hundred grains in twenty- 
four hours. 

In those cases where sugar and the starchy element of the food are the 
sole sources of the diabetic sugar, diet may reduce the quantity and specific 
gravity of the urine to the normal and remove all traces of sugar from the 
urine and blood. In other and more advanced cases animal food is also 
converted into sugar, and in such conditions dieting can only modify the 
urinary symptoms. In a third class of cases the tissues of the body also 
contribute to its formation, and the quantity of sugar eliminated is but little, 
if at all, affected even by starvation. 1 Urea is excreted in abnormally large 
quantities by diabetic patients ; some claim that there is increased decompo- 

1 The following are the best tests to determine the presence of sugar in the urine :— 

Trommer's Test. — To the suspected liquid add a few drops of a slightly alkaline solution of tartrate of 
copper. Boil. Sugar precipitates copper as a yellowish red oxide. 

Fehling's Test is founded on the fact that glucose has the property of precipitating the red cupreous 
oxide from an alkaline solution of sulphate of copper. 

Dissolve 36.64 grammes cupric sulphate in 200 c. c. distilled water ; dissolve 80 grm. sodium hydrate 
in 600 c. c. water, and add 173 grm. Rochelle salts. Mix the two solutions and add' water to make one 
litre. Keep in small, carefully sealed bottles. The copper in one c. c. is entirely precipitated by 5 milli- 
grammes of grape sugar. 

Pour 5 c. c. of the above test-solution into a test tube and heat to boiling ; add the suspected urine, 
guttatim : If grape sugar is present the blue changes to green and the red oxide of copper is precipitated. 
When the blue is discharged the copper is precipitated. — Draper. 

Warren's Test.— In a test tube containing three drams of urine add two drops of a solution of sul- 
phate of copper and one-half as much liq. potass, as the amount of urine ; boil, and if the urine con- 
tains sugar, the red sub-oxide of copper will be thrown down. 

Jfaumene' s Test consists in heating saccharine urine in the presence of bichloride of tin, which 
causes it to throw down a black-brown " caramel " looking deposit. 

Moore's Test consists in boiling liquor potassse with the suspected urine : if sugar is present a bistre 
brown appears. 

The Fermentation Test consists in putting German yeast in a test, tube filled with the nrine, and standing 
it inverted, in a warm place : alcohol and carbonic acid are formed and the bubbles of the latter, tested 
With lime water, give evidence of its character. Non-saccharine urine does not fermenl. 

Twvla form during the fermentation as a scum, and, microscopically, are easily recognizable. 



920 



CHRONIC GENERAL DISEASES. 



sition of albumen into urea and sugar. Albumen does not necessarily indi- 
cate that there are grave kidney changes in diabetic subjects. The amount 
of urine passed in twenty-four hours varies from fifty to one hundred pints. 

The large amount of urine secreted distends the bladder ; and the large 
amount passed, and its saccharinity, cause a constant itching, burning and 
uneasy sensation at the prepuce, along the urethra, and at the neck of the 
bladder ; in females, it may cause redness, irritation, excoriation, or an 
eczematous condition of the vulva. Incontinence of urine is especially fre- 
quent in diabetic children. 

Differential Diagnosis. — Diabetes mellitus may be mistaken for glycosuria, 
for the atrophic form of Bright' 's kidney, and for diabetes insipidus or 
polyuria. 

Diabetes occurs at all ages, and often from undiscoverable causes ; simple 
glycosuria is very common in the aged, in the insane, in fits of ague, 
after sudden excitement, blows on the head, the taking of chloral, etc. In 
diabetes mellitus the amount of sugar seldom varies much from day to 
day; while in non-diabetic glycosuria it varies greatly. 1 Polyuria, poly- 
phagia, and polydipsia are marked symptoms in diabetic glycosuria. The 
symptoms referable to the nervous system and skin are prominent in dia- 
betes mellitus ; they are absent in simple glycosuria. Volumetric analysis 
by Fehling's method is easy in diabetes mellitus ; while in simple gly- 
cosuria it gives obscure results, owing to the presence of kreatinin. 

Diabetes mellitus is at once distinguished from Bright's disease or dia- 
betes insipidus by the presence of sugar in the urine, a condition which 
does not occur in either of the other diseases. 

Prognosis. — Although diabetes is a progressive disease, it has no regular 
course, and the prognosis depends very largely upon the form which the 
disease assumes. In that class of cases where diet reduces the amount of 
sugar, or possibly at first removes it entirely from the urine, the fatal ter- 
mination may be long delayed, but those cases which appear to depend 
upon faulty assimilation are more rapidly fatal. Between these extremes 
the disease may last from a few weeks to ten or twelve years. Pulmonary 
tuberculosis (twenty-five to thirty per cent.) and uraemia (ten to twenty 
per cent.) are the most frequent causes of death. Asthenic inflammation 
with suppuration is frequent in all the tissues, and boils in successive crops, 
and carbuncles., are frequent complications which influence the prognosis. 
Pulmonary gangrene may occur with an odorless breath. Cataract, am- 
blyopia, retinitis, and retinal hemorrhage are often present even in cases 
not attended by albuminuria. 

The prognosis is more unfavorable the younger the subject, the less 
amenable to treatment the case proves to be, and the severer the gastro- 
intestinal symptoms. It is always bad in those who emaciate rapidly. 
Death may occur from marasmus, gangrene, dysentery, anaemia, or not 
infrequently in diabetic coma. 

Treatment. — In spite of the fact that there are no " specifics " for dia- 
betes, the greater number of cases can for a time be brought under control; 
and to this end dieting is of first importance. 



1 Gerin Rozes. 



DIABETES 3IELLITTIS. 



921 



All saccharine form of food, or any article that can be converted into 
sugar, should be withheld. Hence, starchy foods, bread, arrow-root, tapi- 
oca, sago — such vegetables as potatoes, parsnips, turnips, carrots, beans, 
and peas are to be absolutely avoided or partaken of sparingly. Salads, 
greens, acid fruits, all kinds of flesh and fowl, eggs, cheese and butter, 
unsweetened tea and coffee can be taken. Alcohol in any form is harmful, 
but should exhaustion demand stimulation a light sherry or claret may be 
permitted. 1 Koumyss is sometimes given as a substitute for mild stimu- 
lants. To allay the intense thirst acidulated drinks, cracked ice, or alka- 
line waters may be used in as moderate quantities as possible ; while water 
increases the amount of sugar passed, it is not certain that it increases the 
amount formed, and the patient should use water in moderation rather 
than attempt distressing self-denial. A meat diet is therefore to be en- 
joined. 

In the above bill of fare the patient will not find much that is unpleasant 
or distasteful, except deprivation of bread. Gluten breads, bran cakes, and 
biscuits and buns made from almond flour have been devised as substitutes 
Some patients cannot eat bread thus made, and in such cases, if bread 
must be taken, it should be well toasted. Moderate exercise must always 
be advised, and the skin should be kept thoroughly active by means of 
baths ; in the feeble, warm baths, and in the more robust, sea or cold baths. 
But as pulmonary complications are so common, the body must always 
be warmly clothed. The success of dietetic measures depends upon the 
patients rigidly following them. 

The drugs which exert a most beneficial influence are the extract of 
opium, morphia, and codeia. They must be used sparingly, and usually 
only when the meat diet is given up for a time. Small doses should always 
be administered at first. When arthritic muscular and neuralgic pains 
are severe, narcotics are especially beneficial. Cures are reported by high 
and trustworthy authorities from their use. 

On theoretic grounds, lactic acid has been proposed as a substitute for 
sugar. It has been given until arthritic (rheumatic) symptoms have appeared. 2 
Alkalies, bicarbonates, acetates, and citrates are highly recommended. 
And since they are always most beneficial in the form of natural thermal 
mineral waters at the springs, half their benefit may be ascribed to change 
of air, mode of life, and the surroundings that attend a visit to watering 
places. Carbolic acid and creosote have been used as antiseptics, and 
salicylic acid has been proposed as an anti-fermentative ; sulphide of calcium 
is of benefit where there is much suppuration (e. g., boils, carbuncles, etc.). 
Ergot and jaborandi have apparently been beneficial in some cases ; the 
constant galvanic current has been productive of good results. The 
anaemia which attends it demands iron, cod-liver oil, strychnia, quinine 

iDonkin recommends the continuous administration of skimmed milk, three or four quarts a day; 
when the patients are able to pursue this plan it is followed by good results. 

2 Two Neopolitan professors, Primavera and Caucani, claim that a meat diet with 3 ij-iv of lactic acid 
and I ss. of alcohol in 12 oz. of water at a meal, will furnish no materials for the formation of sugar, 
yet will be a substitute for the saccharine and farinaceous elements of the food. 



922 CHROKIC GENERAL DISEASES. 

and a change of air and scene. Surgical operations should on no account 
be undertaken on diabetic patients. 

DIABETES INSIPIDUS. 

Diabetes insipidus, or polyuria, is characterized by extreme thirst and 
the secretion of a large quantity of colorless urine, of low specific gravity, 
free from sugar and albumen. It is also called hyperuresis or polydipsia, 
the latter term having reference solely to the intense thirst which attends 
it. 

Morbid Anatomy. — Polyuria has been produced both by mechanical and 
pathological lesions of the brain just above the floor of the fourth ventricle. 
Disease of the pineal gland, and cerebral disease extending into the medulla 
have also been found associated with it. 1 

Etiology. — Diabetes insipidus may occur at any age and in either sex. 
Some consider its immediate cause to be a dilatation of the capillary vessels 
of the kidney, which has its origin in a disturbance of the sympathetic 
ganglia. Blows on the head, injuries to the medulla or region of the fourth 
ventricle, injuries to the spinal cord, violent emotions, have all apparently 
caused its development. Drinking large quantities of ice-water when 
overheated, and exposure to cold and wet are among its supposed causes. 
Diabetes insipidus temporarily disappears during the course of acute febrile 
disease. 

Symptoms. — This affection may come on insidiously or suddenly. Its 
chief symptom is the passage of a large quantity of limpid urine ; the quan- 
tity varies from thirty to sixty pints per diem. Its specific gravity ranges 
from 1.003 to 1.008 ; it is remarkably clear, faintly acid, and of a greenish 
opalescent hue. Urea, uric acid and kreatin are secreted in larger quanti- 
ties than normal. It contains no sugar or other abnormal ingredients. 
Intense thirst accompanies this increased flow of urine ; so great is it that 
patients who have had all fluid withheld from them have drunk with avidity 
their own urine. The quantity of urine equals the amount of fluid taken. 
The skin becomes harsh and dry ; and the temperature becomes subnormal. 
The appetite, gastric and intestinal symptoms are all very variable. A 
strong corroborative proof of its nervous origin is the occasional increased 
salivation that is clearly due to nerve influence. 2 The other symptoms 
which attend this disease are variable. In some cases the patients are well 
in all other respects : in others there is vomiting, rapid emaciation, and the 
general signs of acute phthisis. 

Differential Diagnosis. — A careful examination of the urine for one month 
will distinguish this condition from all other diseased conditions which are 
attended by the secretion of abnormally large quantities of urine. 

Prognosis. — Eecovery from diabetes insipidus is rare, although it may last 
many years without any disturbance of the general health. Pleurisy and 
acute rheumatism occurring during its course have been followed by com- 



1 Dickenson found degenerative changes in the solar plexus. The blood is said to contain an abnormally 
large amount of solid constituents. 

2 See discussion of " submaxillary gland and chorda tympani nerve" in Foster's Physiology. 



ANEMIA. 



923 



plete recovery. 1 In most instances death is caused by intercurrent dis- 
ease. 

Treatment. — When a cause can be reached, it should be removed. At all 
times the body should be warmly clothed, and the skin kept active. The 
food should be highly nutritious and easily digestible. Great attention must 
be paid to the surroundings and general hygiene of the patient. Narcotics 
have been advocated, but they are not so efficacious as in diabetes mellitus. 2 
Nitrate of potash, iron, alum, lime-water, tannic and gallic acid, creosote, 
bromide of potassium, acetate of lead, jaborandi and belladonna have ail 
been recommended, either for narcotic, astringent or vaso-motorial action ; 
the chief idea in all being to constringe the renal capillaries. The constant 
galvanic current passed between the loins and epigastrium is advocated, and 
deserves more extensive trial. 3 

ANAEMIA. 

Simple anaemia is a condition in which the number of the red corpuscles 
is markedly diminished ; when local it is called ischaemia. If the Wood- 
mass is diminished it is called oligamiia. Spaimmia and hydroemia are 
synonyms of anaemia. 

Morbid Anatomy. — The density of the blood is diminished. There is 
diminution in the number and size, and change in the form and color of the 
red blood discs ; one hundred corpuscles may occupy no more space than is 
normally taken by seventy-five, and the number may fall below one-half 
the normal. Besides quantitative there are qualitative changes in the 
blood ; the amount of haemoglobin in the red discs may be diminished 
twenty-five per cent. When corpuscular abnormalities are due to imper- 
fect development and formation, the condition is called ancematosis ; — 
but when they have been perfect and have subsequently degenerated, the 
name licemophthisis is applied. 

The heart in one who has died in a state of extreme anaemia is flabby 
and pale ; the blood is of a lighter color than normal and more fluid ; if 
coagula exist they are pale and crumbly. There may be a diminution 
in the fibrinogen and fibrinoplastin. There is usually a small amount of 
fluid in the serous cavities. Ecchymoses are common ; and minute hemor- 
rhages may be found at various points. 

Etiology. — Simple anaemia may be caused by anything that decreases the 
number of red corpuscles or that interferes with their production. 

Acute anaemia is the result of sudden and excessive loss of blood ; fe- 
brile anaemia is acute. 

Chronic anaemia may be the result of numerous small bleedings, or of 
exhausting discharges other than blood, which attend many forms of 
chronic diseases. It is a constant accompaniment of many forms of chronic 
visceral diseases, of which Bright's disease is the best example. Chronic 
blood poisons cause what is called toxic anaemia. Interference with nutri- 

1 Dickenson and Desgranges. 

2 Rayer and Trousseau strongly advocate valerian ; and Sidney Ringer regards ergot and ergotin as effi- 
cacious. 

8 Laycock ; The London Lancet, vol. ii., No. 7, 1875. 



924 



CHROMIC GENERAL DISEASES. 



tion, from insufficient or improper quality of food, anti-hygienic sur- 
roundings, etc., are prolific causes of simple anaemia. Women are more 
liable to anaemia than men ; and the condition is much more frequent at 
the two extremes of life, than during the period between twenty and sixty. 
A tendency to an anaemic condition is not infrequently congenital. Struct- 
ural changes in the cytogenic tissues, and disease of the lymphatics, induce 
anaemia. Malignant growths and chronic tuberculosis are attended by con- 
ditions of extreme anaemia. 

Symptoms. — The symptoms of acute anaemia — such as results from pro- 
fuse hemorrhages — are extreme pallor, pinched features, and cold sweats ; the 
pulse is feeble, rapid, is quickly accelerated by slight mental excitement or 
physical exertion ; a blowing cardiac murmur and even a " bruit de diable" 
is present in severe cases. A condition of syncope is of frequent occur- 
rence. Vomiting, delirium, tinnitus aurium, and other nervous phenomena 
are common. The thirst is intense, and the urinary secretion is scanty. 

In chronic ancemia there is a pale, waxy, or sallow hue of the skin, and 
a pale, bloodless condition of the mucous surfaces. The skin becomes cede- 
matous and the muscles flabby. The hands and feet are always cold. A 
cachectic or marasmic condition is developed ; the skin becomes harsh, and 
often desquamates in patches. As a result of long-continued anaemia a 
hemorrhagic diathesis may be established. The urine is pale, contains 
less urea and less pigment than normal. Dropsies are liable to occur when 
anaemia has persisted for a long time. The temperature is frequently sub- 
normal. Extreme exhaustion and muscular feebleness are among its ear- 
liest and most prominent signs. Anaemic patients are irritable, excitable, 
usually hyperaesthetic and suffer from neuralgias. Anaemic females com- 
plain of a pain in the left side and a burning sensation on the top of the 
head. ' They are often hysterical. Temporary aphasia may result from 
anaemia. Anorexia and atonic dyspepsia result from deficiency either in 
quantity or quality of the gastric juice. A morbid, craving appetite some- 
times exists. 

The constant and important signs of anaemia are haemic murmurs, which 
may be cardiac, arterial, or venous. The cardiac murmurs are systolic 
in rhythm, blowing or bellows-like in character, and have their point of 
maximum intensity at the base of the heart. Arterial murmurs are heard 
over the large arteries, and they may be accompanied by a thrill percepti- 
ble in the radial vessels. Over the jugulars, particularly the right, there 
is heard a continuous venous hum. A deep inspiration intensifies, while 
coughing diminishes the intensity of t 7 ie venous hum. It is also dimin- 
ished by the horizontal posture. It may sometimes be felt as a thrill on pal- 
pation. The heart's impulse is always feeble ; the heart sounds are muf- 
fled, and the radial pulse is compressible and small. Severe attacks of 
cardiac palpitation are common. 

Differential Diagnosis. — Acute anaemia from either internal or external 
hemorrhage is not likely to be confounded with any other condition. The 
diagnosis of chronic anaemia is readily made from the history and general 
appearance of the patient, and by the presence of haemic anaemic murmurs. 



CHLOKOSIS. 



925 



Prognosis.— The prognosis in anaemia is determined by the conditions un- 
der which it occurs. The earlier its cause is discovered, and the more readily 
removed, the better the prognosis. Its duration varies from days to years ; 
some individuals, especially women, are anaemic during their entire lives. 
When it is associated with, or dependent upon, organic disease, the prog- 
nosis is unfavorable. Death, in acute cases, results from annulling the 
function of the medulla, or cardiac paralysis; in chronic cases, inanition and 
exhaustion, or some complication, induce the fatal issue. Death may 
occur in syncope, convulsions and coma. 

Treatment. — The treatment of anaemia is always restorative, and must be 
especially directed to improving the blood-making power. Acute anaemia, 
the result of profuse hemorrhage from wounds, accidents, during labor, 
etc., must be treated surgically rather than medicinally. The preventive 
treatment of chronic anaemia when it depends upon exhausting discharges, 
prolonged lactation, and anti-hygienic conditions, is the removal of its 
causes. The diet should be most nutritious, embracing a large proportion 
of nitrogenous elements. If the digestive organs are feeble, food must be 
taken in small quantities and at short intervals. Alcohol is food to anaemic 
patients. Burgundy, Madeira, and rich wines are to be preferred ; but in 
anaemic females the malt liquors are often more beneficial. Daily exercise 
in the open air and exposure to the direct rays of the sun are essential, and 
should be taken regularly without producing excessive fatigue. The clothing 
should be carefully regulated ; in winter warm flannels should always be 
worn, and in the spring and fall great care should be exercised not to allow 
the surface to become chilled. 

Iron is the one drug that best combats anaemia. There are many prep- 
arations, but the chloride, Vallet's mass, Blaud's pills, and, in children, 
reduced iron or the citrate are the forms that have given me the best re- 
sults ; it should be given after meals. The combination of iron with quinia, 
strychnia and phosphorus or arsenic is efficacious in many cases when iron 
alone fails to improve. Emulsions of cod-liver oil are valuable adjuvants 
when they can be borne by the stomach. It should not be given after it 
produces headache or dyspeptic symptoms. 1 Eecently I have found malt 
extracts combined with iron, pepsin and pancreatic preparations efficacious 
when there is deficiency of stomach digestion. The operation for trans- 
fusion of blood or milk in extensive anaemia has never proved successful in 
my experience, although there is good authority for resorting to it. If the 
bowels have a tendency to constipation, aloes should be given with vegetable 
tonics. Travel and a change of climate, often act beneficially when all 
other means have failed. 

CHLOEOSIS. 

Chlorosis is a special form of anaemia, which occurs almost exclusively in 
young females about the age of puberty, without any assignable cause. 



1 Goodhart. Fothergill, and others maintain that ansemia predisposes to cardiac dilatation, and hence 
propose that digitalis should be combined with iron, 



926 



CHRONIC GENERAL DISEASES. 



Morbid Anatomy. — The body is well nourished, the organs are abnormally 
pale, the serous cavities contain fluid, and there is more or less oedema of 
the lower extremities, the red blood corpuscles are diminished in number, 
and the haemoglobin is less in amount than normal. The amount of albu- 
men in the blood-serum is often increased and the mass of the blood is 
increased. 

Virchow states that a constant and characteristic lesion of chlorosis is 
imperfect development of the vascular system. The aorta and arteries are 
generally smaller in chlorosis than normal, and thin walled ; the aorta, 
throughout its entire extent, may only reach the normal size of the caro- 
tids. Fatty degeneration of the tunica intima is very common, and this 
coat may exhibit spots of superficial erosion. The intima exhibits fatty 
change in little spots or streaks, not in large connected masses. The mid- 
dle coat is seldom involved. The heart cavities are usually somewhat 
dilated, and hypertrophy of their walls is not infrequent. Spots of extrava- 
sation and ecchymoses may be found on the mucous surfaces and in the 
serous cavities. The ovaries and uterus are usually abnormally small. 

Etiology. — Chlorosis is regarded by some as a neurosis, the blood changes 
being secondary to the neurosis. The unaltered state of the cytogenic or- 
gans — spleen, lymph glands, and osseous marrow — shows that it is not, 
strictly speaking, a disease of the haematopdetic system. 1 There is always 
more or less anaemia, and there is nearly always some functional derange- 
ment of the sexual organs. All of these causes, however, are not sufficient 
to account for its development in the majority of cases. In very many in- 
stances its cause cannot be reached. It is met with most frequently in 
young girls. 2 There is a form called amenorrhoeal, and another menor- 
rhagic chlorosis. Self-pollution is claimed as an exciting cause of chlorosis. 

Symptoms. — With or without derangement of the menstrual function, 
chlorosis comes on insidiously in precisely the same manner as simple 
anaemia, with which, in its early stage it is so readily confounded. As it 
develops, the mental condition changes, the individual becoming morose or 
despondent. The countenance assumes a peculiar waxy, yellow, or yellow- 
green pallor. The face is puffy, the eyes are surrounded by deep, blackish 
circles, the sclerotic is pearly, and the mucous membranes are pale al- 
most to the verge of bloodlessness. The puffy look of the face is soon 
shared by the rest of the body ; but it is not ©edematous. 3 Sometimes the 
cheek will retain a slight degree of color ; and on excitement, mental or 
physical, the face is suffused. 

In some cases the onset is sudden, and the above-named signs appear soon 
after some menstrual derangement. In all cases lassitude, muscular weak- 
ness, dyspnoea, and fits of cardiac palpitation are common. Muscular pains 
follow violent physical exercise. The appetite is capricious ; the patient 

1 Virchow regards the predisposition to it as dependent upon congenital abnormalities of the heart or 
aorta. Immermann regards chlorosis as due (in part) to functional derangement of the cytogenic organs. 

2 Niemeyer says that "obstinate chlorosis attacks all young girls, without exception, in whom the 1 
menses have appeared in the twelfth or thirteenth year, and before the development of the breast and 
pubes." 

3 Immermann states that a tendency to obesity exists in chlorosis 



CHLOROSIS. 



927 



will crave the most indigestible substances, and will eat with avidity chalk, 
slate pencils, ashes, dirt, or strongly acid and spiced food. Sometimes 
there is anorexia, sometimes bulimia. Cardialgia is a common symptom ; 
it is accompanied by a sense of weight over the stomach and by belching 
large quantities of inodorous gas. It is to be remembered that gastric ulcer 
is frequently met with in chlorotic females. Ohlorotic girls are usually 
melancholy, abstracted and irritable. In some cases they have attacks 
of nervousness, so that the term chlorotic hysteria is used to denote a 
hysteroid attack in young females. The sexual desires are diminished 
rather than increased. The rapid breathing, dyspnoea, and palpitation are 
undoubtedly in most cases purely nervous. Dyspnoea is often a very promi- 
nent symptom and is accompanied by a short, dry cough ; the respiratory 
murmur is feeble, and a full inspiration causes a fit of coughing, which 
may lead to the suspicion of phthisis. There is rarely fever ; when fever 
occurs there is something more than chlorosis. Often late in the disease, 
oedema of the feet and ankles occurs. 

The urine is pale and Watery. The specific gravity is below normal. Urea 
and coloring matter are deficient in quantity. Leucorrhoea, and amenor- 
rhoea or menorrhagia are common attendants of chlorosis. The heart is 
feeble and excitable. A systolic haemic murmur is present which is heard 
in the carotids as in anaemia, but the venous hum in the neck, though not 
infrequent, is still not so common as in anaemia. 

Differential Diagnosis. — Chlorosis may be mistaken for progressive perni- 
cious ancemia, for simple anmmia, Bright' s and cardiac disease. 

In anmmia emaciation is marked ; in chlorosis there is no loss of flesh. 
The peculiar greenish color and the mental state are important points in its 
differental diagnosis. The age, sex, and presence of uterine complications 
are all important in distinguishing chlorosis from anaemia. 

An examination of the urine in the one case and a physical exploration 
of the chest in the other, will soon decide as to the existence of Tcidney or 
cardiac disease. 

Prognosis. — The course of chlorosis is influenced by the hygienic and social 
surroundings of the patient, and by the treatment employed. It is not a 
self-limiting disease, and shows no tendency to spontaneous cure. Its dura- 
tion is very uncertain. As a rule the prognosis is unfavorable, on account 
of the liability to serious complications, as phthisis, valvular endocarditis, 
ulcer of the stomach and thrombotic formations. Rheumatism, septicaemia, 
typhoid fever, and pneumonia are nearly always of a malignant type and 
fatal in one who is chlorotic. Hysteria, chorea, paralysis, and epilepsy 
sometimes complicate, and sometimes are sequelae of chlorosis. 1 It is to be 
remembered, in giving a prognosis, that relapses are common after intervals 
of seeming health. 

Treatment. — When a cause can be reached, such as self-abuse, masturba- 
tion, or disease c n the functions of the uterus or its appendages, the removal 
of such cause will be the first step in the treatment. Chlorotic patients 
should have an out-of-door life with cheerful companions and surroundings ; 



1 Friedreich and others state that Basedow's Disease is unmistakably connected with chlorosis. 



928 



CHKOinC GENERAL DISEASES. 



they should eat regularly of a diet of which meat and vegetables form the 
chief part. Late hours and bad air and gaslight should not be allowed. 
Mental is as important as physical hygiene. The patient should not be idle; 
something pleasant must always occupy the mind. I have found that iron 
does not act as well here as in anaemia ; indeed, in many instances it is not 
well borne. 1 When there is a tendency to fulness about the head it does 
harm ; some authorities state that only small quantities of iron are absorbed 
by this class of patients, others say that large doses are of much more service 
than small. 

Arsenic I regard as the most valuable medicinal agent, either alone or 
combined with iron. Constipation is to be overcome by the careful but 
persistent use of small doses of aloes and nux vomica. Quinine, calumba 
and quassia may be given alone, or in combination with ferric preparations. 
Zinc and the mineral acids will often prove valuable adjuvants to the 
iron plan of treatment. In cases of long standing the rest treatment com- 
bined with massage are followed by good results when all other means 
have failed. 

PROGKESSIVE PERNICIOUS ANiEMIA. 

This form of anaemia has received many names ; 2 but progressive perni- 
cious anaemia is the term now most generally accepted. 3 It may be de- 
fined as that form of anaemia which occurs without discoverable cause, re- 
sists all treatment, and steadily progresses, with greater or less rapidity, to 
a fatal termination. The degree of oligocythaemia is greater than in 
simple anaemia. 

Morbid Anatomy. — The Mood is scanty and pale with a specific gravity in 
some cases as low as 1.030, and shows but slight tendency to coagulate. 
The number of red corpuscles is greatly diminished and their size and out- 
line are altered. There is no increase in the white corpuscles, but they 
seem to be in excess, solely from the great loss in the red. It is stated 
that the amount of haemoglobin in each red disc is diminished ; and that 
the white globules contain traces of it. Myelogenic pseudo-leukaemia was 
the name proposed by those who found that in this disease the adult mar- 
row became foetal, red and adenoid. 4 But the change in the medullary 
structure of the bones is a secondary, not a primary change. Large nucle- 
ated embryonic corpuscles, lymphoma, and multiple sarcomatous growths 
have been found in the marrow. 5 Secondary to the anaemia the heart un- 
dergoes circumscribed or diffuse fatty degeneration. When this is partial 
the papillary muscles and inner part of the heart seem to suffer most. In 

1 Immermann and Niemeyer both regard all else as subservient to iron. The former says a couple of 
boxes of iron pills do more good than anything else. They both regard iron as of more benefit than in 
any other (allied) malady. 

a Addison called it idiopathic anaemia ; Lebert, essential anaamia and puerperal chlorosis ; and Ponfick 
the ancemia of fatty heart. Amematosis and pseudo-leucocythemia, have also been proposed for it. 

3 Andral, Wilks and Wagner describe it under other names. 

4 Cohnheim, Gardner, Litten, Fede, Pepper and Eichhorst all found the bone-changes prominentia 
this disease ; and the last named found microcytes in the marrow. 

8 See a case described clinically by Ehrlich, and pathologically by Growitz, in Charite-Annalen, 1880 
Berlin. 



PROGRESSIVE PERNICIOUS ANEMIA. 



929 



many cases there is more or less dilatation, bnfc no change occurs in the 
valvular apparatus. The inner coat of the larger arteries and certain 
capillary tracts also exhibits fatty degeneration. 

The liver, spleen, kidney and stomach are anasmic, — even Woodless in 
severe cases — and their epithelial elements present similar fatty changes. 
In the kidney multiple sarcomatous formations have been found. 1 The 
liver and spleen may be enlarged ; although some observers maintain that 
anaemia attended by splenic enlargement, disease or swelling of the lym- 
phatics, or any change in the medulla of the bones is to be excluded from 
the class called progressive pernicious ancemia. The body is commonly 
covered with small — rarely large — spots of ecchymosis, and internal hem- 
orrhages are not uncommon. 

Retinal hemorrhage, demonstrable during life, is so common as to have 
been regarded as affording, when taken in connection with the symptoms 
of anaemia, almost positive proof of its pernicious character. These hemor- 
rhages are due to fatty degeneration of capillary aneurisms. The serous 
sacs of the body contain more or less blood-stained fluid, and may also 
exhibit ecchymotic spots. There is not much emaciation, though the 
skin, membranes, and internal viscera are much paler than in simple anae- 
mia ; and rigor mortis is late and slight. 2 

Etiology. — The essential nature of progressive pernicious anaemia is un- 
known. It has been suggested that at times an endemic and specific cause 
may be at work, since the disease has been found to occur with compara- 
tive frequency in certain localities. 3 Women surfer more than men, and 
are liable to it especially during pregnancy. 4 The period between twenty 
and forty is the age when most cases occur ; the disease being rarely seen 
in early youth or extreme age. When no cause can be found for extreme 
anaemia, and when no treatment retards its progress, the case is probably one 
of progressive pernicious ancemia. 

Symptoms. — It comes on insidiously. Whether the patient has been ill 
or in perfect health, the course is the same, and it begins with a sense of 
languor, which increases from day to day. The skin and mucous membranes 
become very pale and assume a dusky yellow color quite distinct from the 
green of chlorosis. The muscles are soft and relaxed, and muscular weakness 
may be so extreme as to force the patient to take to his bed ; and yet there is 
often little or no emaciation. Cardiac palpitation, dyspnoea, and attacks 
of syncope are the results of the oligocythaemia and attendant exhaustion. 
More or less oedema and puffiness appear about the legs and ankles, as- 
sociated with hemorrhages from the nose, gums, bronchi, and female gen- 
itals. At the same time the body exhibits ecchymotic and petechial spots 
and vibices, due to subcutaneous or external hemorrhage. 5 Eetinal apo- 
plexy is not uncommon, and an ophthalmoscopic examination should never 

1 Quincke found an abnormal quantity of iron in the liver, and regarded that as a proof of great destruc- 
tion of red discs. 

2 Brigidi found that the cceliac ganglia showed fatty and pigmentary degeneration of the nerve cells. 
Le Sperimentale. May, 18T8. 

8 Cf. Biermer in the Zuch Canton. 

4 Gusserow proposes the name " extreme ancemia of pregnant women." Lebert also calls it " puer- 
peral chlorosis.'' 

6 Immermann says the bleedings are due to the intense oligocythaemia. 
59 



930 



CHROKIC GENERAL DISEASES. 



be omitted in any suspected case. Persistent diarrhoea is often present quite 
early, and the urine is darker than normal. 

There are early signs of atonic dyspepsia ; and anorexia, nausea, and 
vomiting evidence the great irritability of the gastro-intestinal tract. To- 
ward the end there are periods of pyrexia during which the temperature 
is remittent and may reach 104° F. The rise in temperature is attended 
by other febrile phenomena, such as thirst, furred tongue, etc., etc. Still 
later there is a time of absolute apyrexia, and toward the very last moments 
of life the temperature runs far below normal. Cardiac, venous, and arterial 
murmurs are present and are far more intense than in simple anemia. The 
cardiac systolic murmur is associated with the fremissement cataire. The 
heart is always feeble, and in severe cases intermittent ; sometimes it is 
slightly dilated from fatty degeneration. 

Differential Diagnosis. — Progressive pernicious anaemia may be mistaken 
for simple ancemia, leucocythmmia, pseudo-leukaemia, and chlorosis. 

Ordinary ancemia presents a discoverable cause, is attended by marked 
emaciation, has no febrile symptoms and no evidence of retinal hemorrhages 
or purpuric spots. In progressive pernicious anaemia the case is just the 
reverse: Finally,, simple anaemia is amenable to treatment, while pernicious 
anaemia is not. 

In leucocytlmmia the spleen and lymphatics are enlarged, often enor- 
mously ; and the bones, especially the sternum, may be tender and some- 
what swollen, and the blood will contain an actual as well as relative — 1-20 
excess of white globules. JSTone of these conditions are present in progres- 
sive pernicious anaemia. 

In pseudo-leukaimia the spleen and lymphatics undergo the same en- 
largements as in leucocythaemia, but there are no blood lesions, while in 
pernicious anaemia there is no enlargement of lymph-structures, and the 
diminution of red discs is greater than in any other disease. 

Chlorosis is a disease of young females ; it is uncommon except at the 
time of puberty. Pernicious anaemia is common among women in the pu- 
erperal state, and occurs between twenty-five and forty as a rule. Chlorosis 
is unattended by dropsy, while dropsical symptoms are common in perni- 
cious anaemia. Hemorrhages, spots of extravasation, and febrile phenomena 
form no part of the natural history of chlorosis ; while they are constant 
symptoms in pernicious anaemia. Chlorosis is curable and does not pro- 
gress beyond a certain point ; pernicious anaemia is incurable and progres- 
sive. In chlorosis the face has a yellow-green hue ; in progressive pernicious 
anaemia it is of a dusky yellow. 

Prognosis. — Death occurs in 90 per cent, of all cases. Of course those 
who make death sl necessary factor in their acceptation of the definition, 
justly hold that it is a fatal malady. The duration varies from six weeks 
to six months. Whether it may supervene on a benign anaemia or a chloro- 
sis is uncertain. In very rapid cases hemorrhage and diarrhoea will be ex- 
cessive. Death may occur from inanition, exhausting hemorrhages or apo- 
plexy. 1 



1 Bramwell states that the end is often ushered in by diarrhoea, coma, or delirium. 



LEUCOCYTHiEMIA. 



931 



Treatment. — The treatment is purely symptomatic and supporting. Iron, 
quinine, strychnia and arsenic, in combination with a highly nutritious, 
mostly fluid diet, will be found the most available means in such a line of 
treatment. Change of air and, when the strength allows, sea-bathing are 
highly recommended. Transfusion of blood has been tried, and has failed. 1 
One case was reported as cured by transfusion of two ounces of human 
blood by the Dieulafoy aspirator. 2 Though the outlook is discouraging 
from the onset, yet vigorous supporting treatment should be the rule from 
first to last. 

LEUCOCYTHiEMIA. 



Leucocythaemia is an abnormal blood condition marked by increase in 
the number of the colorless corpuscles, and associated with new formation 
of cytogenic tissue in different parts of the body. 3 It may assume either a 
splenic or lymphatic form, associated, in some cases, with a myelogenous 
leukaemia, in which the medulla of the bones is involved. When two of 
the adenoid structures are simultaneously involved, it is spoken of as 
medullo-splenic or lymphatico-splenic leucocythaemia. 

A temporary increase in the colorless corpuscles (leucocytosis) is not in- 
frequent during and immediately after full digestion, in pregnancy and 
fevers. It is not leucocythaemia. 

Morbid Anatomy. — The blood in leucocythaemia is pale, its specific 
gravity is diminished, and it does not readily coagulate, although the 
amount of fibrin is said to be 
increased. These changes are 
due to a very marked increase 
in the number of white corpus- 
cles, which sometimes equal the 
red. In splenic leukaemia the 
white discs are larger and more 
granular than normal ; while in 
the lymphatic form they are 
smaller. In some instances cor- 
puscles containing several nuclei 
preponderate ; in others the 
white discs are found with only 
one nucleus. Fat is sometimes 
found in the white discs. The 
red blood globules are dimin- 
ished in number, and they lose 
their normal outline. When 
leukaemic blood is defibrinated 
the corpuscles sink and form two 
distinct layers — an upper white layer, and a subjacent red. Some state 

1 Dr. Weldon states that he has cured four cases by the intra-venous injection of milk. 

2 Dr. Cary,in the Buff. Med. and Surg. Jour., Jan., 1881. 

3 Prof. J. Hughes Bennett, in 1845, described tbis condition as suppuration of the blood. Virchow, the 
Bame year, called it leukaemia. Six years later, Prof. Bennett used the name leucocythaemia. 




Fig. 188. 

Blood from a case of Leucocythaemia. 

A. A. White Blood Corpuscles. 

B, B. Red Blood Corpuscles, x 300. 



932 



CHRONIC GENERAL DISEASES. 



that the reaction of leukemic blood is acid, others that it is alkaline. 
Elongated, octahedral, colorless crystals of albuminoid material are often 
found in the blood ; chemical analyses have resulted in the discovery of 
multifarious ingredients, as lactic, uric, formic, acetic, and glycerin-phos- 
phoric acids, leucin, tyrosin, etc., etc., some of which are present (nor- 
mally) in the spleen. 1 It is, however, only when the blood persistently 
shows a proportion of white to red of one to twenty that leukaemia can be 
diagnosticated. 

The spleen usually enlarges uniformly in all cases, and it may reach 




Fig. 189. 

Section of a Leucocythaemic Spleen. 
A, A. Fibrous trabecular of (he vascular sinuses— slightly thickened. 

B t B. Dilated venous sinuses containing lymphoid cells C, C. swollen and proliferating endothelial celh, 
I), D, and large multinucleated cells E, E. 

eighteen pounds in weight. It is usually firmer than normal ; never 
softer. On its cut surface the trabecule stand out as whitish striae, and the 
Malpighian bodies as whitish dots. These last are lymphadenomata of the 
Malpighian bodies, which resemble hypertrophies, the tumors having an 
encephaloid look, and yielding a cancer-like juice. 2 The organ is some- 
times "mottled" with infarctions, the vessels being plugged by white 
blood-cells. In these cheese-like islands the vessels are changed into 
granulo-fatty tracts. Large multinuclear cells and many lymphoid ele- 
ments are found in the venous sinuses. The capsule is somewhat thicker 
than normal, and inflammatory adhesions may bind it to surrounding 
parts. In the hilus of the organ lymphomata the size of an egg are 
sometimes found. 

Virchow thus sums up the splenic changes : "Hyperplasia of this lym- 

1 Physiology, M. Foster. " Metabolic Phenomena," etc. 

2 Cornil and Ranvier say that the diagnosis of lymphadenomata (which may affect other glands than 
the splenic Malpighian bodies) is to be made from cancer, by the fact that the capillaries in leukasmia are 
f ull of white discs which carmine stains. 



LETJC0CYTM1MIA. 



933 



phatic organ induces chemical and morphological changes in the blood." 
In the lymphatic variety the splenic enlargement is slight, and the princi- 
pal change is hyperplasia of the lymphatics. The inguinal, axillary, and 
cervical glands are enlarged and soft, and present a red, pulpy appearance. 
The meshes of their connective-tissue are crowded with lymphoid elements. 

In myelogenic leuhcemia the marrow in the long bones and the spongy 
tissue of the sternum, ribs, and vertebra? is changed to a creamy-white 
puruloid mass. In some cases this hyperplasia produces, or is attended by, 
a red, fleshy appearance, like foetal marrow. The larger vessels in these cases 
have their walls infiltrated with lymph-cells, and the small vessels that re- 
main in the changed marrow are chiefly filled with red cells. 1 

Between the liver cells are found circumscribed or diffused patches of 
white blood cells that have escaped from the overfull capillaries — these are 
called "apoplexies of the white blood corpuscles" — and in connection with 
connective-tissue hyperplasia form the whitish masses found in the organ. 
The liver is enlarged from hyperemia and from inter-lobular and inter- 
cellular infiltration. 

In the kidneys the infiltration of lymphoid elements appears in lines 
parallel to the tubules. Here also lymphadenomata start from the con- 
nective-tissue. Similar new growths are common in the stomach and 
intestines, often measuring from 1 to 1| inches in diameter, and present- 
ing many of the characteristics of cancer. 

The lungs, brain, skin, testicle, and retina are sometimes the seat of the 
leukemic developments. The heart may suffer fatty degeneration, and 
there may be effusions into the pericardium. Indeed, effusions are fre- 
quent in all the serous cavities. Cerebral embolism occurs in about five 
per cent, of all cases. Hemorrhage from mucous surfaces or into serous 
sacs is a very common pathological accompaniment of leucocythoemia. 

Etiology. — Leucocythsemia occurs at all ages and conditions, but it ia 
most frequent in early adult life. It is twice as frequent in men as in 
women. In women there is a notable connection between the generative 
functions and leucocythasmia. Cold, wet, and all anti-hygienic conditions 
predispose to it. When the Peyerian patches are lymphadenomatous, it is 
possible that previous intestinal catarrh was the etiological factor. In the 
majority of instances the etiology cannot be determined. 

Symptoms. — The early symptoms of leucocythsemia are almost identical 
with those of simple anaemia, accompanied by swelling of the abdomen with 
a sense of fulness in the left hypochondrium and wandering pains in the 
splenic region. The sjrienic enlargement may or may not be attended by 
fever. 

In the lymphatic variety, enlargement of the glands in the groin, neck, 
and axillary regions may be the first symptoms which will attract atten- 
tion, and may exist for months before the blood changes can be detected. 

In the myelogenic variety, the bones, especially the ribs and sternum, be- 

i Neuman regards the myelogenous changes as primary, and states that hyperplasia of the marrow 
causes immature corpuscles to enter the blood. Ueber Myelogene Leukcemie, Berlin, Klin. Woch., 1878, 
(6-10). 



934 



CHRONIC GENERAL DISEASES. 



come tender upon pressure, and as the disease advances the patient becomes 
pale and assumes a waxy appearance. There will be more or less pyrexia 
with evening exacerbations, the feyer being usually in proportion to the 
rapidity of the leuksemic development. The pulse is accelerated, feeble, 
and marked by a peculiar throb. The appetite is capricious, and the tongue 
and pharynx may be the seat of ulcerations. Early in the disease the 
bowels are constipated ; but its late stages are attended by exhausting 
diarrhoea. Dyspnoea, arising from the blood condition and from the 
splenic enlargement, is associated with a chronic bronchitis. As a result 
of the blood changes, a hemorrhagic tendency is developed, which may 
cause hemorrhages from any mucous surface, or apoplexy. Ketinal hem- 
orrhages and whitish patches due to apoplexy of the white blood corpuscles 
can be detected by the ophthalmoscope. Ecchymotic spots often appear 
over the body, and the fatal termination is hastened by this hemorrhagic 
tendency. 

If a hemorrhagic diathesis is not developed the disease runs a tedious 
course. In such cases the enlargement of the spleen and lymphatics is very 
great and leads to symptoms of pressure. General anarsarca is of frequent 
occurrence toward the end of the disease, and under these circumstances the 
dyspnoea becomes extreme. The urinary symptoms are not important, 
though the abnormal constituents present the greatest variety. The 
amount passed diminishes with the progress of the disease. 1 As leuksemic 
patients emaciate the dyspnoea increases, and the fever, which was at first 
intermittent, becomes continuous. If no complication occur death results 
from exhaustion, preceded by delirium, stupor, and coma. 

Differential Diagnosis. — Leucocytha?mia may be mistaken for progressive 
pernicious anaemia, for chlorosis, and in its early stages for inflammatory 
and cancerous enlargements, and for pseudo-leukaemia, or Hodglciri's 
disease. 

In all cases the differential diagnosis rests upon the result of a micro- 
scopic examination of the blood. When the ratio between the white and 
red globules reaches one to twenty the case must be regarded as one of 
leucocythsemia. 

Prognosis. — No case of recovery from leucocythEemia has yet been re- 
corded. It varies, however, in its duration. If it comes on abruptly with 
active symptoms it may prove fatal in three or four months ; but when in- 
sidious in its approach three or four years may elapse before the fatal 
result is reached. The average duration of the cases under my observa- 
tion has been about fourteen months. Sometimes the disease does not 
progress steadily, but advances by stages, progressing rapidly for a few 
months, and then remaining stationary for as long a period. 

The more rapidly the patient emaciates, the more frequent and profuse 
the hemorrhages, and the higher the temperature, the more unfavorable the 
prognosis. Dropsy is always an unfavorable symptom. The most frequent 
complications are effusions into the serous cavities and hypostasis in the 

1 A number of cases are recorded where priapism, venereal excess, and seminal emissions have marked 
the ODset and course of the disease, but the value of such symptoms is yet to be determined. 



hodgkin's disease. 



935 



lungs. Pneumonia, pleurisy, and intestinal catarrh stand next ; then follow 
a long list of visceral diseases which appear as coincidences, rather than 
complications. Death may occur from profuse hemorrhage, from cerebral 
apoplexy, from pulmonary and serous inflammation, or from exhaustion. 

Treatment. — None of the many measures proposed and tried have as yet 
produced a cure or proved successful in arresting its progress. Quinine in 
large doses is, however, advocated by all ; it is tonic, and also has a direct 
influence upon the spleen. Arsenic and iron should also be steadily given, 
either alone or in combination with quinine. Faradization of the spleen, 
extirpation of the spleen and transfusion of blood have been tried, the 
latter with, the two former without, success. Nitric and nitro-muriatic 
acid, internally and in the form of baths (locally) are recommended. 
Iodine preparations do not seem to have any efficacy, and the water-cure 
plan has been abandoned. The malady is delayed by cheerful surround- 
ings and simple and nutritious diet. Cod-liver oil and phosphorus are 
valuable adjuvants to the dietetic plan. But the chief indications for 
treatment are found in the accidental complications. 

eodgkin's disease. 

(Pseudo-Leukcemia. ) 

Pseudo-leuksemia is a disease resembling leucocythaemia in all its ana- 
tomical characteristics except the blood changes. It consists in enlarge- 
ment of the lymphatic structures and development of lymphomata ; it so 
invaribly terminates fatally that the term malignant lymphoma has been 
suggested for it. 1 

Morbid Anatomy. — Histologically the lesions of this disease in no wise 
differ from lymphomata. They are divided into hard and soft tumors. 
The soft lymphomata are of encephaloid consistency. Their color is a 
reddish gray, studded with spots of extravasation. The glands undergo 
simple hyperplasia, and as they enlarge become confluent, forming a 
large, soft, fluctuating, lobulated tumor. The capsule is in some cases 
attacked (" periadenitis "), and then the process is not confined to the 
lymphatics, but extends to, and infiltrates the adjoining tissues. The fluid 
expressed from a cut surface resembles cancer-juice. Hard tumors have 
a fibrous feel, and on section exhibit a shining, waxy appearance. The 
capsule and medullary structure are indistinguishable and no fluid can be 
expressed. Many regard the extensive hyperplasia of the soft as the 
initial stage of the hard ; while others consider the greater proportion of 
cellular elements as the cause of the difference. These tumors are rarely 
larger than a hen's egg. Unlike scrofulous glandular enlargement they 
undergo no caseation, suppuration, or retrogressive changes. 

As a sequela of this disease the number of red globules in the blood is 
diminished. The disease first attacks one group of lymphatics and later 

1 Hodgkin, whose name the disease bears, was the first to describe these peculiar lymphatic changes 
(1832). Trousseau called it " Adene." Anaemia lymphatica, Lymph o-sarcoma, Progressive glandular 
hypertrophy, and Lymphadenosis are terms also applied to it. 



936 



CHRONIC GENERAL DISEASES. 



invades those of the whole body. The glands at the angle of the jaw, in 
the axilla and groin are usually first affected. 

The spleen is enlarged, but rarely to such a degree as in leucocythaemia. 
On section, it is seen studded with grayish nodules, the Malpighian bodies 
having undergone hyperplasia. The lymphatic enlargements may be fol- 
lowed by similar developments in the liver, kidney, stomach, lungs, ovaries, 
testicles, brain, retina, muscles, subcutaneous tissue, and in the serous 
membranes. These are called metastatic or secondary deposits ; and de- 
velop especially in and along vascular walls. 

Etiology. — Lympho-sarcomata were formerly thought to be carcinoma- 
tous or a malignant form of tuberculosis. There is no connection between 
pseudo-leukaemia and scrofulosis, or between it and syphilitic affections of 
the lymphatics. The disease has been found in men oftener than in women ; 
but no etiological relations have been established. 

Symptoms. — When pseudo-leukaemia runs its regular course, and begins 
by swelling of the glands in the neck, armpit, or groin, it can be recognized 
without difficulty, and the time of its commencement can be fixed with 
considerable certainty. But when the enlargement commences in the ton- 
sils, the retroperitoneal, mediastinal, or other deep-seated and impalpable 
glands, its diagnosis is difficult. In all forms, however, emaciation and 
anaemia are marked and progressive. In the majority of cases the spleen 
will be more or less enlarged ; and dtiH pains, with a sense of fulness and 
distention, will be felt in the left hypoehondrium. Attacks of cardiac pal- 
pitation are common. The pulse is small and rapid. In the majority of 
cases there is a steady pyrexia (100° to 101° F.) towards the end, attended 
by slight evening exacerbations. With the increasing anaemia there will 
be dropsy, and when the disease is well advanced the muscular weakness is 
marked. When nausea, vomiting, and diarrhoea are prominent symptoms, 
lymphadenomata of the stomach or intestines may be suspected. When 
dyspnoea, cough, impeded venous return, and all the signs of a bronchitis 
exist, the bronchial or mediastinal glands are probably so enlarged as to 
diminish the calibre of the bronchial tubes or venous trunks near them. 
The symptoms of laryngeal paralysis may be induced by a lymphadenoma 
pressing upon the recurrent laryngeal. Pressure on sensory nerves will 
cause more or less pain in the regions supplied. 

The impoverished blood condition is evinced by hemorrhages from the 
various mucous surfaces and by the appearance of petechias over the sur- 
face of the body ; or in children by the occurrence of convulsions or coma. 
Jaundice has occurred in a few cases from pressure on the common bile- 
duct. A large inguinal tumor may exert such pressure on the femoral vein 
as to cause oedema of the legs. 1 

Differential Diagnosis. — Pseudo-leukaemia may be confounded with leuco- 
cythcBmia; the points of differential diagnosis have been considered in leu- 
cocythaemia. It is to be remembered that pseudo-leukaemia has all the 
symptoms of leucocythaemia except blood changes mentioned ; and in 



1 A rare case is reported where a lymphadenoma about the Eustachian tube caused deafness. Anothei 
is mentioned where paraplegia resulted from tumors pressing on the cord. 



addisok's disease. 



937 



addition the cervical, axillary and inguinal glands are early and notably 
enlarged. 

Prognosis. — No case of recovery is reported where the diagnosis has been 
certain. One year is its average duration ; two months and three years are 
its extremes. As in leukaemia, so in pseudo-leukaemia the course may be 
rapid and attended by pyrexia and well marked constitutional symptoms ; 
or it may be slow and essentially chronic. Pseudo-leukaemia is frequently 
complicated by pleurisy, pneumonia, so-called diphtheritic sore throat, ne- 
phritis, lardaceous degeneration of the lymphatic glands, and pulmonary 
tuberculosis. Death may occur from asthenia, exhaustion, anaemia, or from 
complications. 

Treatment. — The general treatment of this disease has been mainly surgi- 
cal, the theory being that if the glands are excised the disease will be 
checked. It is true that the removal of the enlarged glands relieves the 
pressure symptoms, which are often exceedingly painful, but it is of no 
permanent service. Electrolysis, galvano-puncture, the injection of caus- 
tics, iodine, arsenic, and phenic acid have been tried without avail. If 
excision is practised, it should be when there is little or no anaemia and no 
fever. All forms of topical remedies have been tried, but to no purpose. 
Internally, arsenic seems to have some controlling effect. 1 Iron and cod- 
liver oil should be given in all cases, and sea-bathing sometimes arrests for 
a time the progress of the disease. 

addison's disease. 

Addison's disease, or melasma suprarenalis, is a cachexia accompanied 
or caused by degenerative changes in the suprarenal capsules, that re- 
semble tubercular infiltration. Many believe that any of the three condi- 
tions, viz.: tuberculosis, chronic interstitial inflammation, or fibro-caseous 
metamorphosis, or the three combined, may be present in this disease. But 
its real pathogenesis is still in obscurity, for the reason that the physiology 
of the suprarenal capsules is still unsettled. Histologically these capsules 
closely resemble a lymphatic structure. 2 

Morbid Anatomy. — In the early stages of this disease the capsules are 
enlarged. In the centre of the medullary portion of the glands are found 
small, gray, tubercle-like granules. As the development of these masses 
progresses towards the cortex, those at the centre become fused and suffer 
caseous metamorphosis. This change may be so uniform that the whole 
capsule becomes a uniform caseous mass. At other times the process, be- 
ginning in several foci at the same time, causes the gland to assume a more 
or less lobulated appearance. The line of demarcation between the corti- 
cal and medullary portions of the gland is lost, and either the whole cut 
section may be of a yellow color, or yellow masses may be entwined by gray 
tuberculoid fibrous tissue. The gray or yellow color predominates, ac- 



1 Warfynge reports improvement in four cases from its use.— London Medical Record, March 15, 1881. 

2 Kolliker describes the renal capsules as both vascular glands and as appendages to the nervous 
system. Brown-Sequard's physiological experiments accord with these views of Kolliker. 



938 



CHRONIC GENERAL DISEASES. 



cording as the condition has existed for a short or a long time. As the proc- 
ess extends to the cortex the centre begins to soften. In some cases the 
gland is a shell of hard, cheesy material, with diffluent creamy contents. 
Instead of this liquefaction it is not uncommon to find the centre of the 
capsule in a state of calcification. In either case no sign of normal gland 
structure remains. 1 In the stage where gray matter predominates the 
capsules are enlarged ; where yellow material is in excess, especially if as- 
sociated with chalky, degenerative changes, the gland is hard and indurated. 

In some cases the suprarenal glands may become a mass of cicatricial 
tissue, the central portion of which is in a state of caseous degeneration 
The capsules are usually bound to all the surrounding organs or parts by 
firm connective-tissue. 

The shin is discolored. In the lower layers of the rete MalpigMi there 
are granules of pigment matter which vary in color from a very light to a 
dark brown. The coloration is deepest in those parts in which the pigment 
is normally most abundant. In some instances granular pigment is found 
in the papillae and in the cuticular connective-tissue cells. It may be dis- 
tributed along the line of the nerves and blood-vessels. 

The spleen may be enlarged and softened. The adjacent mesenteric and 
retroperitoneal glands are often tuberculous or in a state of cheesy meta- 
morphosis. Peyer's patches and the solitary glands of the intestine are 
enlarged, and the testicles and the prostate are in some cases tuberculous. 
The same changes occur in the liver as in the spleen. Scattered tubercu- 
lous nodules are often found in the brain and apices of the lungs. The 
heart may undergo fatty change and the kidneys are occasionally the seat 
of parenchymatous degeneration. Connective-tissue hyperplasia is marked 
about the nerve-sheaths in the sympathetic nerves near the capsules. There 
is hyperemia of the nerve trunks and ganglia of the large adjoining plex- 
uses. 2 The blood is ansemic, fibrin is diminished, the red discs are altered 
in size and form, and do not run together in rouleaux as normal discs do. 
The white blood globules are increased. 

Etiology. — There is an undoubted connection between tuberculosis and 
morbus Addisonii. In over 80 per cent, of reported cases, tuberculosis ex- 
isted in the capsules or in other organs. 3 The latest and by far the most 
reasonable theory is that the highly nervous capsule contains gland-cells 
which have a close connection with the vascular and haematopoetic system. 4 
Buhl thinks that not only is it a blood disease, but that it is infectious. 
It has been regarded as analogous to leukaemia and pernicious anaemia. 

1 G. Merkel states that there is cell proliferation attended by the formation of a delicate reticulated 
structure containing many fusiform lymphoid and giant cells. In opposition to most authorities, Cornil 
and Ranvier affirm that the process first invades the cortex, and the medullary portion suffers secondarily. 
Upon microscopical examination the yellow and gray matter present the same pathological aspects as 
tubercle. 

2 Cornil and Ranvier say that "the lesions of the nerve centres of the suprarenal capsules and of the 
great sympathetic in part account for the phenomenon of pigmentation. 1 ' 

3 Letulle points to its association with tuberculous disease of the spinal column. Wilks and Moxon 
found pulmonary tuberculosis in 80 per cent, of their cases. Riesel claims that there is a paralytic state of 
the vaso-motor fibres of the sympathetic, and as a consequence the blood is imperfectly and unequally dis- 
tributed. La France Medicale, No. 40, 1880. Also see Ziir Pathologie des morbus Addisonii. Deut. Arch, 
fiir Klin. Med. 18T0, Be. 7. 

4 Henle and Von Brunn. 



addisok's disease. 



939 



It attacks males oftener than females, and is essentially a disease of adult 
life. It has been found associated with cancer, apoplexy, fatty and waxy 
degeneration of the suprarenal capsules, and in some cases the suprarenal 
capsules have been found perfectly normal. 

Symptoms. — This disease may come on so insidiously that the patient 
will be unable to determine the date of its commencement. A feeling of 
extreme languor is its most constant symptom. Its progress may be unin- 
terrupted, either slow or rapid : or it may progress by stages ; in the lat- 
ter case there will be periods when the disease remains stationary for 
months. The countenance becomes pale, the muscles flabby, the pulse fee- 
ble ; there is extreme muscular weakness, asthenia, indigestion, anorexia, 
dyspnoea, and fits of palpitation. Melancholia is not uncommon ; the pa- 
tient is not easily aroused from a drowsy, dreamy languor into which he 
habitually falls. Dizziness and long fits of syncope are not infrequent. 
Gastric irritability, nausea, and yomiting are common. There is a sense 
of distention oyer the epigastrium, acid eructations, and fits of eardialgia. 
The tongue remains normal in appearance throughout. Sometimes there 
is obstinate diarrhoea. 1 In most cases there is intense pain in the joints, 
and along the spine and sacrum. As the disease advances the heart action 
becomes more and more feeble, the pulse more rapid and weak, and arte- 
rial anaemic murmurs are heard. 

Meanwhile the skin changes its appearance. At first its hue is like 
that of melanaernia, then it is distinctly icteroid, then it presents the 
color of a mulatto ; finally, it becomes a lustreless bronze. Xot only 
the whole cutaneous surface, but the mucous membranes of the lips, 
tongue, gums and mouth are strongly pigmented. The parts most exposed 
change in color first, then the parts subjected to pressure and the flexures of 
the joints. Superficial cicatrices are strongly pigmented, while deep ones 
remain unaltered. The roots of the nails and the sclerotic remain un- 
changed, and the soles of the feet and palms of the hands are not discolored 
until late, and then not markedly. As these patients approach death, 
sight and memory fail, conyulsions and choreic symptoms and delirium are 
followed by comatose periods. But eyen when they reach a state of com- 
plete asthenia there is but slight emaciation ; the body often presents the 
appearance of obesity. 

The temperature is slightly sub-normal throughout its course. The 
urine is normal in amount : uric acid, coloring matter, and indican are 
in excess, and urea is decreased. 

Differential Diagnosis. — It may be mistaken for ptyriasis nigra, but 
the itching of the surface and the desquamation of the cuticle in the latter 
disease readily distinguish it from Addison's disease. Anaemic jaundice, 
and the discoloration of the skin from nitrate of silyer or from exposure tc 
the sun will readily be distinguished from the bronzed skin. 

Prognosis. — It is an incurable disease, and no case of recoyery has been re- 
ported. Its duration yaries from sixteen to eighteen months to four orfiye 



1 In 1S71 Prof. Flint stated that degenerative changes in the gastric and intestinal tuhules were prob- 
ably the cause of the intense an?emia. N. Y, Med. Journal. March, 1871. 



940 



CHRONIC GENERAL DISEASES. 



years. Death may occur from asthenia, diarrhoea, convulsions or coma, 
or from complications. 

Treatment. — All remedial measures have thus far proved unavailing. 1 
Faradization and galvanism of the sympathetic have been proposed. Qui- 
nine combined with iron, and iodide of potassium have been strongly rec- 
ommended. In all cases perfect rest, quiet and good hygienic surround- 
ings are important. It must be remembered that sudden and unexpected 
death at any period of the disease may occur when treatment is apparently 
arresting its progress. I have never obtained any positive beneficial results 
from any plan of treatment. 

AMMONAEMIA. 

Ammonaemia is a condition in which an excess of carbonate of ammonia 
is found in the blood, the result of the decomposition of urine retained in 
the urinary tract. 

Morbid Anatomy. — The intestines are the seat of chronic catarrh and 
contain a greenish yellow alkaline fluid. Sometimes ulcers are found in 
the intestines similar to dysenteric ulcers. When ammonaemia occurs with 
ancemia, it is possible for the urea excreted by the intestines to change into 
carbonate of ammonia. 2 A ferment has been obtained from cystitic urine 
that is said to be capable of changing urea into carbonate of ammonia. 3 

Etiology. — The one essential condition necessary for the development of 
ammonaemia is the retention of urine in the body sufficiently long for the 
urea to undergo decomposition. The conditions under which it most fre- 
quently occurs are, stricture of the urethra, enlargement of the prostate 
gland, atony and paralysis of the bladder, pyelitis, pyonephrosis, hydro- 
nephrosis, sacculated kidney and chronic cystitis. 

Symptoms. — There are, clinically, two forms of ammonaemia ; in one the 
conditions which give rise to it come on suddenly ; in the other the causa- 
tive condition comes on slowly but continuously. 

In the first, or, as it is called, acute ammonmmia, there are nausea and 
vomiting, intermittent and irregular chills, acceleration of the pulse, and 
rapid rise of temperature. Diarrhoea and vomiting, if excessive, lead to 
exhaustion and a typhoid condition. The complexion assumes a dingy 
bronzed hue • there is great muscular weakness with a tendency to 
lethargy. (Edema of the face and ankles is of very rare occurrence. De- 
lirium may occur. The tongue is dry, brown and shining — the beefy 
tongue — and the mucous membranes that are exposed to the air, that of 
the throat especially, are remarkably dry. The breath and the perspira- 
tion are ammoniacal. 

Chronic ammonaeinia which accompanies atony and paralysis of the blad- 

1 Greenhovv asserts that glycerine 3 ij. combined with spts. chloroform, et tr. ferri chloridi, aa tt^xv., 
is highly advantageous. 

2 Rosenstein denies any connection between ammonaemia and carbonate of ammonia ; but the weight of 
opinion is in favor of it. Rosenstein, " ueber Ammonaemia^'' Deutsche Zeitschrift f. pr. Med. No. 
20; 1S74. 

3 Pasteur only succeeded in finding a ferment when bacteria were present ; but those who follow Pas 
teur's teachings claim that a specific ferment is the cause of ammonajmia. 



AMMOTC^MIA. 



941 



der and enlargement of the prostate gland, comes on very insidiously. The 
complexion becomes sallow, then of a dingy brown hue. There is pro- 
gressive emaciation and restlessness, headache and insomnia. Irregular 
chills occur at infrequent intervals ; the temperature is constantly above 
normal, and the pulse is accelerated. Vomiting is persistent. The 
mucous membranes assume a dry, glazed, shining appearance ; the skin be- 
comes dry and harsh ; the breath and perspiration are distinctly ammo- 
niacal. But it should be remembered that the amount of perspiration in 
ammonaemia is probably less than in any other disease. When the disease 
is far advanced convulsions may occur. At this time the complexion may 
become quite dark, and emaciation is marked. Diarrhoea alternates with 
constipation. 

As a cachexia develops, insomnia and restlessness give place to som- 
nolence, delirium, lethargy, stupor, or coma, and the patient passes into a 
typhoid state. Old men with enlarged prostates pass into a condition of 
stupor ; and then low muttering delirium, rapid, feeble, and irregular 
pulse and subsultus tendinum terminate in a fatal coma. 

The urinary symptoms are important. The urine is ammoniacal and 
strongly alkaline when passed. It often contains pus, and there is a deposit 
of amorphous phosphate of lime with crystals of ammonio-magnesian phos- 
phate. The odor is offensive and pungent. 

Differential Diagnosis. — Ammonaemia may be mistaken for typhoid fever, 
sub-acute gastritis, pyemia, or septicemia. In gastritis the urinary symp- 
toms are negative, while in ammongemia they are diagnostic. Nausea and 
vomiting are persistent in ammonaemia, and intermittent in gastritis. Ca- 
theterization, or a rectal examination, will rarely fail to discover some 
organic gen ito-urinary obstructive cause for urinary retention; while a 
physical exploration in gastritis gives negative results. 

In pyceuia there will be an initiatory chill, profuse, exhausting, and re- 
curring sweats, a high temperature (103° to 104° R), a sweet, sickly odor 
to the breath, and the evidence of thrombi, infarctions, and multiple ab- 
scesses in some central organ or organs. All these symptoms are absent in 
ammonaemia ; and the ammoniacal breath and urine, and the parched, dry 
skin are in direct contrast to the symptoms of pyaemia. 

In septicemia the temperature is very high— 105° to 107° F. Besides 
there is no ammoniacal odor to the breath or urine; the skin is not dry, 
and genito-urinary obstructive conditions will not be found. The history 
of the case will also greatly aid in making a diagnosis. 

Prognosis. — The prognosis in ammonaemia is determined to a great extent 
by the condition which causes it ; when it is possible to remove the cause 
the prognosis is good, but when the cause cannot be removed the prognosis 
is very bad. In all cases there is slow but progressive impairment of the 
general health. Aged patients rapidly become exhausted, and sink into a 
typhoid state if the causative condition cannot be speedily removed. 

Treatment. — The most important thing to be accomplished in the treat- 
ment of this condition is the removal of its cause. And, since atony of 
the bladder and enlarged prostate are its most common causes, the first 



942 



CHRONIC GENERAL DISEASES. 



step is to empty and wash out the bladder. Very often when the patient 
seems to be sinking into a typhoid state, when there has been nothing 
to direct attention to the bladder, on the introduction of a catheter a large 
quantity of stinking urine will be evacuated ; and after having thoroughly 
washed out the bladder, rapid improvement takes place, and the gastric 
symptoms subside.. The diet should always be supporting and stimulating. 
If tepid water is used to wash out the bladder, carbolic acid, bicarbonate 
of soda, borax, or glycerine may be added ; and the washing should be 
continued till the withdrawn fluid is perfectly clear and free from odor. 
Iron and vegetable tonics are indicated. 

HAEMOPHILIA. 

The hemorrhagic diathesis is an hereditary disease marked by a tendency 
to immoderate bleedings — spontaneous or traumatic — and to obstinate 
swelling of the joints. 

Morbid Anatomy. — No changes in the blood or vessels have been found 
in the few post-mortems that have been made. The swellings of the joints 
are probably due to blood extravasations within the articulation. 

Etiology. — Its most marked cause is hereditary predisposition. It attacks 
men far oftener than women. 1 The tendency descends to sons through 
the mother, who herself may give no evidence of the disease. Fathers do 
not transmit the tendency to their sons. Pregnancy is said to be a devel- 
oping cause. There is often nothing to indicate the existence of this dia- 
thesis prior to the occurrence of the hemorrhage. Whether the hemophilia 
of the new-born is a distinct disease is an unsettled question. Their blood 
has been found to contain fungoid organisms which afford an apparent 
explanation of the hemorrhages. The hemorrhagic diathesis has been re- 
garded as allied to scrofula, chlorosis, gout, and similar dyscrasiae, and 
again as a pronounced manifestation of a rheumatic diathesis, as both these 
conditions occur under the same influences. One of the most recent theories 
is that it is dependent on deficient capillary innervation with resulting 
dilatation. This neurotic theory is favored by the frequency of nervous 
disorders in bleeders and the fact that neurotic remedies exert the greatest 
control over it. 2 In its transmission from parent to offspring it often skips 
one generation. 

Symptoms. — The symptoms appear as a rule during the first or second 
year of life. There is nothing about the appearance that indicates the ex- 
istence of any diathesis. The disease remains latent until a cut, a fall 
on the nose, or the pulling of a tooth starts a hemorrhage, which at times 
is uncontrollable. The blood will ooze for days, and death from acute 
anaemia may result. Usually the bleeding slowly ceases and after a long 
time the patient recovers. The bleedings may come on spontaneously. 
Then there may be prodromata : signs of plethora, of cerebral congestion, 

1 Legg (in Quain's Dictionary, p. 569) gives the proportion as high as 11 to 1. 

2 Mosler states that over fifty per cent, of his cases of leukaemia were complicated by it, and in one 
hundred and fifty cases collected by Gowers, eighty were bleeders. 



SCUKVY. 



943 



stupor, cardiac palpitation, and painful swellings of the joints. In child- 
hood bleeding from the nose is the commonest form of hemorrhage. The 
joints affected are the larger ; the knee is most frequently attacked. 

In bleeders a slight bruise will be followed by extensive blood extrava- 
sations into the connective-tissue. Hemorrhages may take place into the 
stomach, intestines, lungs, bronchi, kidney and brain. Extensive blood 
tumors may form in any part of the body. 

Differential Diagnosis.— There is no condition which is liable to be mis- 
taken for haemophilia, if the history of the patient is accurately taken. 

Prognosis. — Complete recovery is 'rare, but life may be prolonged by ju- 
dicious management ; an example of which can be cited in the case of 
Prince Leopold, who was thirty-two when he died of haemophilia. 

Treatment. — For the traumatic forms styptics and mechanical surgical 
measures should be promptly made use of. When hemorrhage arises spon- 
taneously little can be done. The diet of bleeders should consist largely 
of animal food. Chalybeate tonics should be constantly administered, and 
the patient should lead a quiet life in a warm climate. Xiemeyer rec- 
ommends cathartic doses of Glauber's salts and ergot. Harkin, of Bel- 
fast, recommends the chlorate of potash, — one ounce of the saturated 
solution three times a day — combined with the muriated tincture of iron, 
and claims to have had excellent results. He states that this plan will 
eradicate the constitutional tendency. 

SCTJEVY. 

Scurvy or scorbutus is a chronic blood disease, which may be regarded 
as a peculiar form of anaemia arising from deficiency of vegetable diet. 
Until recently it prevailed very extensively in armies and among crews of 
sailing vessels. Improved means for the preservation of supplies have ren- 
dered it of much less frequent occurrence, and greatly mitigated its severity 
even during long campaigns, and at the present time it is seen but infre- 
quently among sailors. 

Morbid Anatomy. — The red blood corpuscles are diminished and the al- 
bumen and fibrin-factors are increased, although the albumen does not 
coagulate readily, and there is a peculiar viscidity to the blood. There 
is said to be a deficiency of potash salts. 1 The capillaries have been found 
choked with red corpuscles and their endothelial cells altered. Some de- 
scribe the blood as thicker, others as thinner than normal — at one time 
lighter, at another darker. Ecchymoses are very characteristic of scurvy, 
and occur in and beneath the skin, in the muscles, between the periosteum 
and the bone, and within the joints. In these situations they may be very 
extensive. They are also found on all the mucous and serous membranes 
and may partially fill the pleura or pericardium. 2 

The heart, kidney, and liver often undergo fatty or parenchymatous de- 



1 Cornil and Ranvier. 

2 Dr. Ralfe regards disproportion between the various acid* and bases of the blood as the cause of the 
disorganization of the blood, corpuscles and subsequent mucous ecchymoses. 



944 



CHRONIC GENERAL DISEASES. 



generation. The spleen is enlarged, softened, and exceedingly friable. 
Ulcers occasionally form on the mucous surface of the large intestine, re- 
sembling those of dysentery. The changes in the gums are even more 
characteristic lesions. In nearly all cases they become soft, spongy, and 
cedematous, and ulcerated masses overhang the teeth and bleed upon the 
slightest provocation. 

The bodies of those who have died of scurvy are emaciated, the skin is 
ashen gray, and there is more or less oedema, especially of the lower ex- 
tremities. 

Etiology. — Deprivation of fresh vegetable food for a long time will very 
surely induce scurvy, independent of climate, latitude, race, or sex. 1 It is 
rarely met with from any other cause, although an unvaried diet of poor 
quality may induce it. Sudden atmospheric changes, mental disturbance, 
severe and prolonged physical labor with insufficient food, and bad hygi- 
enic surroundings may predispose to scurvy, but seldom develop it so long 
as fresh vegetables in moderate amounts are eaten. 

The theory that scurvy is due to a specific infection, while improbable, 
cannot absolutely be rejected. 2 

Symptoms. — The earliest noticeable changes are in the skin of the face 
and eyelids, which changes color and appears bruised and swollen. The 
pulse is soft and the temperature lower than normal. The patient rapidly 
becomes less and less capable of mental or physical labor, the face grows pale 
and bloated, there is great despondency and a sense of weight in the lower 
limbs. The skin is dry, rough, and of a muddy pallor ; later it becomes 
sallow and leaden. The conjunctivas are pearly white, the tongue is clean 
and pale, the teeth loosen and are surrounded by bright red ulcerated or 
fungous-looking gums that present a purple line where they join the teeth, 
and contrast strongly with the pale or livid lips. The breath is exceed- 
ingly offensive, frequently from necrosis of the jaws. The eyes are sunken 
and surrounded by a dark blue circle. 

Ecchymoses and petechial spots cover the body and extend over a large 
surface on the slightest blow or injury. Severe darting pains which simulate 
rheumatism are felt in the limbs, about the calf of the leg and the popliteal 
space. The legs may become fixed, owing to the hardness of the muscles 
of the calf and thigh. Node-like swellings occur over the tibia from sub- 
periosteal ecchymoses. The pulse is slow except upon excitement, when 
palpitation and dyspnoea are also marked. Slight exertion may occasion 
syncope in those in whom the disease is advanced. Anaemic murmurs are 
heard upon auscultation. The bowels are constipated, unless there be scor- 
butic dysentery. The urine is high colored, sometimes albuminous, and 
there is a diminution in its normal ingredients except potash salts and 
phosphoric acid. The chlorides are abundant. Insomnia and disordered 
vision are common. 

Differential Diagnosis. — The history of a case and a close inspection of 



1 In the Crimean war more died from scurvy than from any other cause. It was the caus<? of death in a 
large proportion of those who died during the potato famine in Ireland. 

2 Fabre regards scorbutus as a miasmatic affection which especially affects the nervous system. 



PUEPURA. 



945 



the gums will enable one to distinguish scurvy from mercurial poi- 
soning. 

Scurvy is distinguished from purpura by the spongy gums, painful 
swellings, and more profuse though less numerous hemorrhages. Purpura 
frequently occurs in those whose health has not been impaired by faulty 
nutrition ; scurvy very rarely. Purpura is not affected by lime juice or 
change in diet, while either will at once produce marked improvement in 
scurvy. Purpura occurs in isolated cases ; the vital powers are not as de- 
pressed as in scurvy, and muscular swellings are absent. 

Prognosis. — Scurvy is not a fatal disease ; appropriate treatment in un- 
complicated cases always effects a cure. It may be complicated by dysen- 
tery, syphilis, the various forms of malaria, typhus, typhoid, and chronic 
alcoholismus. The former diseases assume a scorbutic character. Death 
may occur from complications, exhaustion, general dropsy, hemorrhage, 
diarrhoea, dysentery, pleurisy, pericarditis, or pulmonary oedema. It is 
said, that meningeal hemorrhage is sometimes a cause of death. Hemera- 
lopia often occurs as a sequela. 

Treatment. — In long voyages or campaigns lemon or lime juice or cit- 
ric acid should be taken daily when fresh or preserved vegetables cannot 
be obtained. By their use in the English navy scurvy has been diminished 
nearly ninety per 'cent. One who is seriously ill of scurvy should be kept 
in bed, and the diet at once be made to consist largely of fresh vegetables 
and acid fruits with fresh meats in such proportion as the patient can 
easily masticate and digest. Mustard, radishes, cabbage, and water-cresses 
are anti-scorbutics. Three or four ounces of lime or lemon juice, largely 
diluted with cold water, should be taken daily. If stimulants are required 
malt liquors are to be preferred. A wash of chlorate of potash will afford 
relief to the oral symptoms, and potash may be given internally ; quinine, 
iron and strychnia act both as tonics and appetizers. 

PUKPTJKA. 

Purpura is a general disease, characterized by sanguineous effusions into 
the upper layers of the cutis and beneath the epidermis. 1 

Morbid Anatomy. — Either from changes in the walls of the vessels or in 
the blood itself (excess of salts, or water, etc. ), or quite probably from both 
combined, extravasations occur into the connective-tissue spaces of the 
rete mucosum and papillary layer of the cutis or in the spaces between the 
ducts and hair follicles. The serum is soon absorbed and the more solid 
elements may gradually undergo complete absorption or result in permanent 
pigmentation of the parts. Similar lesions are found in the mucous mem- 
branes, attended by hemorrhage from the free surfaces. Such hemorrhages 
are more common in the nares and along the alimentary canal. Serous mem- 
branes are less frequently affected, but extravasations have been found in the 
pleural, pericardial and peritoneal cavities and in the meshes of the pia, mater. 



1 It may be simple, rheumatic, hemorrhagic or symptomatic. 
'■ i Morbus Maculosus Werihojii.'''' 
60 



Purpura hemorrhagica is also called 



946 



CHRONIC GENERAL DISEASES. 



Rarely are the muscles, periosteum, bones, conjunctiva, and retina the 
seat of extensive blood effusions. 

Etiology. — Age appears to have no bearing upon the development of pur- 
pura, but it is found more frequently in women than in men. It appears 
in some cases without any discoverable cause in the healthy and robust ; 
sometimes its causes seem almost identical with those of scurvy. Rheu- 
matic purpura may complicate acute polyarticular rheumatism or occur 
in those. of a rheumatic diathesis. Purpuric spots are not infrequent with 
valvular disease of the heart, Bright's disease, phthisis, cirrhosis of the 
liver, and various forms of malarial fever. 

Its occurrence with leucocythsemia is interesting on account of Pen- 
zoldt's discovery of the peculiar form of the blood discs in Werlhof s dis- 
ease. 1 Purpuric spots have followed large doses of chloral and iodide of 
potash. Distinct exciting causes, if such exist, are obscure ; fright, severe 
coughing fits, and epileptic attacks are said to have induced it. There is 
no doubt but that the enfeebled condition of the vessels often depends 
upon a state of general debility either hereditary or acquired. 

Embolism and thrombosis have been suggested as causes, while disor- 
dered vaso-motor innervation, which might possibly account for its occur- 
rence after exhausting diseases, has also been considered the primary 
lesion. 2 

Symptoms. — In many cases for days or weeks before the eruption occurs 
there will be a general feeling of malaise accompanied by digestive derange- 
ment. In all varieties of purpura the eruption has the same general char- 
acters. The spots appear upon the extremities and trunk as a rule, but in 
severe cases they cover the head and face as well. They vary in color from 
a bright red to a livid or purple ; they are round or irregular with serrated 
edges, and vary in size from a pin's head to a large pea, or a spot may 
measure an inch or more in circumference. They do not disappear upon 
pressure. The smaller extravasations are spoken of as petechia?, and the 
larger as ecchymoses, and when they occur in lines or stripes they are 
called vibices. . 

If the hemorrhage is so extensive or of such a form as to cause the spots 
to be elevated above the level of the skin the disease receives the name pur- 
pura papulosa, or lichen lividus when they are conical and located around 
a hair follicle. The elevated wheal-like nodules are designated as purpura 
urticans, and if they form bulla? containing serum and blood the name 
purpura bullosa is given. 

While the primary spots are undergoing absorption, as indicated by the 
gradual change of color from the dark blue through the green to yellow, 
another livid red crop is appearing. In ordinary cases a crop lasts from a 
week to ten days. Desquamation never follows, and once formed a spot 
does not increase in size, except by fresh hemorrhage in its vicinity. 

Sometimes there are no constitutional symptoms whatever in purpura 
simplex; but in purpura rheumatica slight fever and rheumatic pains in 



1 Bluthefund bei der 'Werlhof' 'schen Krankkeit, 1878, Erlanger. 

3 Cavalie reports a case associated with organic disease of the brain. 



MYXCEDEMA. 



947 



the knees and ankles are accompanied by red and swollen joints, gastric 
and intestinal disturbances, colicky pains, etc., in addition to the usual 
eruption. In purpura hemorrhagica, preceding and accompanying the 
eruption, there is great constitutional disturbance ; the spots are large and 
numerous, and invade the whole body ; there are free hemorrhages from 
all the mucous tracts and from the lungs. So extensive may these hemor- 
rhages be that acute anaemia is rapidly followed by typhoid symptoms and 
death. The amount of hemorrhage does not depend upon the extent of' 
the eruption. Cerebral symptoms may occur from ventricular or menin- 
geal hemorrhage. 

When purpuric spots accompany the exanthems and contagious fevers the 
usual symptoms of those diseases and the eruption are purely symptomatic 
of the extensive degenerative changes engendered by the primary infec- 
tion. 

Differential Diagnosis. — The points of diagnosis between purpura and 
scurvy have already been given. The fact that there is no itching, no 
desquamation, no suppuration or discharge, and no change in purpuric 
spots upon pressure suffices to distinguish them from the eruption of any 
form of shin disease. 

Prognosis. — In uncomplicated purpura the prognosis is good ; but when 
venous thrombosis, scurvy, diarrhoea, or an incurable organic disease exists, 
life is endangered by the liability to hemorrhage from mucous surfaces, and 
the occurrence of extravasations into the serous cavities or brain. Anaemia 
and dropsy are often causes of death. 

Treatment. — At one time the treatment consisted in administering quinine 
and sulphuric acid. At the present day rest, a highly nutritious concen- 
trated diet, and moderate stimulation with, a nutritive wine are the princi- 
pal measures employed. Tinctura ferri perchloridi, — 15 to 20 minims 
three times a day, — is very efficacious, and should be given in connection 
with some one of the mineral acids, preferably sulphuric. Ergot, turpen- 
tine, gallic acid, and other haemostatics are all highly recommended when 
the hemorrhages become dangerous. When hemorrhage from the lungs 
occurs, the treatment is the same as in other forms of bronchial hemorrhage. 
Recently, small doses of mercury have been given, and apparently effected 
a cure. Shand has obtained excellent results from Faradization (Lond. 
Lancet, July 9, 1879). 

MYXEDEMA. 

Myxcedema is a name given by Prof. Ord to a progressive disease where 
the tissues of the body are invaded by a jelly-like, mucus-yielding dropsy. 

Morbid Anatomy. — All over the body the connective-tissue is found ab- 
normally abundant, the fibrillar element being especially increased and un- 
usually well defined. In Prof. Ord's cases the corpuscular elements were 
enlarged and multiplied, and the interstitial element greatly augmented. 
The skin in myxcedema yields many hundred times as much mucin as nor- 
mal or ordinarily dropsical skin. Besides the overgrowth of connective- 
tissue, it seems to have undergone a retrograde degeneration. In the skin 



948 



CHRONIC GENERAL DISEASES. 



the mucous infiltration causes swelling, translucency and defective secre- 
tion. The connective-tissue stroma of the mucous membranes, of the outer 
coat of the arteries, the glands, muscles, and the central nervous ganglia 
is similarly infiltrated and degenerated. 

Prof. Ord states that the structure of the thyroid glands maybe entirely 
destroyed by the material ; and he thinks its inroads on the Malpighian 
bodies and tubal es of the kidney cause the albuminuria which occurs late 
in the disease. Dr. Mahomed, on the other hand, argues strongly in favor 
of the identity of myxoedema and Bright's disease. Recently it has been 
almost conclusively proven that the central nervous system is affected, and 
in two cases marked bulbar paralysis has been found. 

Etiology. — Myxoedema, in the few cases first described, only occurred in 
adult females, and of these more married than single women were affected. 
Recently, however, Dr. Andrew Clark states that in his experience males 
suffer oftener than females, in the proportion of seven to three. The 
number of recorded cases is, however, too small to admit of positive 
statements. 1 

Symptoms. — The face is swollen as in real dropsy ; but the skin has a 
waxy anaemic look, and the oedema involves not only the dependent por- 
tions, but every feature of the face. Both lips are equally enlarged ; the 
nose is thickened, and the rounded cheeks have a pinkish hue, contrasting 
peculiarly with the rest of the waxy white skin. There is no pitting on 
pressure ; on the contrary, the skin is rather elastic. The shape and form of 
the hands is lost. 2 The dry, rough, translucent skin seldom or never per- 
spires. The thyroid body disappears or diminishes, while there is elastic 
tumefaction of the skin in the lower triangle of the neck above the clavicle. 
The expression of the face is stolid and sad ; the speech is monotonous, 
slow, and leathery ; the limbs move slowly and lazily ; a fixed attitude 
cannot be maintained, and consequently the patient is apt to suddenly fall. 
The intellect becomes dull, sensation is slow but finally sure, and the mus- 
cles are so relaxed at rest that a long contraction occurs before a proper 
equilibrium can be maintained ; hence a quiver often runs through the 
body as one foot is raised from the ground and the body is balanced on 
the other. The muscles of the neck are so lax that the head droops on 
the chest. Sometimes the patella is fractured by the forward bending of 
the body. There is no real loss of muscular power, no wasting, and no loss 
of sensation. 

Thoughts and expressions are tardy and deliberate, but correct. The 
bodily temperature ranges between 98° and 94° F. These patients are 
constantly chilly. Late in the disease patients grow morose and irritable, 
and are subject to delusions, hallucinations, loss of memory, and finally 
complete mental failure. 

Differential Diagnosis. — There is no disease with which myxoedema can 
be confounded when the mucoid oedema is well marked. 

1 In the sixteen cases on which Ord based his descriptions, pregnancy in one or two cases preceded the 
myxoedema. 

2 Sir William Gull calls them spade like. 



SCKOFULA. 



949 



Prognosis. — This is always unfavorable ; its duration varies from six to 
eight years. Death may occur from coma, uraemia, or inanition. 

Treatment. — Besides warm clothing, tonics, and good food little can be 
done. Prof. Ord found that ten to sixty minims of the fluid extract of 
jaborandi, administered four times a day, was followed by marked relief. 
He says the signs of myxcedema almost entirely disappeared under this 
treatment. Nitro-glycerine benefited one case. Vapor baths are advo- 
cated. Dr. Andrew Clark says that baths, assiduous friction, a careful 
diet, and arsenic and iron as tonics, may sometimes cure the disease. 

SCKOFULA. 

Scrofula is a term applied to many different physical conditions de- 
pending upon a diathesis which is regarded as identical with the tuber- 
culous. 

Morbid Anatomy. — The characteristic lesions of scrofula are to be found 
in the lymphatic glands, although the skin, mucous membranes, bones, 
joints, and organs of special sense may be involved. 1 Inflammation ante- 
dates the scrofulous change, and whether occurring in the glands, skin, 
mucous membrane, subcutaneous connective-tissue, bones, joints, kidney 
or testicle, the inflammatory product is the same. When fresh it is rich 
in cells, consisting of a dim, glistening protoplasm with a large single or 
double nucleus. The exudation is either nodular or diffused. It may 
undergo resolution, suppuration or organization ; all taking place slowly 
and imperfectly, on account of poor vascularity. Anaemic necrosis some- 
times occurs in the glands. 

On the skin the lesions appear as eruptions. Impetigo of the eyelashes 
and external otitis are common strumous diseases. In one who has this 
diathesis any skin disease takes on a scrofulous character. Scrofulous in- 
flammation of mucous membranes is marked by a thick, sticky exudation, 
with a tendency to form scabs. The bones most frequently involved are 
those of the ankle, lower part of the femur, the vertebrae, and rarely the 
fingers and toes. The scrofulous development may assume the form of 
synovitis, osteitis, periosteitis, or general arthritis. 

Etiology. — The scrofulous diathesis is very largely an inherited condition 
whose exact nature is unknown, and whose etiology is perhaps equally ob- 
scure. It usually has been considered a functional disturbance of impaired 
vitality, but some recent observations afford ground for the suspicion that 
it may possibly possess an anatomical basis. 

The children of intemperate, phthisical, syphilitic, very old or very 
young parents develop early all the characteristic features of the scrofulous 
diathesis. It is also very apt to appear in the children of parents closely 

1 Virchow taught that the primitive strumous lesion is a simple hyperplasia of the gland tissue, but 
Schiippel has proven that a sc?vfulous gland is a tuberculous gland. Tubercles stud the glands, which 
soon become enlarged and soft. When cut they either resemble a normal gland or contain a white, soft 
cheesy mass mixed with thick pus. Abscess or ulceration may ensue and leave an unsightly scar. Simple 
chronic hypertrophy results in the formation of knotty groups of glands. Of all the tissues the lymphatic 
is the most embryonic, the most plastic or potential. 



950 



CHKONIC GENERAL DISEASES. 



related by blood. Heredity is by no means always present, however, for a 
marked scrofulous diathesis is acquired in early infancy by healthy children 
from improper food, over-crowding, and anti-hygienic surroundings. 

Lack of fresh air, exercise, and sunlight exerts an equally powerful influ- 
ence in reducing the vitality and the reactive power of the system under 
irritation. 1 Scrofula and the tuberculous diathesis, if not identical, are so 
closely related as to be interchangeable. 2 

Symptoms. — Scrofula presents no lesions that may not occur in other dis- 
eases, and the scrofulous inflammation has no characteristics, beyond a 
tendency to extreme chronicity and to undergo caseous changes. It is 
principally a disease of childhood ; rarely, however, appearing before the 
second year. 

Children with a scrofulous habit are markedly different in appearance 
from their healthier mates. Most of them have a transparent, white skin, 
with delicate blue veins ; large, lustrous eyes ; bright red lips, and alto- 
gether look more like wax figures than healthy children. They are apt to 
show abnormal mental development, with an irritable nervous system. On 
the other hand, they may have a large head with coarse features, a thick 
skin, which has a flabby, spongy feel, an enlarged abdomen and cervical 
glands. About the upper lip and the nose there is frequently an over- 
production of fat. 3 In their development no two cases present the same 
characteristics. Chronic inflammations of the skin, especially about the 
face and scalp and at the junction of skin and mucous membranes, are 
frequent, either alone or associated with persistent chronic catarrh of the 
adjacent mucous surface. Coryza, conjunctivitis, ulceration of the cornea, 
and otorrhcea often follow an eczema of the face and neck or alternate with 
it. Laryngitis and bronchitis are obstinately persistent, and may extend to 
the- alveoli and eventuate in phthisis. Pyelitis, cystitis, and vaginal or 
vulvar catarrh are rarer indications of the depraved condition. 

The articular manifestations may appear as a simple synovitis or tumor 
alius, or some slight injury may be the starting-point of caries and ne- 
crosis, with suppuration, burrowing of pus, and complete destruction of the 
joint. 

Glandular enlargements so invariably develop sooner or later in scrofulous 
patients as to be accepted as the most characteristic lesion. This enlarge- 
ment, which is non-inflammatory and due to cellular hyperplasia, is very 
gradual, and forms a smooth, firm tumor, which, with similar adjacent 
glands, may unite in an irregular, shapeless mass. Occasionally these 
hypertrophied glands subside, but more frequently they finally excite in- 
flammation with suppuration or caseous changes. 

The disease progresses slowly with periods of apparent well-being, but 
toward puberty pulmonary disease is apt to be established ; or, if there has 
been much suppuration, waxy degeneration may occur in the viscera or in- 



1 Buhl favors a specific virus theory, but the parasitic origin rests on no certain anatomical facts. 
* Birch-Hirschfeld found tubercles in nine out of ten lymphatic glands removed from the necks of 
scrofulous patients. 

3 Canstatt calls this latter the torpid, and the former the erethitic form of scrof ulosis. 



EICKETS. 



951 



testinal tract. Such a condition will not long continue without the devel- 
opment of extreme anaemia and a characteristic cachexia. 

Differential Diagnosis. — Scrofulous developments per se can hardly be 
mistaken for any other disease, and a question of diagnosis can only arise 
as to the nature of chronic degenerative changes other than glandular. 
Such a diagnosis can be made from the obstinacy of the disease and coinci- 
dent evidence of the peculiar diathesis. 

Prognosis. — The prognosis is good when the patient is seen early, and 
means exist for a change of diet and surroundings. Scrofulous children 
may die from tuberculous intestinal disease, acute hydrocephalus, or croup. 

Treatment. — The prophylactic treatment embraces a consideration of all 
the laws of health. Until unhealthy, old and closely related individuals 
cease to marry, until children receive the proper amount and kind of food 
for the first two or three years of life, scrofula will exist. 

The diet of scrofulous children should be the same as that advised in the 
treatment of chronic phthisis (q. v.). Cod-liver oil will be the chief agent 
for arresting its progress and development, and should be given daily dur- 
ing the greater portion of infantile and adult life. Iodine is no longer re- 
garded as a specific. Chloride of calcium and the sulphites have been recent- 
ly highly recommended. Sea or brine baths or even ordinary cold water 
baths are frequently of the greatest benefit. The treatment of the skin, joint, 
and eye complications, and the question of extirpation of scrofulous glands, 
belong to the domain of surgery. 

EICKETS. 

Rickets or rachitis is a disease of general malnutrition with characteristic 
lesions in the osseous structures. 

Morbid Anatomy. — Deficient ossification is the essential pathological 
change ; bones already ossified are softened, and ossification in parts still 
cartilaginous is prevented or delayed. Growth of the bone is retarded or 
advances in an irregular manner, and while the medullary cavity increases 
the osseous shell becomes deficient, owing to proliferation of unossified 
matter at its circumference. There is an undue development of the car- 
tilaginous epiphyses and fibrous periosteum, 1 causing the clumsy appearance 
of rachitic bones. The flat bones are greatly thickened at their circumfer- 
ence, from proliferation of the periosteum, but thinned at their centres, — a 
condition called craniotabes: — this is especially marked in the occipital and 
other cranial bones. In the lower jaw the anterior wall of the alveolus is 
sometimes perforated by the milk teeth. 

The liver, kidneys, spleen and lymphatic glands are often enlarged from 
irregular hyperplasia of their fibroid and epithelial elements, conjoined 
with a deficiency in earthy salts. The brain enlarges from increase in its 
neuroglia. The muscles are small, pale, flabby, and soft, and their striae are 

1 Virchow thus describes the changes in the diaphyses:— (1) Increasing density of periosteal prolifera- 
tion and progressive rarefaction of the substance in the areolae and cancellated tissue. (2) Deficient os- 
sification of the cancellated tissue and continuance of the deep layers of compact exterior substance. (3j 
Partial formation of cartilage in the areolae. 



952 



CHKONIC GEKERAL DISEASES. 



very indistinct. The ligaments are also wasted. The fontanelles close 
very late in rachitic children, and, on this account, chronic hydrocephalus 
maybe suspected. 

Etiology. — Our knowledge of the primary "blood changes which result in 
deficient ossification is largely theoretical. It has been supposed to be : 
(1) the presence of lactic acid holding the salts in solution ; (2) deficiency 
of lime salts ; (3) an inflammation of the epiphyseal cartilages and perios- 
teum (4) some irritant in the blood. 2 Clinically, rickets is caused by 
anti-hygienic surroundings. Poor or deficient food and foul air are the 
most potent factors. Acute disease and troublesome dentition predispose 
to it. It is more apt to occur in children of rachitic, syphilitic, or phthisi- 
cal parents. 

The disease usually develops during the first year of life, and is rare be- 
fore the seventh month or after the seventh year of life. 3 Foetal and con- 
genital forms occur, and in many cases no cause can be ascertained. 

Symptoms. — Usually gastro-intestinal disturbances are the earlier symp- 
toms of rickets. There may be vomiting, and the motions are frequent, 
pasty and offensive. The child, when awake, is listless and drowsy, and 
when asleep is restless and sweats profusely, mainly about the head and 
upper parts of the body, regardless of the temperature of the room. He 
dislikes to be disturbed and frets when any one approaches his cot. There 
is an intolerance of the bedclothes, which the child is constantly throw- 
ing off. 

The final distinct evidence of the osteal changes is the enlargement 
of the lower extremity of the radius and tibia and of the corresponding 
portion of the ulna and fibula. The softened bones yield readily to 
pressure, and if the child is allowed to stand or walk, the legs become bent 
and twisted, and the gait unsteady and swaying. The limbs may remain 
perfectly straight, though stunted, thin and flabby, when the disease oc- 
curs very early in life. The head is large and elongated antero-posteri- 
orly, the fontanelles are wide and the sutures thick. The forehead is very 
prominent, while the face is small and wizened, with the skin wrinkled as 
in old age. The lower jaw is shortened, so that the upper teeth overlap 
the lower. The teeth appear late, the incisors may not appear until the 
end of the first year, and dentition proceeds very irregularly. The spine 
is curved, and distortions of the ribs induce an unsymmetrical or oblique 
thorax. 

Eachitic children are usually pigeon-breasted, and there is often marked 
deformity of the pelvis. The joints are large, loose, and lax. The child is 
short for his age, and the limbs are short in proportion to the trunk 
and head. The abdomen is prominent, and the liver and spleen will 
usually be enlarged ; sometimes their enlargement gives the first indication 
of rachitis. The large cranium, thin face, and distorted limbs cause a 
rachitic child to present the appearance of a monstrous deformity, when 
intellectually it is bright and mature beyond its years. Eachitic children are 



i Niemeyer. 2 Wagner. 

3 Rehn states that he never saw it develop after the third year.— Centralb.f. KindrJi., 1877 to '78. 



ALCOHOLISM. — DELIRIUM TREMENS. 



953 



anaemic and very sensitive to changes of temperature. 1 The nervous sys- 
tem is very impressionable, and general convulsions or spasms of the larynx 
are frequent. All rickety children do not emaciate, and some only suffer 
pain when they attempt an exertion. 

Persons who were rachitic in infancy not infrequently become very 
strong as they reach adult life. They remain of short stature and the 
deformities persist. In foetal rickets the body is large and plump, the ab- 
domen protrudes, all the abdominal organs being large, the skin is thick, 
and the extremities are short and thick. In these cases the chicken- 
breast is not present. 

Differential Diagnosis. — The nocturnal sweats about the head, the osseous 
changes, the enlargement of the spleen and liver, the weakness of the legs, 
the rims around the cranial bones, the large, lax joints, and the gastro- 
intestinal disturbances form a train of symptoms that prevent rickets 
from being confounded with any other disease. 

Prognosis. — As a rule, when the cause is removed the disease will dis- 
appear. The greater the thoracic deformity and the longer the disease has 
existed the worse the outlook. Bronchitis, pneumonia, enteritis, laryn- 
gismus stridulus, convulsions, difficult dentition, diarrhoea and chronic 
hydrocephalus are not infrequent complications. Death may occur from 
the wasting and anaemia, from the complications, or from asphyxia due to 
thoracic deformity. 

Treatment. — Cleanliness, fresh air, and nutritious food suitable to the 
age of the patients are of the utmost importance. Children kept too long 
at the breast often become rickety ; they should be weaned at once and have 
liquor calcis saccharatus added to their food. Cod-liver oil should be taken 
as early and in as large doses as the child can digest. Scraped raw beef r 
with a small amount of wine, often produces marked improvement. The 
intestinal derangements are best corrected by castor oil or rhubarb and 
soda. In older children quinine, iron, and lime preparations may be ad- 
ministered. 2 The hydrate of chloral is to be used for any nervous derange- 
ments. Rickety children should not sleep on feather beds or high pillows, 
and must not be allowed to run about or exert pressure on any part that 
may become deformed. Orthopaedic measures are treated of in works on 
Surgery. 

ALCOHOLISM. DELIRIUM TREMENS. 

Alcoholismus may be acute or chronic. Acute alcoholismus often mani- 
fests itself as delirium tremens. 

Morbid Anatomy.— In acute alcoholismus the mucous membrane of the 
stomach and duodenum is intensely injected. Patches of aphthae are found 
upon it, and the mucous surface of the stomach is covered with ropy mucus 
slightly tinged with blood. The gastric juice is altered in quantity and 
quality. The brain, lungs and kidneys are the seat of active hyperaemia, 

1 Barthez regards a blowing sound audible over the cranial sutures, as diagnostic of the affection. 

2 Recently the phosphates have been more recommended than cod-liver oil. The fluorides and arsenic 
are esteemed highly by German physicians. 



954 



CHRONIC GENERAL DISEASES. 



and the pericardium and pleura are often filled with bloody serum. In 
chronic alcoholismus there is chronic gastritis, congestion or cirrhosis of 
the liver, emphysema and bronchitis, fatty degeneration and dilatation of 
the heart, atheroma of the vessels, and Bright's disease of the kidneys. 
Chronic meningitis and pachymeningitis are common. In long-standing 
cases cerebral softening occurs, and in such the viscera are fatty and the 
subcutaneous tissue and omentum are loaded with fat if the subjects are 
beer or wine drinkers ; those who drink spirits are emaciated and grow pre- 
maturely old, on account of the increase in connective-tissue. Frequently 
the abnormal accumulation of fat in the abdomen is in striking contrast 
with the thin, wasted limbs. 

The blood in chronic alcoholismus contains more fat than normal ; one 
of the first effects of alcohol is a true chemical combination with nerve- 
tissue, and as the ingestion of spirits is constant, the nerves progressively 
atrophy and harden. This is hastened by general interference with nutri- 
tion from poor blood. The face of the confirmed toper shows turgid and 
varicose veins, — especially about the nose, which becomes clubbed, — in- 
jected conjunctivae, and pimples of acne rosacea. Puffiness under the 
eyes indicates the changes taking place in the kidneys. 

Etiology. — Even more deleterious than alcohol itself are the adulterations 
of fusel oil, wormwood, and cocculus indicus. Delirium tremens comes on 
after a prolonged debauch in an old drinker, or when one unaccustomed to 
alcohol takes a comparatively large quantity of raw spirits. After ex- 
posure to cold, prolonged abstinence from food, or some exhausting dis- 
ease, a small amount of alcohol may induce acute alcoholismus. Chronic 
alcoholismus is often met with in families where epilepsy, hysteria, in- 
sanity, and allied disorders show themselves. In such cases a peculiar 
constitutional condition which renders abstinence from alcohol especially 
difficult, is undoubtedly present. 

Symptoms. — In acute alcoholism, after a period of exhilaration and semi- 
delirium, acute coma is very apt to supervene ; in this condition the breath- 
ing is stertorous, the face is pale, and the pupils as a rule are dilated. 
The skin is co'id and clammy, and the temperature below normal. The 
urine may be albuminous, and always contains more or less alcohol. Some- 
times control over the sphincters is lost. In rare cases delirium tremens 
occurs after the first debauch. 

In clironic alcoholismus there is muscular tremor and pyrosis, or vomit- 
ing on waking, with entire loss of appetite, the sleep is disturbed, and there 
is headache and vertigo ; the will-power and memory are progressively 
weakened until entirely lost, the gait becomes ataxic, the face is flabby and 
the eyes watery. The breath and sweat have a peculiar, offensive odor, 
the generative functions are enfeebled, muscular tremors become constant, 
and the patient is in a continued state of dread or anxiety. 

Delirium tremens occurs most frequently in old topers after a severe 
drinking bout, or it follows the sudden withdrawal of stimulants. 

The early stages are marked by great mental depression and anxiety — 
the condition known as "the horrors." There is complete anorexia, the 



ALCOHOLISM. — DELIKIUM TKEMEKS. 



955 



muscular tremor becomes prominent, and the patient's sufferings are 
increased by a persistent insomnia. At this stage the pulse is weak and 
feeble, though often rapid, and the surface cool and often covered with a 
free perspiration. 

For several days this condition continues, the patient's mind remaining 
clear notwithstanding the extreme depression. The advent of the second 
stage is marked by temporary mental aberration. Gradually these wander- 
ings become more prolonged, and the victim no longer appreciates, as he 
did at first, the unreality of sights and sounds which torment him. These 
delusions and hallucinations may begin very simply as imaginary questions, 
voices, or visions of persons. More frequently they begin, and in any case 
quickly become, extremely horrible in character. Visions of snakes and 
toads and all manner of crawling vermin, of wild beasts and still more 
ferocious men, fill the sufferer with the most agonizing fear. He may 
cower in a corner paralyzed with fear, or attempt to grapple with his 
imaginary tormentors. Such patients may attack their attendants with an 
insane fury. During this delirium the patient talks incessantly ; is con- 
stantly moving in a quick, nervous manner. His eyes assume a wild or 
vacant expression, the face is drawn, and gives evidence of the mental 
distress. The pupils are contracted, the pulse is still more rapid, and, as 
exhaustion supervenes, what has been a weak pulse becomes distinctly 
dicrotic. From the first the muscular tremor is persistent, and may even 
increase as the delirium becomes more violent. Insomnia is still the most 
dangerous symptom. Four or five days may pass before the patient can be 
made to sleep, or before be passes into a state of coma vigil. In the former 
case the delirium is lost in sleep, and usually does not reappear when the 
patient wakens, or, at most, is speedily ended by renewed sleep. When 
such a patient can fall aslee]3, he usually passes to a more or less speedy 
recovery. But when the delirium passes into coma vigil it is attended by 
marked typhoid symptoms, whicb are the precursors of death. Under such 
conditions a partial delirium continues until complete coma supervenes, 
shortly before the fatal termination. At times an attack of delirium tre- 
mens becomes distinct alcoholic mania or an acute melancholia, which per- 
sist for long periods. Other cases of chronic alcoholismus develop chronic 
dementia with suicidal tendencies, and may become permanently insane. 
Such cases are rare with acute alcoholismus. 

Differential Diagnosis. — The coma of alcoholism may be confounded with 
urcemic coma, which has already been considered. Its diagnosis from apo- 
plectic coma will be considered under apoplexy. 

It can only be distinguished from opium poisoning by an examination of 
the contents of the stomach, and by an examination of the urine. 

The delirium of acute diseases will not be confounded with delirium tre- 
mens if the history of the case and the patient's temperature be taken. 

Meningitis is distinguished from alcoholismus by the firm, hard pulse, 
the pyrexia, the projectile vomit, the retracted abdomen, the photophobia 
(absent in alcoholismus) and the agonizing headache. 

Chronic alcoholic tremor has been confounded with shaking palsy (q. 



956 



CHRONIC GENERAL DISEASES. 



v.), with locomotor ataxy and softening of the brain; their differential 
diagnosis will be considered in connection with the history of these dis- 
eases. 

Prognosis. — The prognosis is good if the patient is manageable. Death 
may occur in acute alcoholic coma, and from acute lobar pneumonia which 
so often complicates it. A patient in delirium tremens may suddenly pass 
into a comatose state, which will soon be followed by death. The degen- 
erative changes which take place in the vessels and viscera in chronic 
alcoholism predispose to a long list of diseases, and tend to shorten life. 
Insanity, impotence, epilepsy, melancholia, and organic brain diseases, are 
its frequent sequelae. 

Treatment. — In acute alcoholismus the stomach may be washed out and 
the head douched with cold water, or the patient simply allowed to sleep 
off his "drunk." In acute mania the stomach should always be unloaded, 
and cold affusion applied freely. A patient with delirium tremens should 
be restrained in a large, quiet room, from which bright light is excluded, 
and should be watched carefully by a strong, trustworthy attendant. In 
severe cases it may be necessary for the patient's safety to employ a 
strait-jacket. His diet should consist solely of pej)tonized milk, and 
stimulants must be given as demanded by the pulse, and always in moder- 
ate quantities during the period of acute delirium. Alcohol is not to be 
continued after sleep is obtained, or during convalescence. The bowels 
must be kept open by mercurial and saline cathartics. The one great 
object is to secure sleep. This is best accomplished by bromide of potash 
and chloral in full doses, assisted, as may be necessary, by morphia. Mor- 
phia must be given with care, and its use is not to be prolonged. When 
the heart is feeble, strychnia not only increases its force, but augments the 
action of other remedies given to produce sleep. The bromide and chlo- 
ral may be continued until the patient wakes from his sleep free from 
delirium. Large doses of digitalis have been advised, but they fail to sus- 
tain an enfeebled heart. During convalescence the vegetable bitters and 
iron are of service. 



TBICHIKOSIS. 



957 



TEICHmOSIS. 

Trichinosis is a parasitic disease, classed by some among the acute in- 
fections diseases. 

Morbid Anatomy. — Trichina spiralis, in the form of a minute worm, meas- 
uring about one thirty-fifth of an inch in length, enters the human system 
through the intestinal tract after the ingestion of trichinous flesh. The 
muscle larvae mature two days after, and in six days the embryos are born. 
In about fourteen days the migrating progeny reach the muscles. Some 
believe that the blood-vessels are the channels of their conveyance. The 
most prevalent idea, however, is that they pass through the intestinal walls 
and peritoneal cavity and then enter the muscular system. Once in the 




Fig. 190. Fig. 191. 

Encapsulated Trichince in voluntary muscle. Trichinae with calcareous deposits and de- 

x 300. generation of the capsules, x 300. 



muscles, oToid protective capsules are thrown around the entozoa, each of 
which is curled up spirally like a hair spring. The muscular fibrillae sub- 
sequently break down into a granular debris, interstitial connective-tissue 
forms in abundance, and in the neighborhood the muscles have an inflamed, 
gray-red appearance. 

The voluntary muscles are tho:e usually invaded. The ends of the 
muscle — where it becomes tendinous — exhibit the greatest number. The 
diaphragm, lumbar, intercostal, cervical, and laryngeal muscles, and those 
of the eye are the favorite sites. As a rule, the farther from the trunk the 
fewer the trichinae. At times the heart has been infested with them. The 
number of the trichinae in the muscles is greater the longer the disease has 
lasted. 1 Later the capsules become dense, fibrous, cheesy, and even chalky. 



1 Cohnheim states that the muscles have no other changes except those met with in acute infectious 
diseases. 



958 



CHRONIC GENERAL DISEASES. 



At the autopsy of one who has died of trichinosis during the first week, 
only the signs of more or less intense intestinal catarrh are found ; after 
the fourth or fifth week, distinct signs of interstitial and parenchymatous 
inflammation of the muscles are found as fine grajdsh -red striae. Intestinal 
catarrh, enlarged mesenteric glands, peritonitis, venous thrombosis, and 
hypostatic congestion of the lungs are also quite frequently found. En- 
cysted trichinae retain their vitality for a number of years. 

Etiology. — Trichinosis in the human being results almost exclusively 
from eating trichinous pork. The raw flesh is most dangerous ; the more 
underdone the pork the greater the danger. Pork cooked in any way that 
does not kill the trichinae is dangerous. Sausages, ill-smoked ham, or 
quickly-broiled ham, or any form of pork that has not been subjected to a 
moist heat of 170°, is liable to induce it. Salting meat does not necessarily 
destroy the trichinae. Each trichina may give birth to a thousand young ; 
about one-half a pound of pork containing trichinae could rapidly produce 
thirty millions of trichinae. 1 

Symptoms. — The symptoms of trichinosis are first gastro-intestinal and 
then muscular ; associated with these there is more or less fever. After a 
varying time following ingestion of trichinous meat, nausea, vomiting, 
vertigo, anorexia, a feeling of malaise, and a slight febrile movement 
occur. There is almost always diarrhoea, the passages being first brownish, 
fchen yellow ; after a short time there are wandering pains in the limbs, 

which become stiff and painful to the 
iouch, and the muscles are swollen 
rind rigid. In from four to ten days 
oedema of the eyelids, perhaps of the 
entire face, occurs. The temperature 
ranges from 101° to 106° F., the 
pulse from 110 to 120 ; there is photo- 
phobia, and movements of the limbs 
or of the eyes are accompanied by ex- 
cruciating pain. The pain in the 
limbs becomes so great that the patient 
cannot sleep. (Edema of the lower 
extremities is common ; and there 
may be general anasarca. Copious 
perspiration with sudamina charac- 
terize the fever of trichinosis. The 
diarrhoea becomes exhaustive, the 
limbs are paralyzed and the patient 
lies in a state of utter helplessness. 

Abdominal pains are sometimes 
present and the muscles of the ex- 
tremities may become strongly flexed. Deafness and aphonia occur when 
trichinosis of the stapedius muscle or of the muscles of phonation respect- 




Fig. 192. 

Temperature Record in the fourth week of a case 
of Trichinosis. Death on the 29th day. 



i Trichinae have been found in rats, mice, dogs, cats, badgers, etc., and swine get them by eating the 
excrements of the^e auinials or the dead animals themselves, rats and mice especially. 



SYPHILIS. 



959 



ively takes place. 1 When recovery is to occur the symptoms all gradually 
abate. This occurs iu from four to five weeks after the first evidence of 
its commencement. When death occurs it is usually during the fourth 
week, and it may or may not be preceded by delirium. 

Differential Diagnois. — Trichinosis may be confounded with typhoid 
fever, myalgia, Asiatic cholera and inflammation of the muscles. The 
points of diagnosis between trichinosis and typhoid fever have already been 
considered. 

From myalgia, or inflammation of muscles, trichinosis is distinguished by 
the abdominal pains, the diarrhoea, febrile movement, and the history of 
the case. 

Cholera is distinguished from it by the sub-normal temperature, absence 
of sudamina and copious perspiration, and by the presence of the charac- 
teristic rice-water discharges. It is said that the nematoid can be found 
in the faeces. In all cases a diagnosis can be reached by excising a piece of 
the deltoid muscle and examining it microscopically. 

Prognosis. — There are no reliable statistics by which its rate of mortality 
can be determined. It may be complicated by hydrothorax, pneumonia, 
bronchitis, haemoptysis, gastritis, enteritis, peritonitis and anasarca. 

Treatment. — Preventive treatment consists in eating no pork that has not 
been so prepared as to kill any trichinae that might exist. The first indi- 
cation for treatment is to support the patient by a nutritious diet and mod- 
erate stimulus. We know of no means of destroying the trichinae after 
they have once entered the muscles. Very early in the disease a prompt 
emetic or a, brisk purge may remove the trichinae from the intestinal tract. 
Calomel, jalap, scammony and colocynth are efficient for such purpose. 
To allay the fever and overcome the subsequent anaemia quinine and iron 
are of service. The treatment is mainly symptomatic. 



SYPHILIS. 

Syphilis is a specific infectious disease produced only by inoculation. It 
presents a characteristic acute, initial lesion, and multiform chronic mani- 
festations, which follow a uniform order of development, and are of two 
distinct forms, called secondary and tertiary lesions. 

Morbid Anatomy. — The pathological changes in the primary and second- 
ary stages are essentially inflammatory. About the point of inoculation 
there is hyperaemia and cell infiltration, followed by necrosis or ulceration, 
and resulting at first in a papule, and later in a simple excoriation or a 
shallow, indolent ulcer, with characteristic induration and a dirty-gray base, 
which eventually leaves a discolored, retracted cicatrix. This ulcer is the 
typical Hunterian chancre. For its many deviations due to adventitious 
circumstances reference must be made to surgical works. In connection 
with the inflammatory changes of the secondary stage there is proliferation 



1 Cohnhelm states that the position of one suffering from trichinosis is that in which the various 
groups of muscles are least extended. 



960 



CHRONIC GENERAL DISEASES. 



of connective-tissue with new formations which soon subside or merge with 
the tissue in which they occur, producing ostoses, or in vascular organs in- 
duration and atrophy. In the tertiary stage the process assumes the form 
of specific neoplastic formations termed gummata, which may be circum- 
scribed and isolated, but more frequently are infiltrated through the af- 
fected tissue. They may appear as firm, gray, opaque nodules, or as soft, 
translucent masses. They consist histologically of a cell-growth, resembling 
granulation tissue, and, unlike the earlier manifestations, show little tend- 
ency to resolve, but evince a marked tendency to undergo caseous and 
calcareous changes and to produce necrotic processes in the infiltrated tis- 
sue. 

In the skin, mucous membranes, and smaller cartilages and bones, this 
degenerative process results in fatty degeneration, ulceration, and slough- 
ing, and may result in widespread destruction of tissue. In the deeper 
organs it produces more or less circumscribed tumors, composed of ca- 
seous matter, granular detritus, calcareous deposits and fibroid indura- 
tion. The distinction between secondary and tertiary lesions is often more 
distinct clinically than pathologically. The glandular changes which 
appear soon after the initial lesion are permanent, and are due to cellular 
infiltration and hyperplasia, but are not usually attended by suppura- 
tion. 

Etiology. — There is no doubt as to the specific nature of syphilitic poison, 
or its transmission solely by inoculation, which may be mediate, immediate, 
or through the processes of conception. The poison is most frequently 
communicated during sexual intercourse, but inoculation may occur from 
deposition of the poison upon any abrasion of the surface or upon delicate 
membranes, as those covering the sexual organs, without any solution of 
continuity. Thus infection may take place in kissing, or from the use of 
pipes, drinking vessels, etc., upon which the poison has been deposited. 
Nursing children may infect, or receive the poison from their nurse. 
Physicians not infrequently receive it accidentally upon the fingers, or are 
the agents in its transmission by vaccination. 

Even more unfortunate are the victims of syphilitic parents. The poi- 
son in the mother invariably manifests itself in the child, and when in the 
father, infects the offspring and, secondarily, the mother through the foetal 
circulation. The syphilitic poison is most virulent in the primary sores and 
glandular affections, but is present in the blood in decreasing quantity 
through both the secondary and tertiary stages. Late in the disease it is 
found only in the discharges from those organs which are involved in the 
specific processes. One inoculation of syphilitic poison, with rare excep- 
tions, confers protection from all subsequent poisoning. 

Symptoms. — Primary. The period of incubation is variable, but is sel- 
dom less than ten days and averages about twenty-five. The first change 
is the appearance of a dark-red papule, which slowly enlarges, becomes in- 
durated early, is not painful, and may even escape notice. Although it 
may run its full course without becoming moist, generally the apex be- 
comes eroded, leaving a moist surface, or undergoes ulceration. The true 



SYPHILIS. 



961 



chancre does not secrete pus unless it becomes inflamed, but remains a sim- 
ple excoriation, either moist or scabbed, through its entire course. The in- 
duration may be thin and superficial, may simply underlie the excoriation, 
or may spread extensively into adjacent parts. In the course of six or eight 
weeks the sore begins to heal, the induration subsides, and finally there is 
no trace left, or if ulceration has been present, there remains a white or 
slightly pigmented cicatrix. Soon after the appearance of the primary 
sore, the nearest lymphatic glands indurate and enlarge but rarely suppu- 
rate. Nor do they resolve with the healing of the chancre, but remain en- 
larged for months and years, and are eventually joined by other glands 
throughout the body. 

Secondary syphilis includes the earlier and generally lighter affections of 
the skin and mucous membranes, with some of the affections of the organs 
and nerves. The most prominent are those of the skin which usher in the 
eruptive stage of syphilis. They appear from six weeks to three months 
after inoculation, and in nearly one-half the cases before the initial lesion 
has healed. This stage is often attended, at its invasion, by some slight 
fever and constitutional disturbance, marked by weakness, emaciation, and 
wandering pains in the limbs and joints. The cutaneous syphilides assume 
nearly all the types of skin diseases, and present in this multiplicity of 
form a distinctive characteristic. The earlier eruptions are generally the 
simpler forms of erythema, and papules, and are diffused over the surface 
quite uniformly. Later, there appear vesicles, pustules, tubercles, and 
scaly eruptions which are more apt to be gathered in groups. Not infre- 
quently several or all the forms may be present. In all syphilides there 
is a general roundness of form, an absence of pain and itching, and a pe- 
culiar livid coppery color which gradually changes in cicatrices to a glis- 
tening white. 

Secondary syphilis most frequently affects the mucous membranes of the 
fauces and pharynx. In connection with the earlier symptoms there may 
be only a diffuse hyperemia and a redness with or without ulceration ; but 
with the later secondary and earlier tertiary, there is a peculiar dusky red 
appearance, the result of chronic congestion, and more or less thickening 
and induration about ulcers and mucous patches. This condition seldom 
causes any pain or discomfort, and the ulcers may disappear spontaneously. 
Mucous patches appear most abundantly about mucous orifices, as the 
mouth and anus, but may appear on the skin. They are round or 
oval, slightly elevated spots of varying size, with a moist excoriated sur- 
face, which does not ulcerate unless irritated. They appear with the 
earliest eruption and continue with decreasing frequency into the tertiary 
stage. 

The secondary affections of the eye assume the form of iritis with ex- 
tensive exudation, and retinitis, which, appearing with but little pain or 
photophobia, is attended by extravasations and partial or complete abolition 
of function. In connection with the general tegumentary inflammation 
the hair-bulbs are involved, and the hair becomes thin or is lost en- 



962 



CHRONIC GENERAL DISEASES. 



Tertiary.— Secondary symptoms usually pass away after a few months 
and the patient may never suffer further, or, more frequently, he enjoys a 
period of apparent health of from two months to two years, in some eases 
extended to twenty or more years. In other instances there is no break, but 
the secondary lesions merge into those of the tertiary stage. The special 
characteristics of tertiary lesions, as already stated, are the formation of new 
tissue — gummata— and the tendency to cause degenerative and necrotic 
changes. Fibroid change and induration are less frequent results. They 
involve deeper parts, and are not symmetrical, but are persistent and re- 
current. Tertiary syphilis is rarely attended by any fever, and even a ca- 
chexia is wanting in most cases. When present this cachexia is indicated 
by anaemia, with possibly some anasarca and general depression, both physi- 
cal and mental. The skin is dry, harsh, and dirty looking, the face thin, 
the eye dull, and the general appearance that of decay. In the skin, 
gummy tubercles, which may be single or in groups, result in ecthyma, 
rupia, and extensive ulcers, which leave characteristic cicatrices. Sub- 
cutaneous gummata may soften, break through the skin, and form deep 
ragged cavities which heal slowly. Similar processes occur in mucous 
membranes, more particularly of the mouth, pharynx and nose, and may 
destroy the tonsils, fauces, and soft palate, or entirely clear out the nasal 
cavities. The resulting cicatrices produce permanent stricture of the fauces 
or oesophagus, and other deformities. 

Syphilis of the viscera is most frequent in the liver, where it appears as 
gummata or general fibroid induration. All the organs are liable to sim- 
ilar deposits, as the heart and arteries, lungs — syphilitic pneumonia — and 
bronchial tubes, or any abdominal organ. In the bones, caries and necro- 
sis are often chronic states, and diffuse or circumscribed periostitis with 
the formation of painful, tender nodes is very characteristic. These 
nodes do not often suppurate, but are quite permanent. Of even greater 
importance are the lesions of the nerves. The cranial bones and cerebral 
membranes are the seat of nodes and gummy tumors which cause convul- 
sions or paralysis and disturbances of function, as epilepsy and insanity, 
by direct pressure or through inflammatory processes. In the brain sub- 
stance inflammatory softening and induration are the most frequent changes. 
In the eye the cornea, iris, and retina are more frequently affected, and 
the changes differ in degree rather than in form, from those found in the 
secondary stage. 

Inherited Syphilis. — Syphilis may be inherited from either the father 
or the mother. If from the father, the mother will not escape infection 
during pregnancy unless he is in the tertiary stage. Syphilitic mothers 
usually abort two or three times, then produce a weak, unhealthy child 
that dies within a few days. Finally, an apparently healthy child is born. 
It does not develop properly, however, looks old and withered, and in a 
few months secondary eruptions make their appearance with excoriations, 
mucous patches and ulcers about the mouth, nose, anus and genitals. At 
the same time it develops the characteristic snuffles. The nose discharges 
an irritating secretion at first, producing excoriations on the lips. Becom- 



SYPHILIS. 



963 



ing closed it fills with mucus and pus which produce ulceration and ne« 
crosis. Tertiary symptoms appear early, and gummy tumors and fibroid 
indurations may occur in the viscera in connection with the secondary erup- 
tions. Such children have a very characteristic appearance ; they are thin 
and poorly nourished, the skin is pale, coarse and wrinkled, the forehead 
and cheek prominent, the eyes and nose sunken, and the teeth present the 
peculiar pegged appearance. Interstitial keratitis causes defective sight 
and photophobia, and the child, with some deafness, a coarse, harsh voice, 
wrinkled brows and apathetic look, presents a pitiable sight. 

Differential Diagnosis. — For the diagnosis of the primary lesions reference 
should be made to surgical works. As the diagnosis of secondary and ter- 
tiary lesions depends so largely upon their location, they are considered in 
connection with the diseases of the various organs. In inherited syphilis 
the coryza and snuffles, the cracks, excoriations and fissures about mucous 
orifices, with mucous patches, are the early characteristics. Later there are 
the scars on the face and in the throat, the sunken nose, and peculiar teeth. 
In many cases, however, the differentiation can be made only by the results 
of treatment. 

Prognosis. — As a rule the prognosis is favorable before destruction of tis- 
sue has begun, and even afterward the necrotic process may be arrested. 
It varies greatly, however, with the nature of the lesions and their situation. 
In confirmed drunkards, and when the disease assumes a rapid or malignant 
form, the prognosis is grave. In inherited syphilis the prognosis varies 
with the date of the appearance of symptoms. If the eruption is present at 
birth or occurs early the child seldom lives. The longer the disease remains 
latent, the more favorable the prognosis. 

Treatment. — The treatment of syphilis is primarily specific, and confined 
to the use of two drugs, — mercury and iodine. Secondarily it is hygienic 
and tonic, a relation which for a time is reversed in some cases. Specific 
treatment is often unavailing when used alone, but becomes brilliantly suc- 
cessful when assisted by 'fresh air, good food, exercise and rest, with oil, 
iron, quinine and other tonics. 

As a rule mercurials are more efficacious in the earlier, and iodine in 
the later manifestations. Mercury should be given as soon as a diag- 
nosis of chancre is established, but were better omitted until the appear- 
ance of secondary symptoms than used on an uncertain diagnosis. When 
treatment is begun thus early, it should be continued for at least a year, 
and followed by one or two years of a mixed treatment of mercury and 
iodine. 

"When treatment is begun late in the course of the disease either iodides 
alone or a mixed treatment will most speedily remove the lesion, after 
which the patient should continue treatment for a year or more. Gener- 
ally it is well to continue a mild mercurial course for at least six months 
after all lesions have disappeared. The present tendency is toward a more 
extended use of mercury in the later stages of the disease. The methods 
of administering mercury are too numerous to be described in detail : the 
more common, aside from that by the stomach, are, hypodermically, by 



964 



CHRONIC GENERAL DISEASES. 



fumigation, baths and inunction ; the latter being the most desirable for 
children with inherited syphilis. Iodine may be used in its combinations 
with potash, soda, ammonia, mercury, iron, etc. The doses of both 
mercury and iodine must be determined by trial for each case. With 
mercury they should fall short of salivation, but with iodine should 
increase to the limit of the "patient's endurance, or until the lesions yield to 
treatment. 



SECTION VI, 



DISEASES OF THE NEEVOUS SYSTEM. 

{Including Diseases of the Brain, Spinal Cord, and Functional Nervous Diseases.) 
GENERAL SYMPTOMATOLOGY. 

The symptomatology of nervous diseases presents many peculiarities 
which render their diagnosis especially difficult. Nearly every physical 
and rational symptom may be the result of so many different lesions that 
at best it is indicative of the seat and extent of the lesion only, and not of 
its nature, and often only determines the division of the nervous system 
which is affected. Symptoms are, therefore, often entirely negative when 
taken singly, and find their significance only in the order and manner of 
their development, or in their combinations with others equally valueless 
per se. All lesions of nervous tissues result in (1) impairment or abolition, 
(2) exaltatioo, and (3) perversion of function, and may manifest themselves 
through the motor, sensory, co-ordinating, or psychical systems, by symp- 
toms which will vary with the location, nature, and extent of the lesion. 
I shall first consider some of the more important symptoms in their gen- 
eral relations to nerve lesions. 

Motor Paralysis. — Loss of motor power, or voluntary nervous control of 
muscular movements, may exist in all degrees, from the slightest weaken- 
ing or delaying of the nervous impulse to absolute abolition of the impulse, 
or its complete arrest in transit to the muscles. The lighter and interme- 
diate grades are termed paresis, while paralysis is applied to extensive or 
entire loss of motor power. The nature and extent of the paralysis is evi- 
denced in the muscles, so that the muscular condition becomes a matter of 
primary importance. 

(a) Reflex Action. — In many instances, and more especially in spinal 
paralysis from circumscribed lesioos, the muscular force, as indicated by 
reflex movements, is not diminished. Under suitable irritation the appa- 
rently powerless muscles execute violent movements and become powerfully 
contracted. These reflex movements are not always limited to the irritated 
limb, but may appear in other paralyzed muscles. For diagnostic purposes, 
then, reflex action indicates unimpaired nervous connection between the 
paralyzed muscles and the spinal centres, and can never be present when 
the paralysis is due to a disseminated destructive lesion of the nuclei of 
origin of the affected nerves or the nerve trunks, but is generally most dis- 
tinct in disease interrupting the transmission of voluntary motor impulses. 
A very common and patent form of reflex action is known as tendon reflex. 



966 



DISEASES OF THE NERVOUS SYSTEM. 



If in health the tendon of any muscle be struck a sharp, quick blow, there 
will immediately follow distinct contraction of its attached muscles, most 
marked, of course, in the larger muscles, as those attached to the patella 
or tendo Achillis. Abolition or exaggeration of tendon reflex is an impor- 
tant point in diagnosis. Either may be associated with decrease or increase 
of reflex action from irritation of the skin. A third form of reflex action 
is called ankle clonus. This consists in a clonic tremor of the muscles, par- 
ticularly of the leg, occurring whenever the muscle is stretched by flexion 
of the foot, and continues during flexion. In severe eases it may be excited 
by putting the toe to the floor, and then often involves the entire limb. 
Abolition of reflex action may be due to degenerative changes, either in the 
nerve trunk or spinal centre, but exaggeration is generally the result of 
central irritative lesions. 

(b) Electrical Irritability. — Electrical contractility of paralyzed muscles 
may remain normal, be increased, or impaired. When not otherwise speci- 
fied, it is understood that the muscular contraction is produced by a cur- 
rent applied to the motor nerves. When muscles atrophy from disease, or 
are the seat of degenerative changes, Earadic contractility is proportion- 
ately decreased. As dependent upon nerve changes it is not only generally 
retained in both cerebral and spinal paralysis due to interruption of nerve- 
currents, but is frequently, and especially in the latter form, increased. 
When disease involves central nuclei or nerve-trunks, Earadic contractil- 
ity is often rapidly and extensively lost. Such muscles may still react, 
however, to the slowly interrupted galvanic current, even after they fail 
entirely to respond to the Faradic. Indeed, galvanic contractility may 
increase as Faradic decreases, and eventually become more marked than in 
healthy muscles. When nerve-trunks no longer respond to electricity, the 
muscle itself may, in some conditions, still show an increasing electrical 
irritability. This, in its various forms, is called reaction of degeneration. 

(c) Muscular Nutrition. — Muscular nutrition and tonicity generally keep 
pace with contractility ; and the muscles remain firm and are but slightly 
reduced in bulk, or they may become small and flabby, or in some cases 
contracted and rigid. The former condition prevails when disease lies 
above the origin of the implicated nerve, but sudden onset of the disease 
or implication of nuclei or nerve trunks results in flaccid and wasting 
muscles. Eigidity and contraction follow irritative lesions or complica- 
tions and also occur in paralysis of long standing, in which case they are 
mostly due to secondary descending degeneration of the cord. 

General Paralysis. — Lesions resulting in general paralysis of necessity 
involve such important parts as to be followed in most cases by immediate 
death. General paresis occurs in connection with insanity from diffuse 
disease of the cerebral cortex. It implicates all the voluntary muscles, not 
excepting those of deglutition and phonation, but is slight in degree, sel- 
dom extending beyond weakness and sluggishness of movement. 

Bulbar paralysis is perhaps the nearest approach to general paralysis. 
Disease of the pons or medulla generally results in bilateral paralysis, and 
is the cause of the mixed and crossed paralyses occasionally met with, as 
paralysis of both arms, both legs, or one side of the face and the oppo- 



GENERAL SYMPTOMATOLOGY. 



967 



Cerebral Causes. 



site side of the body. Motions of the eye, phonation, deglutition and res- 
piration are especially liable to be interfered with, and death is seldom 
long delayed. 

Hemiplegia is a motor paralysis limited to a lateral half of the body. 
It is generally the result of a lesion above the medulla, and most fre- 
quently of the corpus striatum, but may result from injury to a cerebral 
hemisphere or crus. It occurs on the side opposite to the disease or in- 
jury. Its most frequent cause is undoubtedly apoplexy, but it may be 
due to other cerebral injuries or disease, and not infrequently is functional. 
The causes of hemiplegia may be classified as follows : 

Compression from bone, blood, pus, or inflamma- 
tory exudations. 
Tumors, especially carcinoma, sarcoma, gummata* 
Partial anaemia from thrombosis, embolism, soft- 
ening, aneurism, apoplexy. 
Encephalitis, — abscess. 
^ Atrophy and sclerosis. 

S inal Causes \ ^ s a k° ve > or an y disease affecting a lateral half of 

^ " "" \ the cord. 

Functional Causes.. i H y steria ' c,lorea > e ? ih ^> diphtheria, malaria, 
( poisons, etc. 

Although the paralysis is of central origin, the muscles are seldom af- 
fected uniformly, and it has been noted that those which suffer least are 
such as act in conjunction with their counterparts on the non-paralyzed 
side. The muscles of the arm and leg are chiefly affected, while those ol 
the trunk and neck often escape entirely, so that the body and head remain 
erect and firm. The paralysis is generally descending in its onset, and as- 
cending in its recovery, the leg being last involved and the first to regain 
its power. Occasionally, however, the leg escapes entirely, or it may suffer 
a more complete paralysis than the arm. Of the cranial nerves the third, 
fourth and sixth seldom suffer unless the lesion is in the crus, when the 
third will probably be involved. The fifth, also, as a rule, suffers but 
little, but may be paralyzed in either or both roots, a condition indicated 
by anaesthesia of the face and cornea and paralysis of the muscles of mas- 
tication on the affected side. The facial, on the other hand, seldom 
escapes entirely in lesions at the base. The face becomes blank and mo- 
tionless, the mouth is drawn toward the healthy side, and the paralyzed 
cheek puffs on expiration. The muscles of the tongue may escape or suf- 
fer with the others, and the tongue will then be protruded with the tip 
pointed toward the affected side. When hemiplegia is uncomplicated its 
diagnosis is evident, but if associated with coma it may not be readily ap- 
preciated. The paralyzed limbs, however, will be more flaccid, and when 
raised and released will drop more heavily and limply than on the unaf- 
fected side. If the face is implicated the peculiar expression and retrac- 
tion of one angle of the mouth will be readily appreciated. In the differ- 
ential diagnosis of the causes of hemiplegia the location, nature, and ex- 
tent of the paralysis will be of value, but the most important points will 



968 



DISEASES OF THE ^EKVOUS SYSTEM. 



be found in the history of the case, the manner of invasion and the pe- 
culiar combination of other symptoms. It has been noticed that paralysis 
caused by lesions in the motor tract above the ganglionic cells in the anterior 
cornuaof the cord is seldom followed by much muscular atrophy, or more than 
would be caused by inacti vity, while disease affecting these cells or the peri- 
pheral nerve-trunks produces marked muscular atrophy as well as paralysis. 

Paraplegia. — Bilateral paralysis, of whatever extent, is termed paraple- 
gia, and, when of organic origin, affects only those parts of the body sup- 
plied by nerves leaving the spinal cord at or below the seat of the lesion. 
Its causes may be classified generally as follows : 

Brain { Small clot in the pons. 

^Compression of a lateral half of the cord from bone as in 
« • i J fracture, caries, dislocation, spina-bifida, from blood 

^ j (traumatic), pus, exudations, tumors, all diseases of the 

I cord, shock and concussion. 
Peripheral . . \ Inflammation or degeneration of nerve-trunks. 
Functional.. -{ Hysteria, catalepsy, rheumatism, syphilis, poisons. 
Reflex \ Diseases of genito-urinary organs, diseases of intestines. 

Organic paraplegia, therefore, is commonly of spinal origin, and in extent 
varies with the seat of the lesion. If this is located in the dorsal region 
the lower extremities alone are affected ; the paralysis becomes more exten- 
sive the higher in the cord it has its origin ; when this is in the cervical 
region the entire body, including the diaphragm, may be paralyzed. In 
all forms, however, the sphincters are liable to be involved. Generally if 
the disease is high up there will be spasm and retention ; if low down, 
paralysis and incontinence. Paralysis may be of all grades and varieties, 
according as more or less of the thickness of the cord is involved. There 
may be simply slight paresis, decided paralysis with sensation unimpaired, 
or complete paralysis of both motion and sensation. Disease of the cord 
has a special tendency to be un symmetrical, and confined to particular 
tracts As a result, the effects are very varied. When the changes are 
confined to a lateral half, motor paralysis affects the parts below on that 
side ; but owing to the immediate decussation of sensory fibres on entering 
the cord, and their consequent implication with motor fibres of the other 
side, anaesthesia is found on the opposite side of the body below the lesion, 
with possibly a distinct line of anaesthesia marking the upper boundary of 
motor paralysis. The limitation of spinal lesions to distinct tracts has given 
rise to such characteristic combinations of symptoms as to lead to their being 
considered as special diseases. 1 

Aside from the foregoing forms of paralysis for the most part due to inter- 
ruption of the connection between nerve-nuclei or trunks and the higher 
centres, paralysis may result from direct injury to, or destruction of, these 
nuclei or trunks. In such cases the paralysis is confined to the distribution 
of the affected nerves, is generally more complete and permanent than in 
other forms, and is attended by rapid loss of Faradic irritability, with wast- 
ing of the muscular tissue and the reaction of degeneration. 



1 See Locomotor Ataxia, Progressive Muscular Atrophy, etc. 



GENERAL SYMPTOMATOLOGY. 



969 



Spasms, Convulsions. — In determining the seat and nature of the disease 
causing spasms the same anatomical facts are to be considered as in the 
diagnosis of paralysis. It is probable that irritative lesions of the same 
centres as are affected in paralysis result in motor disturbances ; hence con- 
vulsions of a lateral half of the body may be ascribed to irritation of the 
opposite cerebral hemisphere, corpus striatum or crus. In a similar man- 
ner spasms confined to the lower portion of the body and bilateral are to 
be considered of spinal origin, while general convulsions may be the result 
of general cerebral disturbance or of a general affection of the cerebro-spinal 
system. Basing the diagnosis upon our knowledge of the motor areas of the 
cerebral cortex, it is possible in many cases to locate the lesion quite exactly 
by careful consideration of the location and extent of the convulsive move- 
ments. Spasms are even more varied in their distribution than paralysis, 
affecting single muscles, muscular groups, a single limb, half the body or 
all the muscles, not excepting those of respiration and deglutition, and 
they vary in degree from light fibrillary twitching to such violent cramps 
as to rupture muscles or to fracture bones. When the contractions are 
persistent they are termed tonic, but when rapidly alternating with relaxa- 
tion are called clonic. Convulsions appear as symptomatic of both organic 
and functional disease. Tremulousness of the muscles often accompanies 
paresis, and paralysis is frequently followed by tonic contractions. Fibril- 
lary twitchings are common in debilitated conditions, in general paresis, 
the typhoid state, paralysis agitans, etc. ; while the severe forms are illus- 
trated in inflammatory conditions of the brain and cord, epilepsy, tetanus, 
strychnia poisoning, hydrophobia, etc. 

Sensory Paralysis, Anaesthesia. — Anaesthesia, like motor paralysis, may 
be located in any part of the body, may be of all degrees, and may be super- 
ficial or extend to deep parts. When slight it is only a sense of numbness 
which gives the impression of some soft substance covering and protecting 
the parts, and is generally attended by formication or burning prickly pains. 
In complete anaesthesia the patient is unconscious of the severest injury, 
and bed-sores may denude the bones without his being aware of their ex- 
istence. In some cases sensations of heat and cold are still appreciated, 
while all other sensibility is lost. Among perverted sensations may be 
placed those conditions in which sensation is delayed, and the patient ap- 
preciates the impression only after the lapse of some seconds, or is unable 
to determine its nature. In many cases he suffers severe neuralgic pain in 
the anaesthetic parts, due to the central nervous irritation. Anaesthesia 
may be general with general paresis in insanity, but rarely so in other con- 
ditions. It more commonly appears as hemi-anaesthesia, from causes sim- 
ilar to those of hemiplegia, but is less frequent than the latter. It most 
frequently depends upon lesion of the external capsule or fibres of commu- 
nication between the optic thalamus and hemisphere, and frequently impli- 
cates some of the nerves of special sense. Lesions of the tegmentum of the 
crus also result in opposite hemi-anaesthesia. Spinal anaesthesia is also far less 
frequent than paraplegia, but when present is almost always associated with 
paralysis. The condition of reflex action will indicate somewhat its nature. 



970 



DISEASES OF THE NEKYOTJS SYSTEM. 



When paraplegia and anaesthesia are the result of destruction of nerve nu- 
clei in the cord, or of injury to the nerve-trunks supplying the paralyzed 
part, reflex activity will be abolished. When, however, the paraplegia is of 
parts below a spinal lesion, reflex action is normal or often increased. As 
noted before, a lesion of a lateral half of the cord may give a paraplegia 
compounded of motor paralysis on the side of the lesion and sensory paral- 
ysis on the opposite side. 

Hyperesthesia. — Hyperesthesia, either general, partial, or of the nerves 
of special sense, is of common occurrence in nervous disease, since it may be 
the result of the most trivial disturbances. It is present in the congestive 
or early stages of inflammatory conditions of the brain and cord, and in 
functional disturbances. It is often a symptom in the earlier stages of fe- 
brile diseases and in inflammation of the skin. When normal sensation 
becomes painful, it is termed dysesthesia, and appears as gastralgia, enteral- 
gia, or, in the nerves of special sense, as sparks and flashes of light or even 
the appearance of distinct forms of men and animals, ringing or violent ex- 
plosive sounds, and, in some cases, continuous conversation, or as disturb- 
ances of taste and smell. 

Disorders of co-ordination are of rare occurrence except in connection 
with sclerosis of the posterior columns of the cord. Disease of the cerebel- 
lum is indicated by lack of co-ordination, a staggering gait, or entire ina- 
bility to maintain the erect position. 

Mental Disturbances. — All forms of cerebral disease are attended by 
more or less perversion of the mental powers, but such symptoms are sug- 
gestive only of the general nature of the cerebral changes, and but remotely 
of the character of the lesion. Hyperemia and inflammatory conditions 
generally produce at first exaltation of mental processes which may vary 
from simple excitement to the wildest delirium. On the other hand, any 
lesion which causes sudden shock to nerve centres or interferes with nutri- 
tion, either by simple pressure or through destruction of the cerebral tissue, 
is generally indicated by depression or abolition of mental power. Patients 
evince the most varied forms of mental disturbance, and at different times 
suffer in their emotions, intelligence, or will. They may be happy, 
hilarious, angry, or sober, melancholy, sullen and distressed. In intel- 
ligence they may appear brilliant, vivacious, and the exaltation may extend 
to delusions and hallucinations, or they may lose all reasoning power and 
memory and become idiotic. Delirium of meningeal origin is generally 
active or even maniacal, but becomes low and muttering, as in the typhoid 
state, when the lesions implicate the cerebral ganglia and result in general 
nervous depression. Like all other symptoms of similar origin it com- 
monly ends in coma, with abolition of sense, sensation and voluntary 
motion. Although com,a is the usual termination of cerebral disease, it is 
dependent upon many other and diverse causes, and often demands a 
differential diagnosis as to its origin. Its causes are classed as cra- 
nial or extra-cranial, although they all act directly upon the cere- 
brum. 



GENERAL SYMPTOMATOLOGY. 



971 



The more common causes are : 

( Hyperemia, Anaemia, (Edema, Compression, Tumors, 

Cranial . . •< Thrombosis, Embolism, Apoplexy, Abscess, Soften- 

( ings, Shock, and Concussion. 

C Hysteria, Epilepsy, Uraemia, Ammonaemia, Cholaemia, 
Extra Cranial.. -< Poisons of drugs, Narcotics and Anaesthetics, Anti- 

( spasmodics, Alcohol, Poisons of fevers, Malaria, etc. 
Trophic Changes. — Many forms of nervous disease are attended by pecu- 
liar and rapid trophic changes throughout the body. They appear in the 
skin, muscles, joints, bones, and viscera. The more common are bed-sores 
and inflammations of the urinary tract. It may suffice to say generally 
that trophic changes are associated only with inflammatory or irritative 
lesions, which implicate the nerve-trunks or their nuclei of origin in the 
case of motor nerves, but in the case of sensory nerves maybe located in the 
gray matter of the posterior portion of the cord. Injury of motor nerves 
generally results in muscular or arthritic changes^ while cutaneous changes 
are dependent upon lesions affecting sensory nerves. 



972 



DISEASES OF THE NERVOUS SYSTEM. 



DISEASES OF THE BRAIN 

will be considered under the following heads : — 

I. Cerebral Hyperemia — active or V. Cerebral Softening, 

passive. VI. Cerebral Apoplexy. 

II. Cerebral Ancemia. VII. Abscess of the Brain. 

III. Meningitis. VIII. Cerebral Tumors. 

IV. Cerebral Thrombosis and Em- IX. Sclerosis of the Brain. 

holism. X. Hypertrophy of the Brain. 

CEREBRAL HYPEREMIA. 

{Congestion of the Brain). 

Cerebral hyperemia is an increase in the quantity of the blood within the 
capillaries of the brain. It maybe active or passive. In active hypere- 
mia there is increased current, and the blood is "arterial, while in passive 
hyperemia the current is retarded, and there is an excess of venous blood. 
It seems probable that both forms of hyperemia may really produce ane- 
mia, so far as the cerebral nutrition is concerned, by compression of the 
capillaries and lymph spaces. 

Morbid Anatomy. — In passive hyperemia, the veins and sinuses are en- 
gorged with blood, and, when long continued, the dura mater appears 
distended, and sometimes the cerebral convolutions are flattened, with a de- 
cided pinkish color in the gray substance. On microscopical examination, 
the perivascular lymph spaces are seen greatly diminished, or possibly ob- 
literated. In the former case, large pigment granules are scattered outside 
the vessels along their line. 

On section, the white substance is seen dotted with numerous blood 
points, and the cortex is grayish red. At the lower portions of the cere- 
bellum there are dark red patches. In active hyperemia the small arteries 
are enlarged, and the capillaries of the meninges are distended. This may 
be accompanied or followed by oedema of the pia mater and distention of 
the ventricular cavities. 1 The condition of the membrane is no guide, 
either to the existence or degree of hyperemia, and transitory active or pas- 
sive hyperemia often leaves no trace discoverable at the autopsy. 2 

Etiology. — Active hyperemia may be due to increase in the blood press- 
ure, from excessive action of the heart, from contraction of the surface 
capillaries during a chill, from prolonged mental labor, intense emotion, 
digestive disturbances, acute blood poisoning, increased atmospheric press- 
ure, and gravitation from a prolonged recumbent posture. Local arterial 
anemia in other parts of the body, such as arises from sudden cold to the 
surface, intense muscular exertion, and pressure of tumors or dropsical 
fluids on the main branches of the aorta, may also induce active hyperemia. 3 

1 Ecker states that the capillaries and small vessels are sometimes double their normal calibre. Niemeyer 
and Nothnagel state that atrophy of the brain may result from chronic passive hypersemia. 

2 Many pathologists, while admitting the possibility of partial congestion, ascribe to post-mortem 
changes what others denominate local congestion. 

3 Watson states that men have been arrested as drunk on cold nights, when they were only suffering 
from active cerebral hyperemia. 



CEREBKAL HYPEREMIA. 



973 



Paralysis of the vasomotor nerves of unknown origin, or severe nervous 
shock, and poisons, alcohol and certain drugs, especially nitrite of amyl, 
will give rise to active cerebral hyperemia. It occurs more frequently in 
hot climates than in cold, and is said to follow breathing exceedingly rar- 
efied air. Insolation is probably more than intense active hypersemia. 1 

Passive cerebral hyperemia, when general, is the result of obstructed 
venous circulation, itself the result of pressure upon the jugular or vena 
cava descendens. Prolonged fits of coughing, playing on wind instruments, 
and prolonged straining at stool may induce it. Any cardiac valvular le- 
sion that obstructs the blood in the pulmonary vessels, or any disease of the 
lungs which offers obstruction to the onw^ard current, will lead to passive 
hyperemia of the brain. Tricuspid regurgitation stands pre-eminent among 
these causes. Partial or complete stenosis of the larynx will induce it, as 
in croup and oedema glottidis. Thrombi in the cerebral sinuses may induce 
passive hyperemia; and it sometimes occurs from feebleness of the incoming 
arterial How. 

Symptoms. — The symptoms of cerebral hyperemia may be grouped in two 
classes : — those of excitement and those of depression. In all cases these 
symptoms are increased by a recumbent posture, by a forced inspiration and 
by stimulants. The symptoms of excitement are a diffuse pain and throb- 
bing in the head, accompanied by dizziness, vertigo, flashes of light, ringing 
in the ears, restlessness, insomnia, and perhaps delirium and convulsions. 
Photophobia is present ; and there may be nausea and vomiting. Sleep is 
usually broken and disturbed from the onset. The gait is unsteady, the mind 
confused, and sometimes the speech embarrassed. In active hyperemia the 
pulse is accelerated, full, bounding, and hard, and the carotids and tempo- 
rals pulsate forcibly. An ophthalmoscopic examination reveals injection of 
the retinal vessels, and the conjunctivae are often suffused. In most cases 
there are both motor and sensory disturbances. As a rule, the mental state 
in active hyperemia is one of exaltation. These patients are irritable, 
peevish and^ highly excitable. They are apt to talk a great deal. When 
coma occurs, the hypersemia is described as apoplectic ; when convulsions or 
spasms are present, it is called epileptic ; and when there is delirium we 
have the maniacal form. The latter is mania ephemera or impulsive insan- 
ity.' 1 Paralytic symptoms are rare in active hyperemia. 

The symptoms of depression are dull headache, vertigo, ringing in the 
ears, with confusion of mind and dulness passing into somnolence, stupor, 
or complete coma. Illusions and hallucinations are uncommon. 3 Con- 
vulsions may occur in children. When due to passive hyperasmia, as is not 
uncommon, there is a cyanotic hue to the face and neck, the jugulars and 
venous system are over-distended, and the arterial system is scantily filled. 
The pulse varies with the etiological (cardiac) lesion. In old people, after 

1 See the interesting experiments of S. Mayer and Pribram (Sitz. der Men. Akad., 1872), in which elec- 
trical or mechanical irrilMtion of the walls of the stomach produced a reflex increase of the vascular press- 
ure and considerable diminution in the frequency of the pulse. 

2 Trousseau and Nothnagel both claim that the epileptic and apoplectiform varieties are either true epi- 
lepsy or are due to actual cerebral hemorrhage. 

s Griesinger describes a peculiar fear of places that seizes patients when in the midst of a crowd or 
while in a certain place or street. 



974 



DISEASES OF THE NERVOUS SYSTEM. 



depression of spirits, or a long period of taciturnity, there follows wander- 
ing delirium, usually nocturnal, talkativeness, and a state often bordering 
on hysteria. The mind becomes more and more inactive, and sensation as 
well as motion is diminished. This condition is followed by coma, with 
stertorous breathing and relaxation of the sphincters. This coma, which 
is frequently interrupted by local or general convulsions, generally ends in 
death. 

Differential Diagnosis. — Cerebral hyperemia may be mistaken for apo- 
plexy, embolism, urcemia, acute alcoliolismus, epilepsy, and cerebral an- 
cemia. 

In cerebral hemorrhage the onset is more sudden ; the coma is more com- 
plete and prolonged, and following the attack there is always hemiplegia. 

In cerebral embolism the onset is sudden ; the face is pale, the head cool, 
the respirations and pulse-rate are rapid and irregular, there is usually evi- 
dence of cardiac valvular disease, aphasia follows the attack, and the symp- 
toms are more permanent than in acute hyperemia. 

In urcemia the coma is deeper and generally preceded by convulsions. 
There is oedema of the eyelids or of the lower extremities, and the urine 
will be found to contain albumen and casts. 

In epilepsy there is usually an aura, and the patient falls as if from a 
blow, uttering the epileptic cry. In the fit, which is of short duration, the 
convulsions are first tonic and then clonic, and there is a bloody froth about 
the mouth. 

The diagnosis between stomachic and cerebral vertigo will be found under 
Diseases of the Stomach. 

It is often impossible to distinguish between acute meningitis and cere- 
bral hyperemia in children, except from the results of treatment, until the 
disease is well advanced. 

In cerebral hyperemia the headache is generally diffused and the pupils 
are contracted, while in cerebral anaemia the headache is vertical and the 
pupils are dilated. In hyperemia there are loss of memory and hallucina- 
tions, in anaemia we have simply incapacity for mental work. In anaemia 
the respirations are hurried, the pulse is quick, feeble, and irritable, there 
are murmurs at the base of the heart and in the vessels of the neck, and 
the face is pale and cold. 

Prognosis. — The prognosis depends upon the cause ; as a rule, therefore, 
passive is less favorable than active hyperemia. The maniacal or apo- 
plectiform variety is the most, the convulsive the least, dangerous. The 
outlook for recovery is best in those whose habits are good, who can ex- 
ercise mental control and avoid excitement, and in those between twenty- 
five and fifty. In youth and old age the prognosis is more unfavorable on 
account of the condition of the cerebral vessels. Accompanying cardiac 
and pulmonary disease, passive hyperemia is a symptom of secondary im- 
portance. 

Treatment. — During an attack of cerebral hyperaemia from whatever 
cause, the patient must be kept absolutely quiet in bed with the head 
raised, and the diet should be the simplest and most easily digested, and 



CEREBEAL ANEMIA. 



975 



taken in small quantities at short intervals. In active hyperemia cold 
to the head and heat to the feet, with the administration of a brisk purge, 
are to be the first measures. The bromide of potassium is beneficial in 
most cases. In severe active hyperemia blood-letting is permissible in the 
form of leeches to the temples or nose. The constant current may be used 
to stimulate the sympathetic nerve, and thus contract the cerebral blood- 
vessels. Some advise zinc in combination with bromide of potassium. 
Ergot and antimony have been used with some success in active hyperemia. 

In passive hyperaemia stimulants may be given with bromide of potash 
or soda. Digitalis is usually indicated. Sulphuric ether, inhaled or given 
internally, often produces good results. In coma due to passive cerebral 
hyperemia, all remedies will prove ineffectual, except quinine, which 
should be given in small doses at short intervals. When cessation of the 
menses or of an old hemorrhoidal flux is followed by cerebral congestion, 
leeches to the anus, sitz-baths, emmenagogues, etc., should be given in 
connection with the other remedies. A change of residence with rest 
from mental work is often of great benefit. 

CEEEBEAL ANAEMIA. 

Cerebral anaemia is a condition in which there is a deficiency in the 
quantity or quality of the blood in the capillaries of the brain. 

Morbid Anatomy. — The principal change in cerebral anaemia is pallor of 
the brain, which may be partial or general, accompanied by serous effusions 
into the meshes of the pia mater. The ventricles are often distended with 
fluid and the veins and sinuses are engorged. 1 In some cases hyperaemia of 
the meninges coexists with cerebral anaemia. Partial cerebral anaemia is not 
often demonstrable. It exists about neoplasia and adventitious products ; 
and may be the result of local pressure, or partial occlusicn of an artery. 

Etiology. — It may be due to general systemic anaemia from excessive 
hemorrhages, or to sudden pulmonary hepatization and congestion in 
other organs. Exhausting discharges, prolonged lactation, etc., induce 
it. Spurious hydrocephalus following infantile diarrhoea is a condition of 
cerebral anaemia. It may result from defective blood nutrition, as in 
chlorosis, or cardiac weakness, mitral or aortic valvular disease, or cardiac 
insufficiency occurring in acute febrile diseases. Eatty heart is even more 
potent than valvular lesions in producing it. Any mechanical interference 
with the supply of blood to the head, as pressure on, or ligation of, the 
carotids, may induce cerebral anaemia. The arteries that form the circle 
of Willis are, in twenty per cent, of cases, so distributed that only im- 
perfect communication exists between their two lateral halves. Mental 
influences through vaso-motor spasm may produce it ; thus fright, joy, or 
anger will, in many, produce syncope due to cerebral anaemia. 

Cerebral anaemia sometimes follows the application of strong electrical 
currents to the spinal region and irritation of the peripheral nerves. It is 
claimed that zinc oxide, the bromides, tobacco, calomel, and tartar emetic, 



1 Golgi claims that there is enlargement of the perivascular lymph-spaces. 



976 



DISEASES OF THE KEEVOUS SYSTEM. 



if long continued, will cause cerebral anemia. Partial cerebral anaemia is 
always due to local obstructions, which may result from narrowing of the 
vessels from disease of their walls, from spasm of their muscular coats, 
from embolism or thrombosis, and from pressure of tumors, blood, bone 
or inflammatory products. 

Symptoms. — The symptoms of cerebral anaemia may appear suddenly or 
slowly. In the former case they are the ordinary phenomena of a fainting 
fit ; the individual becomes dizzy, nauseated, and the sight is obscured ; 
there is ringing in the ears, the pupils dilate, the gait is unsteady, cold 
perspiration covers the surface, the pulse becomes feeble, rapid, and thready, 
and the respirations hurried ; and the patient may fall to the ground with 
slight spasmodic twitchings. Such a condition is common from reflex 
causes. If due to extensive hemorrhage the loss of sight in those that re- 
cover may be permanent. 

When cerebral anaemia comes on slowly it is attended by headache, 
drowsiness, vertigo, muscae volitantes, tinnitus aurium, sometimes attacks of 
total blindness, inability to perform work, insomnia, extreme sensitiveness 
to light and noise, and at times delirium and hallucinations. Notwith- 
standing the maniacal character of the delirium, melancholia is often its 
predominant feature. Though usually of brief duration, it may end in per- 
manent insanity. In most cases the pupils are sluggish and dilated, the 
retina is anaemic, and the headache is confined to a small circumscribed 
spot. The recumbent posture induces insomnia, and the erect position 
often causes a sense of general muscular weakness and faintness. The face 
is pale and cold. In the cerebral anaemia of children — spurious hydro- 
cephalus — restlessness, jactitation, grinding of the teeth, and muscular 
twitchings are followed by symptoms of collapse and coma. 

Differential Diagnosis. — The points of differential diagnosis may be found 
under the heads of Tubercular Meningitis and Cerebral Hyperaemia. 

Prognosis. — The prognosis in cerebral anaemia will be determined in most 
cases by its causes. Where acute anaemia results from hemorrhage, death 
may result, although the hemorrhage has been arrested. The prognosis is 
more favorable when there is no organic disease of the heart or vessels. The 
more speedily the cause can be removed the better the prognosis. In the 
so-called spurious hydrocephalus the prognosis is favorable, if met by 
prompt and suitable treatment. 

Treatment. — In acute anaemia with syncope the head must be lowered at 
once and the patient may even be inverted, cold water may be dashed over 
the face, the vapor of ammonia inhaled, and bandages applied from the 
feet upwards. As soon as consciousne..3 is regained, champagne, ether, 
ammonia, coffee, or other cardiac stimulants may be administered. If these 
measures fail transfusion should be resorted to. Alcohol is to be given 
very cautiously in cerebral anaemia ; and exercise of either brain or body 
must be carefully undertaken. Bromides are never to be given. 1 For 
chronic anaemia the treatment can only be determined by causal indica- 
tions. 



1 Nothnagel advises small doses of morphine for the excitement that precedes anaemic delirium. 



MENINGITIS.— ACUTE MENINGITIS. 



977 



MENINGITIS. 

The membranes covering the brain are the pia and dura mater ; the pia 
mater is a delicate and exceedingly vascular membrane which is intimately 
adherent to the brain, sending prolongations into the sulci and fissures ; 
its connective-tissue is very extensive. The external layer of the pia mater 
is the structure formerly called the arachnoid. The meshes of the pia 
mater were formerly denominated the subarachnoid space. 1 The dura mater 
acts as the periosteum of the cranial bones ; it is firm, not very vascular, 
and encloses venous sinuses between its folds. Its inner surface is covered 
with a layer of endothelial cells. 

Inflammation may have its seat in the dura mater, the pia mater, or both 
may be involved. Inflammation of the pia mater is usually called menin- 
gitis. The term pachymeningitis is applied to inflammation of the dura 
mater. 

When inflammation of the pia mater is attended by rapid changes in the 
membrane and by the effusion of sero-fibrin and pus, with varying quanti- 
ties of red blood globules, it is called acute meningitis. 

So-called sub-acute meningitis is a mild type of acute, in which extensive 
serous effusions are the chief, and at times almost the sole, event, although 
small quantities of lymph, white and red blood cells, and fibrin are usually 
present. 

Inflammation of the pia mater, when chronic, results in thickening, 
opacity, and adhesions. It might be called interstitial meningitis, while 
the acute and sub-acute belong to the class of exudative inflammations. 

The dura mater has an external and an internal layer, the external is in- 
timately connected with the inner surface of the calvarium. Inflammation 
of this layer is called pachymeningitis externa, and is marked by thickening, 
opacity and localized adhesions of the dura with the skull. 

Pachymeningitis interna is an inflammation of the inner surface of the 
dura mater, and may be acute or chronic ; it is usually localized. Chronic 
pachymeningitis interna often results in the formation of flat, oval, lami- 
nated sacs containing blood which lie between the dura and pia mater, 
avA are called hematoma of the dura. 

ACUTE MENINGITIS. 

Acute meningitis is also called simple meningitis of the convexity (from 
its usual site), cerebral fever, and arachnitis. When the unqualified word 
meningitis is used, acute, non-specific inflammation of the pia mater is 
understood. 

Morbid Anatomy. — The inflammatory process may be established in any 
portion of the pia mater ; but it usually involves the hemispheres. Only 
in rare cases is it confined to the base of the brain. There is always more 
or less thickening and redness of the membrane, and it loses its glistening 

1 Handb. d. Hist.— Strieker. 



978 



DISEASES OF THE NERVOUS SYSTEM. 



appearance. Around the vessels where the connective- tissue is most abun- 
dant, there is first a slight serous effusion, which is quickly followed by 
cellular infiltration. An opaque zone of exudation surrounds the vessels. 
In mild cases the exudation is limited to the perivascular lymph spaces. 




Fig. 193. 
Acute Meningitis. 

Portion of the under surface of the Brain, including the middle lobe of the Cerebrum and the 

Cerebellum. 

The opaque exudation is seen upon the cerebral meninges completely covering the pons and surrounding the 
medulla. The basilar artery is dimly seen through the exudation. 

The character of the exudation varies ; it may be serous or sero-purulent, 
and occupy the deeper meshes of the pia mater, or a thick puro-fibrinous 
exudation may cover the convexity of the brain as a firm membrane or a 
creamy diffluent mass. 1 This layer of fibro-pus or false membrane is 
thickest and most abundant in the fissure of Sylvius and the sulci and 
along the vessels, which are visible as red, inosculating lines in a yellow- 
green or distinctly green mass. On raising this layer the brain beneath is 
found studded with minute hemorrhages from the ruptured vessels con- 
necting the pia and gray substance. The white substance may also show, 
on section, numerous puncta vasculosa. The convolutions are flattened, 
the sulci deepened, and the ventricular cavities will contain very little, if 
any, fluid. 2 When the cerebellar pia mater is involved, as in young subjects, 3 
the roots of the cranial nerves about the medulla are sheathed in the exuda- 
tion, and there is inflammatory infiltration of the neighboring plexuses. 

Etiology. — Meningitis of the convexity is most frequent in early adult 
life and in young children. It is more common in males than in females. 
Acute alcoholismus and prolonged and intense mental anxiety and grief are 
among its predisposing causes. Injuries of the cranial bones, as fractures, 
severe blows, or punctured wounds are the most frequent exciting causes. 
Disease of the cranial bones and suppurative inflammation of the middle 

1 Klob is of the opinion that the^ws is furnished in great measure from the arachnoidean epilhelia. 
- Hugnenin states that in meningitis of unknown origin the pia mater is often so adherent that it tears 
away portions of the brain substance when it is removed. 
3 Beduar. 



ACUTE MENINGITIS. 



979 



ear may induce meningitis, and inflammation of the dura mater is often 
complicated by simple meningitis. Diabetes, and irritation caused by cere- 
.bral tumors, or suppuration in the eyeball, and large carbuncles about the 
cranium, have caused it. In many cases of apparent idiopathic meningitis 
it is probable that an infection whose origin has been overlooked is the 
direct exciting cause. 

Meningitis occurs as a complication in certain diseases — as measles, small- 
pox, scarlet fever, ulcerative endocarditis, Bright's disease, acute croupous 
pneumonia, typhus, typhoid fever, diphtheria,- pyaemia and rheumatism. 
Acute alcoholism is said to induce meningitis in children. 1 Long-continued 
exposure to intense heat of the sun under conditions favorable to the de- 
velopment of miasmatic contagious diseases may result in meningitis. 
Finally, meningitis is sometimes idiopathic. 

Symptoms. — The symptoms of meningitis may be divided into the three 
stages of headache, delirium, and coma. Premonitory symptoms, such as 
general malaise, wandering pains in the head and limbs, irritability, in- 
somnia and a sense of impending trouble, are all indefinite " prodromata." 
It may be ushered in by a distinct chill or by repeated rigors. 

Usually the first prominent symptom is intense and persistent headache, 
localized in the frontal, temporal, or occipital region, which increases in 
severity from hour to hour. In severe cases the headache is diffuse, al- 
though it may extend obliquely across the head, or shoot from temple to 
temple. Accompanying the headache 
there is vertigo, intense photophobia, 
loud ringings in the ears, nausea, and 
projectile vomiting. There is cuta- 
neous hyperesthesia, and convulsive 
movements of certain groups of mus- 
cles. The upper and lower extremi- 
ties, and the posterior cervical mus- 
cles suffer most. The face is rarely 
flushed, but has a pale, anxious ex- 
pression. The conjunctive are in- 
jected, and the pupils are contracted 
and respond slowly to light. The 
degree of contraction of the pupil varies 
considerably in different patients dur- 
ing the twenty-four hours. It may 
only be contracted on the same side 
as the meningeal inflammation. 
Aphasia has been noticed as occurring 
in a few cases ; loss of co-ordinating 

power is a marked Symptom, SO that Temperature Record in a case of Acute 
f . _ . . J r * Meningitis. 

the individual has an unsteady, tot- 
tering gait. The temperature, which rises rapidly, reaches 103° or 105° F., 
rarely higher ; it may have a morning remission and evening exacerbation. 



105 
104- 

iot°- 
ioo° 

og°. 



Z. 



3. 



9. 



93° 
97- 



1 Ramskill states that in some instances when impetigo and eczema about the face and head suddenly 
disappear, the symptoms of acute meningitis of the convexity are developed. 



980 



DISEASES OF THE KEKYOUS SYSTEM. 



In those cases which are rapidly fatal there is continuous high tempera- 
ture. The pulse is firm, hard, wiry, and small, varying in frequency with 
the temperature range. The bowels are constipated and the abdomen is 
retracted. In old people the stage of headache may pass unnoticed, and 
the delirium first attract attention. In children general convulsions may 
be the initiatory symptom, with marked strabismus from its very onset. 
If constipation is not present the discharges are scanty and offensive. In 
this class of cases the first stage is always preceded by peevishness and irrita- 
bility, which lasts from a few hours to two or three days. 

In adults the stage of delirium is ushered in by an increase in restless- 
ness, jactitation, irritability, and mental confusion. It is sometimes wild, 
simulating acute mania ; at first it may be present only at night, coming on 
with the evening rise in temperature. In the aged the delirium is typhoid 
in character, or marked by incessant talking. Sometimes the aged are only 
lethargic and stupid. In adults muscular twitchings of the extremities 
and face are present in this stage ; the eyeballs roll about vaguely, the 
flexor muscles are often powerfully contracted in one or both limbs, and 
there may be opisthotonos or even hemiplegia. Paresis of the thoracic and 
faucial muscles causes dyspnoea, irregular respiration, and dysphagia. In 
metastatic meningitis delirium may be the first symptom, and simulate 
delirium tremens, or the patient may be absolutely mute. The result, if 
death does not occur, is sometimes permanent insanity. 1 As this stage ad- 
vances the temperature rises to 104° F., the pulse becomes more frequent 
and irregular ; the abdomen is retracted, the vomiting continues projectile, 
and the respirations become sighing in character. During this stage the 
pupils are uneven — one may be of normal size while the other is quite 
small ; when the delirium is subsiding they dilate and contract by turns, 
or oscillate. The tdche cerebrate may appear, and herpetic eruptions are 
not infrequent. This stage lasts from one to three days. 

The stage of coma comes on gradually. The delirium subsides, and is 
followed by a tendency to stupor, lethargy, and deep sleep. Headache, 
jactitation, and hyperesthesia disappear. The pulse becomes slow, irregu- 
lar, and intermittent. The pupils are markedly dilated, the breathing is 
superficial and irregular. The patient is insensible to all impressions ; he 
rolls his head and grinds his teeth, picks stupidly at the bedclothes, and 
the face becomes alternately white and red. Gradually the coma becomes 
complete, and the urine and faeces are retained, or the latter are passed in- 
voluntarily. Drawing off the urine may temporarily rouse the patient 
from the coma. The head is drawn to one side, and as the circulation 
is retarded the extremities and face are often of a purple hue. Subsultus 
tendinum is marked. The pulse runs up to 160 to 170, or until it cannot 
be counted at the wrist ; the C hey ne- Stokes" respiration of ascending and 
descending rhythm becomes established. The expirations are puffing. 
The body is bathed in cold sweat, and death results from central paralysis, 
causing asphyxia, or heart-failure and pulmonary oedema. The temperature 
may rise very high or fall to a subnormal just before death. 

1 Vigla, Actes de la Soc. Med. des Hop. de Paris. 



ACUTE MENINGITIS. 



981 



Differential Diagnosis. — Acute meningitis may be confounded with acute 
urcemia, typhus fever, variola, and delirium tremens. 

In urmmia the face will be turgid, and there will be puffiness about the 
eyelids ; in meningitis the face is pale and anxious, and there is no oedema. 
In uraemia the urine will contain albumen and blood or exudative casts ; m 
meningitis only a small amount of albumen is present and no casts. Con- 
vulsions, preceding the coma, are far more common m uraemia than in 
meningitis. The pulse, temperature, and the subjective symptoms of 
meningitis are absent in acute uraemia. In some cases only a microscopic 
examination of the urine will enable one to make a differential diagnosis. 

In typhus fever, although the cerebral symptoms closely resemble those 
of meningitis, the temperature range is higher, often reaching 106° to 
107° F. The pulse is more rapid and compressible in typhus than in 
meningitis. In typhus the countenance has a dull, leaden, or mahogany 
hue ; in meningitis it is pale and anxious. Surface sensibility is blunted 
in typhus, and is exaggerated in meningitis. Vomiting is infrequent in 
typhus, in meningitis it is persistent and projectile in character. The 
characteristic typhus eruption appears on or about the fifth day ; there is 
no characteristic eruption in meningitis. In typhus the pupils are equal, 
in meningitis they are unequal. 

In small-pox the face is flushed, the pulse is full and bounding, there is 
intense pain in the back and loins, the vomiting is retching in character, 
and at the end of the third day the characteristic eruption occurs along 
the roots of the hair. These symptoms are all absent in meningitis. In 
many cases, however, it is necessary to await the appearance of the eruption 
before a diagnosis can be made. 

In delirium tremens there is a busy delirium, the patient imagines 
persons and animals about him, and is wild in his gestures and utterances ; 
in meningitis the delirium is incoherent and milder, but marked by a de- 
sire to get out of bed. The surface is bathed in a profuse, clammy sweat 
in delirium tremens ; it is hot and dry in meningitis. In delirium tre- 
mens the temperature, pulse-rate and pupils are normal ; there is no head- 
ache. 

Prognosis.— The prognosis in acute meningitis is very unfavorable ; severe 
cases terminate fatally, mild cases may recover. The duration varies from 
two days to four weeks ; fatal cases rarely last more than eight days. If 
recovery takes place convalescence may not be fully established before the 
third week. The average duration of the disease is about eight days. 
Strabismus, hiccough, and local paralyses are very unfavorable symptoms. 
The prognosis is better in children than in adults. 

Treatment. — The most important local measures at the onset of the dis- 
ease are local blood-letting and the application of cold to the head. 
Leeches may be applied to the nuchal region or temples. The best method 
of applying cold is by means of the ice-bag or coiled tube, and that it may 
be thoroughly applied the head should be shaved. The patient must be 
placed in a large, quiet, darkened room, with the head elevated and all 
obstruction to the return circulation removed. The bowels must be freely 



982 



DISEASES OF THE NERVOUS SYSTEM. 



acted upon by croton oil, and some drastic purge and saline diuretic are 
indicated if the urinary secretion is scanty. 

In the stage of coma blisters to the back of the neck are of service. To 
relieve the great restlessness which often precedes the stage of delirium, 
hydrate of chloral and opium may be given. Iodide of potash and mer- 
cury are strongly recommended in all stages of this disease, but I have 
never obtained any positive beneficial effects from their use. Strong broths 
and alcoholic stimulants, if indicated, may be administered throughout the 
whole course of the disease. The condition of the bladder and the bowels 
must be carefully looked after during the stage of coma, and especially in 
the meningitis of old age. 

SUBACUTE MENINGITIS. 

Subacute meningitis differs from acute in that it is always secondary, is 
of longer duration, and is attended by less active symptoms. 

Morbid Anatomy. — Upon the convexity of the brain there is found a sero- 
fibrinous exudation, containing few pus globules, and fibrin only in small 
quantities. The effusion will occupy the meshes of the pia and the ven- 
tricular cavities. As a result of the effusion the convolutions are flattened 
and the sulci are deepened. Flocculi of lymph will be found most abun- 
dantly along the line of the vessels of the convexity, and the vessels of the 
pia mater will be more or less distended. The pia mater will be lifted 
from the surface of the brain, will lose its glistening appearance, and in old 
cases will be slightly opaque. 

Etiology. — This form of meningitis may occur during the course of any 
exhausting disease, as chronic diarrhoea, cancer, chronic Bright's disease, 
typhoid fever, etc. 

Symptoms. — Being subacute and always secondary, its early symptoms are 
obscure. The stage of headache is wanting or lasts only a few hours, and 
is never severe. The delirium, which is often preceded by extreme jactita- 
tion, comes on gradually and is always quiet in character, and is character- 
ized by an attempt on the part of the patient to get out of bed and walk 
around the room ; the patient in walking staggers and is apt to fall for- 
ward. The stage of delirium may last only a few hours. In most cases 
headache and delirium are rapidly followed by coma. Thus, if a patient 
with chronic Bright's disease, after a short delirium, passes slowly into a 
state of coma, there is reason to suspect the development of this form of 
meningitis. 

When the active delirium of typhus fever becomes muttering in charac- 
ter, when the pupils dilate and the pulse becomes slow and irregular, sub- 
acute meningitis may be suspected. As the coma begins the respirations 
become sighing and puffing in character, and the urine collects in the blad- 
der. As it deepens, the pulse, which has been slow, is accelerated and in- 
termits ; the expirations are short puffs, and the interval between expira- 
tion and inspiration becomes lengthened. The typhoid state is rapidly 
developed, deglutition becomes difficult, there is blueness of the finger- 



CHKONIC MENINGITIS. 



983 



nails with cyanosis, and the coma ends in death, or is slowly recovered from 
and followed by a long convalescence. 

Differential Diagnosis. — The history of the case will aid very much in its 
diagnosis. Coma being its prominent symptom, the differential diagnosis 
is from other forms of coma. 

From coma of acnte meningitis, of tumors, compression, concussion, or 
cerebral softening, the previous history is sufficient to distinguish it. 

From coma of poison and narcotics it is differentiated by examination of 
the secretions and excretions and by the state of the pupil ; thus, in lead 
poisoning the line on the gums, in alcoholic coma an examination of the 
urine, and in opium coma the pin-head piipils will at once decide. 

Hysteria, epilepsy, and catalepsy are attended with such distinctive signs 
that they cannot be mistaken for sub-acute meningitis. 

Prognosis. — The prognosis of sub-acute meningitis is determined by the 
disease with which it occurs. When it occurs with Bright's disease it is 
usually fatal, but when complicating typhus and other fevers it is fre- 
quently recovered from. 

Treatment. — The chief indication is to remove the cause. In Bright's 
disease, elimination of urea, which is causing the meningitis, should be 
attempted. In typhus fever free ventilation, stimulants, and concen- 
trated nutrition will remove the cause so far as possible. In most instances 
blisters applied to the neck will be followed by marked improvement, 
and not infrequently by recovery. 

CHKONIC MENINGITIS. 

Chronic meningitis is an interstitial 'inflammation of the pia mater, 
which causes thickening and opacity of the membrane. It may be lim- 
ited to the convexity. 

Morbid Anatomy. — The pia mater is thickened, callous, and opaque, and 
maybe infiltrated with serum, pus, and new connective-tissue cells. 1 There 
is thickening of the walls of the blood-vessels of the pia, and of their 
branches which enter the brain substance. These last adhere to the sur- 
rounding brain substance, so that it is torn when the pia mater is lifted 
from the brain. 2 Attendant upon all forms of chronic meningitis there is 
more or less interstitial inflammation of a very low grade of the Irain- 
sulstance (diffuse interstitial encephalitis), although meningitis chronica 
is. not ordinarily diffuse, but limited in extent. When the pia and dura 
mater are bound together, pachymeningitis has preceded the development 
of adhesions. The ventricles usually contain more or less fluid. The 
development along the f alx of glandulce pacchionii is due as much to senil- 
ity as to chronic meningitis. 3 Atrophy of the cortex results from long- 
continued chronic meningitis. 

1 Ramskill states that osseous plates have been found embedded in the thickened membrane. 

2 Some authors describe a degenerative change in the vessels resulting from previous peri- or endarter- 
itis, which is said to resemble colloid metamorphosis. This change is rare. 

3 Foster states that he has seen cheesy degeneration of the exudation lying in the sulci, and that a cyst- 
wall of connective-tissue has formed. 



984 



DISEASES OF THE NERVOUS SYSTEM. 



Etiology. — Chronic meningitis is a disease of adult life, especially after 
fifty years of age. It is often idiopathic, and is met with among the poor 
and badly nourished. It is very frequently a complication of chronic 
alcoholismus, syphilis, 1 rheumatism, gout, and chronic Bright's disease 
(small granular kidney.) It is sometimes of traumatic origin, and is fre- 
quently found in the general paralysis of the insane. 2 

Symptoms. — The symptoms of chronic meningitis are always obscure. In 
some cases there are no symptoms ; patients die of other diseases and 
meningitis is found at the autopsy. In others there are well-marked 
symptoms. The patient grows stupid, dull and apathetic, the mental 
faculties are blunted, and there is headache and a constant desire to sleep, 
or the patient may become morose and fretful. In the old the headache 
comes in paroxysms, and is attended by marked flushing of the face, fre- 
quent pulse and high arterial tension, occasionally attended by delirium. 
In nearly all cases vomiting becomes a prominent symptom, producing 
great exhaustion. Muscular weakness attends the decline in mental pow- 
ers ; the legs tremble in walking, control of the sphincters is lost, and the 
urine and faeces may be passed involuntarily. In many cases, chiefly the 
aged, there is paralysis of the bladder. The appetite' is good, but diges- 
tion is slow and the bowels are constipated. The speech is thick, or the 
power to articulate certain words is lost. Vertigo, tinnitus aurium, and 
muscas volitantes are present, with localized numbness or hyperesthesia. 
The very aged often lie in a stupor, exhibiting no mental or physical signs 
of life except to breathe and take food. 

There is no typical temperature range. Indeed, in many cases there is 
no pyrexia during the whole period of the disease, in others there will be a 
chill and fever resembling in its variations that of malaria. In some forms 
of chronic meningitis hemiplegia occurs, both with and without facial pa- 
ralysis. When the trigeminus is involved the eyeball may slough. 3 Ptosis, 
strabismus, and variations in the size of the pupils indicate that the third 
nerve is involved. • These irregular symptoms may continue with increasing 
severity for months or years. Toward the end convulsions may occur, and 
death takes place in deep coma: 4 

Differential Diagnosis. — The diagnosis of chronic meningitis is always dif- 
ficult. It may be mistaken for cerebral tumors or softening. 

With tumors, the headache is more intense and circumscribed, paralysis 
of nerves of special sense or of certain sets of nerves is common, and the 
signs of general decline in mental and physical power are less marked. 
Chronic meningitis appears in its whole symptomatology to be of a more 
general nature, while tumors produce local symptoms; speech and intellect 
are usually unimpaired. When neoplasias excite chronic meningitis in their 
vicinity the diagnosis is often impossible. 

1 Virchow states that when constitutional ' syphilis exists in the human body, its localization depends 
greatly upon previous states of the system. 

2 Calmeil. 

3 See Effect of cutting fifth cranial nerve, in M. Foster's Physiology, p. 381 to 382. 

4 Many attribute the symptoms of chronic meningitis occurring in the insane, epileptic, and imbeciles to 
a cortical encephalitis frequently found at the autopsy, with the changes of meningitis. 



TUBERCULAK MENINGITIS. 



985 



Softening of the brain is also often associated with chronic meningitis. 
In softening there may be a history of a previous apoplectic seizure ; mus- 
cular contractions are common, and the headache is not so severe as in 
chronic meningitis. In chronic meningitis there is more mental excitement 
than in cerebral softening, and the hemiplegia is more complete after apo- 
plectic seizures. 

Prognosis. — The prognosis is bad; the disease is a progressive one. Only 
in cases of a syphilitic origin can we offer any hope of recovery. Many be- 
come permanently insane, and some die from inanition. Death may also 
result from exhaustion, from cerebral pressure, and from complicating dis- 
eases, as pneumonia, etc. 

Treatment. — The patient is to be kept quiet mentally, and the diet must 
be fluid and nutritious ; stimulants being only administered to sustain vi- 
tality. The bichloride of mercury and iodide of potassium, in small doses, 
are the remedial agents most frequently employed. Blisters may be applied 
to the back of the neck, or a seton introduced there. The bowels need 
careful attention. The urine, if not passed freely, should be drawn and 
the bladder washed out. 

TUBERCULAR MENINGITIS. 

(Acute Hydrocephalus.) 

Tubercular meningitis 1 is an inflammation of the basal pia mater, 
caused by an irruption of gray, miliary tubercles, and occurring most fre- 
quently in children. 

Morbid Anatomy. — The dura mater is rarely involved. The pia mater in 
some cases is congested, in others pale, and it may be infiltrated with 
serum, fibrin, and pus. The vessels along the Sylvian fissure and the an- 
terior peduncles of the cerebellum are studded, especially at their bifurca- 
tions, with miliary tubercles, which lie in the perivascular lymph-spaces. 
The lymph-spaces may become filled, and a covering be thus formed over 
the vessel ; or the miliary granules dot the vessel like a string of beads. 
As they develop they compress and finally occlude the vessels. These gran- 
ules are sometimes met with in small numbers on the convexity and along 
the longitudinal fissure, but are always more abundant at, if not confined 
to, the base, from which they may extend to the pia mater of the cervical 
cord. Even at the base they may be few and limited, or so abundant and 
extensive as to obstruct the circulation and impair the walls of the vessels, 
causing multiple hemorrhages and red softening. 

The inflammatory exudation at the base is a turbid, serous effusion, or 
more commonly a thick, yellow, semi-plastic layer which extends from 
the fossa Sylvii, where it is most abundant, to the inferior surface of the 
cerebellum. When the pia mater of the convexity is involved it may show 
no evidences of exudative inflammation, but present a bright, rosy hue. 
The ventricles are distended by a serous fluid, usually turbid from admix- 

1 Is also called by the Germans basilar meningitis ; and by the English acute hydrocephalus. The dis 
ease was properly named tubercular meningitis by the French. 



986 



DISEASES OF THE NEKVOUS SYSTEM. 



ture of cellular elements, which flattens the convolutions and causes cede- 
matous softening. The membrane of the ventricles is thick and opaque. 
In cases running an acute course, the only lesion except the tubercles may 




Fig. 195. 
Tubercular Meningitis. 

Region of the Sylvian fissure showing at A, A, miliary tubercles along the line of the blood-vessels. 



be a large serous effusion into the ventricles. In most cases tubercular 
meningitis is associated with general tuberculosis. 

Etiology. — Tubercular meningitis is rare before the first and after the 
fifth year. It occurs almost exclusively in children of a scrofulous diathe- 
sis, either inherited or acquired. In such children the tuberculous process 
is latent, and any debilitating disease may excite it, such as diarrhoea, the 
exanthemata, especially measles, whooping-cough, otorrhcea, and skin and 
scalp diseases of a chronic nature, dentition, insufficient or improper 
food, and injuries to the head, more particularly at the base of the 
brain. The immediate cause is the same as in all forms of tuberculosis. 
The bacilli may be carried to the brain from any tubercular focus or from 
sites of non-tubercular suppuration. 

Symptoms. — The symptoms of tubercular meningitis are due not so much 
to the tubercular developments, as to the exudative products of the inflam- 
matory process, as the pia may be studded with tubercles both at the con- 
vexity and base without the slightest symptomatic indications of their pres- 
ence. Its advent is generally very insidious ; if convulsions usher it in, its 
course is rapid. 

The premonitory stage is marked by changes in the nutritive and diges- 
tive processes ; the appetite is diminished and capricious ; the breath is 
offensive, the tongue coated, constipation and diarrhoea alternate. The 
child becomes dull, languid, apathetic, and desires quiet ; its sleep is 
restless and troubled. The face assumes a dull, anxious appearance, and 



TUBERCULAR MENINGITIS. 



987 



when at play the child will stop suddenly and rest its head on its hands or 
the floor. During the progress of these symptoms a cachexia is developed 
and there is progressive emaciation, which in connection with the etiology 
gives rise to the suspicion that the disease is developing. These prodro- 
mata may last from a few days to a month, and will often attract the 
attention of strangers before they are observed by the parents. In most 
Instances there is a slight evening rise in the temperature and a short 
backing cough at intervals. The symptoms may be divided into three 
stages. 

The first is the irritative stage or period of in vasion. In this period the 
little patients dislike to be disturbed ; light and noise annoy them ; they 
answer questions intelligently, but unwillingly and slowly. The expression 
of the countenance is anxious. The cheeks will be alternately flushed and 
pale. Headache, which is often severe, is paroxysmal and seldom constant. 
It is usually frontal and may be accompanied by dizziness. In some cases 
the intermissions are short and the pain is diffused. The sufferer will moan 
and clasp the head with his hands. In young children pressure on the fon- 
tanelles increases the pain. There is mild delirium alternating with dis- 
turbed and fitful sleep, from which the child starts with a piercing hydro- 
cephalic cry. They grind their teeth, roll their eyeballs, and the facial 
muscles are contorted. The hands will be clenched and the thumbs flexed 
on the palms. Muscular tremors pass over the face and body in quick suc- 
cession. The abdomen is retracted and hard, due to contraction of the 
intestines from central irritation. Projectile vomiting occurs at varying 
intervals, independent of the ingestion of 
food, and resists all treatment. The bowels 
are constipated. The tongue is dry, covered 
with a white coating, and the tip is red. 
The pupils are contracted, there is photo- 
phobia and possibly strabismus ; the con- 
junctivae are injected and the brows con- 
tracted. On drawing the finger firmly over 
the skin, a red line, after a moment, will 
follow the removal of the pressure. The 
evening temperature is a degree or two 
higher than that of the morning, but rarely 
rises above 103° F. Sometimes, in cases 
where convulsions usher in the disease, the 
temperature will reach 104° or 105° F. The 
exacerbations and remissions are always 
irregular. The pulse is at first full, com- 
pressible and regular, or it maybe normal in 
character. After the first twenty -four hours 
it shows a marked tendency to become accelerated and slightly irregular 
upon muscular exertion or excitement. The respirations at times are rapid 
and irregular, at others slow and regular, during sleep perfectly natural. At 
first drowsiness alternates with periods of excitement, but gradually becomes 
more persistent, and the child is disposed to sleep constantly unless aroused. 




Fig. 196. 

Temperature Record in a case of Tuber- 
cular Meningitis. The disease was ush- 
ei'ed in by convulsions, and terminated 
in death on the ninth day. 



988 



DISEASES OF THE NEEVOUS SYSTEM. 



After a few days, a week in most cases, these signs of cerebral irri- 
tation give place to evidences of depression which attend the second 
stage. The pupils are unequal and respond slowly to light. The photo- 
phobia and irritability disappear. The muscles at the back of the 
neck become rigid ; the head is retracted and rolled slowly from side to 
side ; sometimes distinct opisthotonos occurs. This state is irregularly 
interrupted by sudden spasms with the hydrocephalic cry, or by parox- 
ysms of delirium. The pulse becomes slow, irregular, and intermit- 
tent ; the irregularity is very distinctive. It may be doubled in frequency 
on slight excitement. There are partial or general convulsions ; ptosis, 
strabismus, loss of sight, anaesthesia, local paralysis or complete hemiplegia 
may occur. There is constipation arid retention of urine or involuntary 
passages. The projectile vomiting ceases. Deglutition may become diffi- 
cult, and the unparalyzed hand will grasp at the mouth and throat to re- 
move supposed obstructions. The respirations are irregular and sighing, 
and Cheyne-Stokes' respiration is common. As a rule complete anorexia 
exists ; the tongue and mouth are covered with sordes ; and the passages 
are unnatural and offensive, often having a slimy, greenish appearance. 
The urine is diminished in quantity, of high specific gravity, dark colored, 
and contains chlorides, phosphates and albumen in varying proportions. 
Facial convulsions are not infrequent. In young children, the temperature 
may be subnormal during this stage, even when convulsion follows convul- 
sion in quick succession. The ophthalmoscope reveals varicosities 1 of the 
retinal veins, points of hemorrhage, serous peri-papillary infiltration, and 
white miliary granulations on the retina and choroid. Optic neuritis is 
sometimes present. It is said that ocular disturbances will be present in 
this disease only when the chiasm, is involved. 2 They are not present in 
tubercular meningitis of the convexity. 

At this stage of the disease apparent recovery is of common occurrence. 
The child sits up in bed, is free from pain or delirium, eats with avidity, 
and will play as though completely convalescent. This is deceptive ; for 
after a few hours he lapses into a deeper stupor than before. 

The last stage is indicated by a change in the pulse and by deepening 
coma. The pulse runs up to 150 or 170 per minute, is feeble, small and 
irregular. The pupils are widely dilated ; the fontanelles in the very 
young may become prominent ; the paralyses — which may have been tran- 
sient — are now permanent, and convulsions occur during the development of 
the coma. The breathing is sighing or snoring in character. Dysphagia 
is marked. The contents of the bladder and rectum are passed involunta- 
rily ; the body is covered with a clammy s veat, and one side may be hot, the 
other cold. The patient lies, when convulsive movements are absent, on 
his back, the head drawn to one side or still rolled from side to side. One 
side of the mouth, and one nostril, show that paralysis has occurred. Soon 
only reflex movements can be excited. Contractions about the jaw and 
neck are frequently observed. The abdomen becomes tympanitic, subsul- 
tus tendinum is marked ; the capillary circulation is more and more inter- 



1 Cohnheim and Bouchut. 



2 Union Medicate, 1867, Galezowski. 



TUBERCULAK MENINGITIS. 



989 



fered with, respirations become less distinct, and death may occur quietly 
in deep coma, or from asphyxia at the height of a severe convulsion. 
During these last hours the temperature may reach 106° P., is of varying 
intensity, and is rarely subnormal. In some severe cases the stage of .coma 
is reached in a few hours, and death occurs within forty-eight hours ; again 
there may be no actual coma throughout. I have occasionally seen cases 
begin with paralyses (facial hemiplegia, etc., etc.), and with aphasia. 

Differential Diagnosis. — Tubercular meningitis may be mistaken for acute 
meningitis, gastro-enteritis, acute Bright 9 s disease, spurious hydrocephalus 
and infantile remittent fever. 

Acute meningitis has none of the prodromata that in over 80 per cent, 
of the cases precede tubercular meningitis ; it is sudden in its onset and 
rapid in its progress ; the temperature is higher and has none of the exacer- 
bations and remissions that cause the* tubercular form to simulate infantile 
remittent fever. The ocular symptoms and the boat shaped abdomen 
are more prominent in the tubercular than in other forms of meningitis. 
The hydrocephalic cry, and the irregular, slow development are character- 
istic of the tuberculous variety. 

Gastro-enteritis is accompanied by diarrhoea, abdominal pain and tender- 
ness. But headache, contracted pupils, photophobia, the slow, irregular 
pulse, reflex movements during sleep, projectile vomiting, and the hydro- 
cephalic cry of acute hydrocephalus are wanting. 

In Bright 's disease the oedema, the characteristic facial expression, and 
the absence of prodromes, taken in connection with the presence of albu- 
men and casts in the urine, will establish the diagnosis. 

A comatose state following cholera infantum, called spurious hydroceph- 
alus, will be recognized by a feeble, rapid pulse, a low (even sub-normal) 
temperature, a dilated pupil, a distended abdomen, and the absence of the 
characteristic nervous phenomena of meningitis ; the fontanelle is depressed 
in spurious hydrocephalus, elevated and strongly pulsating in tubercular 
meningitis. 

Infantile remittent is attended by a high temperature that remits with 
regularity ; the exacerbations and remissions of tubercular meningitis are 
irregular, and the fever is rarely over 103° F. In infantile remittent the 
vomiting is retching in character, diarrhoea is prominent and the discharges 
pea-soup in character, the abdomen is distended and tender; there is great 
thirst, rapid pulse, and normal pupils. The photophobia, irregular pulse, 
hydrocephalic cry, and the grinding of the teeth so common in acute 
hydrocephalus are absent. The severe cerebral symptoms that often attend 
the invasion of acute pneumonia, pleurisy, bronchitis, or the exanthematous 
fevers in children are to be distinguished by a physical exploration of the 
chest or by the appearance of the eruptions and the high fever and pulse-rate. 

Prognosis. — Tubercular meningitis is one of the most fatal diseases of 
childhood. Many authors state that it is always fatal after its character- 
istic symptoms are developed. The duration varies from five days to four 
weeks ; from sixteen to twenty-one days after the initial symptoms death 
may be expected. If ushered in by convulsions its duration is short. 



990 



DISEASES OF THE NERVOUS SYSTEM. 



Treatment. — It is unnecessary to refer to all the different measures which 
have been resorted to for the cure of this disease, for they have all failed. 
Prophylaxis alone is effective. A child whose antecedents lead us to fear 
the advent of acute hydrocephalus should be given a healthy wet-nurse 
from its birth, and the greatest care exercised as to its hygiene and diet for 
the first few years of life. Children who exhibit the premonitory symp- 
toms, and in whom its development is feared, should be given cod-liver 
oil, kept out of doors as much as possible, and placed under the most 
favorable hygienic conditions possible ; a frequent change of surroundings 
and of climate is important. 

The treatment after the disease is established is almost entirely symp- 
tomatic. The bowels are to be kept open, and absolute quiet enjoined. 
Ice-bags may be placed on the head ; but depletion of all kinds is contra- 
indicated. Iodide of potassium (pushed to toxic effects), 1 the mercury 
salts, and soda phosphate have been advocated, but their utility is ques- 
tionable. I have obtained the greatest benefit from opium and bromide of 
potash during the stage of excitement, to relieve the restlessness and jac- 
titation. I have never found that any of the plans of treatment proposed 
for this disease have any power to arrest its progress. 

Tubercular meningitis in the adult is of rare occurrence, and is found 
only in connection with general tuberculosis. The pathological changes 
are the same as those found in children, and its etiology is identical with 
that of general tuberculosis. When latent, it may be excited by severe 
mental emotions or over-work. Symptomatically, it differs from infantile 
hydrocephalus in degree rather than kind, the symptoms being perhaps less 
violent. In all other respects the description just given will apply in all 
points to the same disease in adults. 

CHKONIC HYDROCEPHALUS. 

Chronic hydrocephalus is a cerebral dropsy from some cause not well 
understood. It is divided into external hydrocephalus, in which the serous 
effusion is in the meshes of the pia mater, and internal hydrocephalus, 
where the accumulation of fluid is in the ventricular cavities. When both 
coexist, it is called mixed hydrocephalus. Chronic hydrocephalus may be 
intra-uterine or extra-uterine. 

Morbid Anatomy. — The essential lesion of chronic hydrocephalus is a 
serous effusion either into the ventricles or upon the surface of the brain. 
The fluid consists chiefly of water, containing albumen, sodium chloride, 
traces of lime and potash salts, epithelial and blood cells, rarely scanty 
lymph-flocculi and urea. 2 The ventricles may contain from twenty to 
thirty pounds of fluid. 3 The upper wall of the lateral ventricles may be 
ruptured ; the brain substance is either softened or abnormally tough and 
resistant. The brain will be enlarged, and the convolutions flattened. In 
congenital hydrocephalus the bones of the skull are thin, the fontanelles 

1 Niemeyer. 

9 BrighVs Reports, vol. i., p. 433. 

3 Trousseau {Clin. Med.) mentions a case in which the amount was fifty pounds. 



CHROKIC HYDROCEPHALUS. 



991 



and sutures are enlarged ; or, if united, numerous ossa triquetra are found 
between them ; and the supra-orbital, temporal, and occipital regions are 
distinctly depressed. The head may measure from eighteen to forty inches 
in circumference. The large ganglia at the base are pressed downward. 
The optic chiasm is flattened, and the pons and cerebellum are compressed ; 
the various septa and commissures are thinned or ruptured ; and, finally, 
there may be left only a thin layer of brain matter together with the 
thalami and corpora striata. When the lateral ventricles are distended 
and the ependyma thickened and granular, the term chronic or granular 
ependymitis is given ; in this condition there may be new tissue formation, 
and bands of cicatricial tissue join the walls of the ventricles. 

Hydrocephalus ex vacuo is the result of defective development of, or 
atrophic degenerative changes in, the brain ; the space thus left is filled 
by a serous, sometimes slightly bloody fluid, seldom in great quantity 
(hydrocephalus senilis). The membranes (in the very young) are seen 
studded with ossific granules. If the bones should unite, there is subse- 
quent thickening, and the head is either unsymmetrical, or nearly globu- 
lar. 1 It is not uncommon to find evidences in the membranes of acute or 
sub-acute inflammatory processes. 

Etiology. — Hydrocephalus may be congenital or acquired. When ac- 
quired it usually appears before dentition. A few cases occurring in old 
people are mentioned by Watson 2 and Golis, and Dean Swift is said to 
have died of it in the seventy-eighth year of bis age ; atrophy or imperfect 
development of the brain causes it ; and it may arise from chronic passive 
hyperemia, weakness of the vascular walls, from compression of the veins, 
occlusion of one or both lateral sinuses, or the presence of tubercular 
masses in the brain-substance. Eickets and syphilis in children, and 
dementia and alcoholismus in adults, are regarded as causes. It is met 
with in tubercular and scrofulous subjects, and it is said to have followed 
measles and scarlet fever. 3 Inflammatory changes in the ventricles and 
ependyma are accompanied by hydrocephalus. One hydrocephalic child 
renders it probable that subsequent children will be hydrocephalic. 4 

Symptoms. — The symptoms vary with the rapidity of its development. 
If intra-uterine, hydrocephalus develops rapidly ; the head becomes so 
large that its delivery can only be accomplished by operative procedure. 
If such children are born alive they die within a few days. In those cases 
where the disease is slight, the child at birth appears healthy, but after a 
few weeks the head begins to enlarge ; the sutures do not close, and the 
fontanelles are persistent ; the forehead bulges so that it overhangs the 
face, which is pale, small and weazened, giving a dwarfish expression to 
the child. The limbs do not develop ; the abdomen is distended and tym- 
panitic, and the skin dry and scaly. Fluctuation 6 may sometimes be ob- 



1 Barthez and Rilliet «tate that in a few cases of congenital hydrocephalus the bones were normal. 

2 Practice of Physic ; Sir Thomas Watson. 
8 Tanner's Practice. 

4 Hoppe, Niemeyer and others regard hydrocephalus arising from nutritive changes in the capillary 
walls as analogous to " skin inflammations that produce blebs." 

5 Sir T. Watson ; Dr. Bright. 



992 



DISEASES OF THE NERVOUS SYSTEM, 



tained between the anterior and posterior fontanelles. Often the child is 
unable to hold its head erect even for a few moments ; the pupils are 
dilated and the eyes protruded. There are periods of apparent improve- 
ment, but after a year of gradual decline death occurs in convulsions, from 
starvation or intercurrent disease. 

In another class of milder cases the mental faculties are normal, but 
nutrition is imperfect ; the limbs are small and the muscles flabby. The 
children are irritable, and at times have fever, nausea and vomiting. 
After an unusually severe attack of fever they may gain flesh and seem 
much improved, but the head still increases in size. After a variable time 
of improvement they again become worse, lose strength, and all the active 
cerebral symptoms return. When they attempt to walk they totter, stum- 
ble and fall. Spasms, epileptiform convulsions and paralysis of certain 
groups of muscles follow, and they become idiotic. Such children do not 
die from hydrocephalus but from intercurrent disease. Some of these cases 
live for four or five years, having periods when they seem to be recover- 
ing. When anaemia and asthenia cause death the usual duration is a 
year. 

A few rare cases are recorded where hydrocephalic subjects have lived 
five, ten, and even thirty years. 

Differential Diagnosis. — Congenital, or intra-uterine hydrocephalus cannot 
well be mistaken for any other malady. 

Cranial rachitis does not cause the mental, or even the physical, derange- 
ments induced by hydrocephalus ; but it induces an unsymmetrical en- 
largement of the bones. 

Prognosis. — The prognosis is always unfavorable. The average duration 
is one year. Death may result from any of the complications, from simple 
asthenia and anaemia, from meningitis, ependymitis, apoplexy, rupture of 
the fluid through the brain substance into the epicranial aponeurosis, 1 or 
from general paralysis. The only condition of recovery is a cessation of 
increase in the fluid and closing up of sutures ; the cases of absorption of 
fluid and return of mental power are doubtful. 2 

Treatment. — There is very little to be done for this disease. The treat- 
ment which has been employed may be divided into external or mechanical, 
and internal or medicinal. Mercurial inunctions and strapping the head 
with adhesive plasters have been advised, but are of doubtful utility. Sud- 
den compression of the head may cause death. Pale, flabby children bear 
it best. 

Tapping can be advocated only in external hydrocephalus and where no 
inflammatory or organic changes coexist. The anterior fontanelle is the 
proper point to insert the aspirating needle ; only a few ounces should be 
drawn at a time, the child being carefully watched during and after the 
operation. Subsequently the head should be lightly bandaged. Langen- 
beck passes behind the upper lid through the superior wall of the orbit and 



1 Rokitansky's case. 

2 Otto states, however, " that new cerebral matter may be deposited in place of re-absorbed fluid."- 
Rokitansky's Pathological Anatomy. 



PACHYMENINGITIS EXTERNA. 



993 



enters the anterior horn of the lateral ventricle. But inflammatory action 
is apt to be excited by any such procedure. 

Internally cod-liver oil and the syrup of the iodide of iron and potash 
should be given throughout the disease. Calomel (gr. J— |-) daily has 
been recommended, until purging becomes severe. The food, the hygienic 
surroundings and the clothing should also receive careful attention. 
Change of air is also highly beneficial. If rickets coexist phosphatic salts 
are indicated. 

PACHYMENINGITIS EXTERNA. 

Pachymeningitis is an inflammation of the dura mater which may be 
acute or chronic. The inflammation may involve either the external, 
internal, or both layers of the dura mater. When the external layer is 
primarily involved, it is called external pachymeningitis ; when the inter- 
nal layer is the primary seat of the inflammatory process, it is called 
pachymeningitis interna. External pachymeningitis is almost always a 
secondary inflammation. 

Morbid Anatomy. — In the non-suppurative form of pachymeningitis ex- 
terna the dura is injected, softer than normal, and covered with ecchymo- 
tic spots. New connective-tissue formations occur, which lead to thicken- 
ing and induration of the dura and adhesions between it and the cranial 
bones. Numerous pigment granules stud the thickened membrane. Os- 
teophytes form and the appearance closely resembles periostitis with exos- 
tosis. In many cases bony flakes can be detached from the tough, pale, 
leathery dura mater. 

In purulent pachymeningitis externa suppurative processes are early 
established and the external layer is softened, disintegrated, thinned, and 
rendered very friable. A thick layer of new connective-tissue separates 
the pus from the internal layer of the dura mater. These purulent collec- 
tions are usually of traumatic origin and circumscribed, as inflammation of 
the dura is rarely diffuse, and the pus detaches the dura from the bone and 
may lead to necrosis. When the sinuses are involved in pachymeningitis 
their walls undergo thickening, the intima is roughened, and thrombi form 
at the seat of the lesion, which may break down and be absorbed or give 
rise to emboli or pulmonary infarctions. 

In old age it is physiological for the dura to be thick, leathery, cartilagi- 
nous and of a dull white color. The sheaths of the arteries are thickened. 

Etiology. — Idiopathic pachymeningitis externa is of doubtful occurrence. 
Secondary pachymeningitis may result from injuries to, and caries of the 
cranial bones or upper cervical vertebrae. Hemorrhage of traumatic ori- 
gin may separate the dura from the bone and be followed by inflammation. 
Chronic internal otitis and suppurative inflammation of the orbit may lead 
to it. An external periostitis maybe followed by external pachymeningitis 
without apparent intervening bone-changes. Inflammation in the venous 
sinuses, especially the transverse and petrous, may lead to it, especially 
when the thrombus formed undergoes suppurative changes. 



994 



DISEASES OF THE NEEVOUS SYSTEM. 



Symptoms. — The symptoms of pachymeningitis are generally very ob- 
scure. After an injury of the skull or a chronic otorrhoea, we may sus- 
pect external pachymeningitis when there is somnolence, headache, dizzi- 
ness, photophobia followed by delirium, and perhaps convulsions and 
coma. In cases attended by thrombosis of a sinus there will be hectic 
fever and rigors and symptoms simulating an attack of intermittent fever. 
When metastatic abscesses develop in the joints and internal organs, the 
headache will be severe and localized, and possibly attended by nausea and 
vomiting. If there is cerebral pressure, the pulse becomes slow and irregu- 
lar, rarely frequent and feeble ; the pupils are unequal ; the headache, 
apathy, and somnolence increase and are attended by facial paralysis. Just 
before death the pulse slows and coma is developed. Circumscribed pain- 
ful oedema behind the ear 1 and less fulness of the jugular of that side are 
indicative of thrombosis in the transverse sinus. 2 

Differential Diagnosis. — In one who has received an injury of the skull, 
with possibly fracture of the base, if the signs of cerebral compression per- 
sist, pachymeningitis externa may be suspected. With caries of the cranial 
bones or otitis interna, the diagnosis can be made from the complicating 
cerebral symptoms. But in chronic cases the symptoms are often so obscure 
that a positive diagnosis is impossible. 

Prognosis. — Eecovery is possible and depends largely upon the cause. 
Alcoholic pachymeningitis is almost invariably fatal. That due to otorrhoea 
may end favorably if the pus is evacuated either spontaneously or by opera- 
tion. The great danger is in extension of the inflammation to the internal 
layer of the dura mater and to the pia mater. 

Treatment. — The treatment is mainly surgical. Trephining may some- 
times save life. Rest, a mild diet, a free evacuation of the bowels, cold to 
the head and warmth to the extremities are the principal means of treat- 
ment. Disease of the ear demands immediate attention. I recall a case 
where, after a deep coma of five days' duration, recovery unexpectedly oc- 
curred after a copious discharge of pus from the ear. Should symptoms of 
suppuration be well marked, alcoholic stimulants, quinine, and opium are 
indicated and the question of surgical interference will present itself. 

PACHYMENINGITIS INTERNA. 

Pachymeningitis interna may be acute or chronic. 3 

Morbid Anatomy. — In acute pachymeningitis interna the inner surface of 
the dura mater is intensely hypersemic and covered with a layer of fibrin 
and pus which may be circumscribed or diffused. The substance of the 
membrane may be thickened by new connective-tissue developments ; but 
the larger part of the inflammatory exudation is upon its free surface. This 
form of pachymeningitis is apt to be complicated by inflammation of the 
pia mater. In chronic pachymeningitis interna the dura is covered with a 
layer of organized tissue. This thin, filmy new membrane is very rich in 



1 Griesinger calls this phlegmasia alba dolens en miniature. 2 Gerbor2tt. 

3 Virchow was the first to interpret and classify the changes which take place in this inflammation 



PACHYMENINGITIS INTERNA. 



995 



large capillaries with thin walls. It is composed mainly of cells, having 
very little basement substance, and is usually most abundant at the con- 
vexity of the brain. 

Some pathologists claim that before these changes occur, a thin layer of 
compact fibrin, which can readily be stripped off, occupies the site where 




Fig. 197. 
Pachymeningitis Interna. 
Vertical Section of the Skull and Cerebral Meninges. 

A. Section of the skull. 

B. Dura mater thickened and conn ected intimately with C, the first layer of the inflammatory deposit. 

D. Deposit of pigment. 

E. Superficial layer of exudation containing an hcematoma F, caused by rupture of the capillaries in the 

highly vascular tissue. 

O. A second and superposed hcematoma appearing in a new layer of exudation, x 250. 

subsequently a hematoma is developed. The capillaries in the new tissue 
are easily ruptured and hemorrhages are liable to occur, forming hasma- 
tomata, ranging in size from small clots to large blood sacs covering 
the whole convexity. 1 After a time the walls of the new vessels become 
thicker. In rare instances the blood extravasates in small amounts and 
is absorbed, and only a thin, transparent well-defined membrane marks the 
spot where the pachymeningitis existed. 

The hematoma may become encysted (Virchow's hygroma of the dura 
mater), or its contents may undergo caseous and calcareous changes. 2 In 
some cases the blood has either dissected between the layers of the wall 
of the hematoma, or else, after one hemorrhage, a new layer of pseudo- 
membrane forms, and a second extravasation is followed by a second tis- 

1 In opposition to the above description, Huguenin states that a thick (one-twelfth inch) la3'er of fibrin 
forms on an intact dura. This, he says, is rarely demonstrable ; the new, yellow-stained membranes, in 
which are colorless masses (? white blood corpuscles) of protoplasm, form later. 

8 Rokitansky and Forster. 



996 



DISEASES OF THE NERVOUS SYSTEM. 



sue formation. The ventricular cavities are sometimes filled with a sero< 
sanguinolent fluid. 

Etiology. — Both acute and chronic pachymeningitis interna are usually 
secondary, but in rare instances are of idiopathic origin. The acute form 
may be secondary to pachymeningitis externa, pyaemia, Bright's disease, 
or the acute infectious diseases. Chronic pachymeningitis interna is a 
disease of advanced life, rare before forty, and most frequent between sixty 
and eighty. Chronic alcoholismus is its most frequent cause. Atrophy 
of the brain, hydrocephalus, cerebral tumors, and general paralysis and 
dementia are often followed by pachymeningitis interna. In progressive 
pernicious anaemia, haematoma appears in thirty-three per cent, of all 
cases. 1 Leucocythaemia, the hemorrhagic diathesis, scorbutus, and splenic 
anaemia are blood states especially liable to be accompanied by pachymen- 
ingitis. Valvular diseases of the heart impairing venous return and athe- 
roma are important factors in its causation. 

Symptoms. — The symptoms vary with its extent and the amount of the 
new tissue formation. When the disease is slight, there are no symptoms ; 
when extensive, most of the symptoms are due to cerebral pressure. At 
first there is constant headache, dizziness, vertigo, tinnitus aurium, mus- 
es volitantes, photophobia, constipation, anorexia and insomnia, with 
slight febrile movements. The intellect is impaired, memory fails, and 
sometimes there will be a temporary loss of consciousness and partial loss 
of speech. The symptoms of slight extravasation simulate very closely 
those of a small cerebral apoplexy. The pupils will be contracted, one 
more than the other. There may be slight wandering, and when the attack 
is partially recovered from the mental and bodily conditions are palpably 
impaired. The temperature may be slightly raised and attended by irreg- 
ular exacerbations and remissions. The pulse is slow, becoming irregular 
upon excitement. 

Paralysis comes on gradually, as one hemorrhage follows another. Be- 
tween the attacks localized headache is the prominent symptom. Some- 
times slight epileptiform convulsions occur, followed by temporary loss of 
consciousness. 2 If the hemorrhage in the new tissue is rapid and exten- 
sive, patients may die suddenly from cerebral compression ; or one slight 
hemorrhage which gives rise to few symptoms may be followed by a second 
more extensive bleeding, attended by the ordinary symptoms of apoplexy. 
Recovery after slight hemorrhage not infrequently occurs : but the patient 
afterward will be troubled with more or less constant headache, insomnia, 
and perhaps by localized paralysis. Moderate-sized haematomata have 
been found at autopsies, where, during life, no signs existed. 

During the course of acute and chronic pachymeningitis the venous 
sinuses may become involved in the inflammatory process, causing thrombi 
which give rise to pulmonary or other infarctions, attended by the usual 
symptoms : rigors, followed by a temperature of 103° or 104° F., with ir- 



1 Huguenin. 

a Pon states that pachymeningitis interna begins, often, with the symptoms of the general paralysis 
of the insane upon one side of the body. 



SYPHILIS OF THE DURA MATER. 



997 



regular variations. The pulse at first is rapid, but after a few days it 
becomes slow. As the case approaches a fatal termination the pulse runs 
up to 120 or 140, and is small and feeble. The patient becomes delirious 
and rapidly passes into coma, preceded or followed by convulsions. 

Differential Diagnosis. — The diagnosis of pachymeningitis interna is 
always difficult ; it may be confounded with acute meningitis of the con- 
vexity with which it is frequently associated, with chronic meningitis, and 
softening of the drain. The diagnosis of a hematoma is based on the fol- 
lowing conditions, viz. : continued, vertical, localized headache, contracted 
pupils, strabismus or ptosis, very slight fever, slow pulse, a history of one 
or more apoplectic seizures, or of periods of loss of consciousness followed 
by dysphagia, facial paralysis or hemiplegia. The diagnosis is always 
problematical, complicating, as it does, so many cerebral affections, and 
its symptoms are masked and indefinite. 

Prognosis. — The prognosis is bad, although the course of the disease is 
usually slow. The cerebral symptoms often intermit. Some die from the 
extension of the inflammation ; others from rapid and extensive blood ex- 
travasation ; some become insane or demented ; the larger number die from 
intercurrent disease. When the venous sinuses are involved patients may 
die from the effects of the inflammation or from infarctions. The disease 
lasts, in most cases, from one to three weeks, yet one day and one year are 
given in a few recorded cases as the limits of this affection. 

Treatment. — There is no cure for pachymeningitis interna : all that can 
be done is to treat symptoms. Absolute rest in a cool, quiet room is to be 
enjoined. Irritative or inflammatory symptoms demand cold to the head, 
mild counter-irritation, and heat to the extremities. The bowels are to be 
kept freely opened, and, at the onset, a brisk purge may be given. As the 
disease progresses stimulants and a highly nutritious diet are the best 
means to combat the affection ; and anodynes may be necessary to induce 
sleep and relieve headache. Ergot is indicated on the ground of its 
physiological action on the vascular system, to prevent or diminish future 
hemorrhages. Ramskill advocates iodide of potash as the chief remedy, but 
this and mercury are rarely employed at the present day. 

SYPHILIS OF THE DUE A MATER. 

Syphilitic gummata, developed in the dura mater and accompanied by 
meningitis, are met with in the advanced stage of syphilis. 

Morbid Anatomy. — The lesions differ from the other forms of meningi- 
tis, in that the inflammatory product is circumscribed in the form of gum- 
matous tumors, which are composed of small round, oval, and pyriform 
cells with basement substance. These gummatous masses may degenerate 
and become cheesy, or be converted into a purulent-looking fluid consist- 
ing of serum, degenerated cells, and granular matter. They may be 
developed either on the external or internal surface of the dura mater, 
and are usually multiple. Gummatous masses may develop in the sub- 
stance of the cranial bones and cause more or less destruction of them, or 



998 



DISEASES OF THE KERVOUS SYSTEM. 



it may be complicated by inflammation of the pia mater, and then gummy 
masses may develop beneath the pia mater. 

Symptoms. — As in the varieties of pachymeningitis, persistent localized 
headache is the most constant and prominent symptom ; convulsions and 
temporary loss of consciousness not infrequently accompany the head- 
ache. The intellect is impaired, and the patient lapses into a dull, 
stupid, apathetic condition. They may be wildly delirious. In some 
instances there is loss of sight and hearing. If the gummatous masses 
attain a large size, facial paralysis and hemiplegia may occur. I have 
known a patient with syphilis of the dura mater to become hemiplegic, 
pass into a state of complete unconsciousness, with stertorous breathing, 
relaxed sphincters, and dilated pupils, remain in this condition for ten 
days, and finally completely recover. 

Differential Diagnosis. — The diagnosis rests entirely on the syphilitic his- 
tory in one who has any of the external manifestations of syphilis asso- 
ciated with the cerebral symptoms of pachymeningitis. 

Prognosis. — The natural termination of this disease is in death. If these 
patients are subjected to proper treatment before the gummatous masses 
have become too large or are too far advanced in degenerative changes, re- 
covery is almost certain. Recovery, however, in these cases is rarely per- 
manent, for after the treatment has been abandoned, the disease is apt to 
return. In one who is addicted to the use of alcohol the prognosis is very 
unfavorable. 

Treatment.— The treatment is that of advanced sypnilis. Mercury and 
iodide of potassium, either together or alternately, are the means to be re- 
lied upon. The mercury is best employed by inunctions and baths. My 
rule is to apply each day a drachm of strong mercurial ointment in the ax- 
illa and flexures of the joints until its specific effects are produced. Iodide 
of potassium must always be given in large doses ; from thirty to sixty grains 
may be given in from four to six ounces of water, three or four times daily 
until the desired effect is reached, which is the disappearance of the cerebral 
symptoms. Tonics and cod-liver oil are always indicated, and of service 
between the periods of the administration of the mercurials and the iodide. 
Under no circumstances should this class of patients be allowed to use stim- 
ulants habitually in any form. 

CEEEBEAL THROMBOSIS AND EMBOLISM. 

The cerebral arteries may be obstructed by emboli or thrombi, the cere- 
bral veins and sinuses by thrombi only. The changes in, and effects pro- 
duced by a plug in the cerebral vessels, whether embolic or thrombotic in 
its origin, are identical with similar changes in other parts of the body. 
The walls of a cerebral artery which is the seat of thrombosis are usually 
thickened. The thrombosis may be the result of slowing of the blood cur- 
rent from any cause. The results and symptoms of cerebral thrombosis are 
essentially the same as those of cerebral embolism. 

Cerebral emboli may be bilateral ; several may coexist ; and they have 



CEREBRAL THROMBOSIS AND EMBOLISM. 



999 



been found in all of the cerebral arteries. The left middle cerebral is their 
most frequent seat (forty-six in one hundred cases) ; next the internal ca- 
rotid, the basilar, and vertebral. Ninety per cent, are in vessels that sup- 
ply the ganglia at the base. The artery of the corpus callosum is rarely 
implicated. 1 Embolism in the cortex is rarely attended by serious results, 
on account of the free anastomoses between the cerebral capillaries and 
those of the pia mater. 

When the left middle cerebral artery is plugged, it being a terminal ar- 
tery with no anastomoses, well-marked symptoms occur and destructive 
lesions follow. This artery has the most direct communication of any of 
the cerebral arteries with the left ventricular cavity. This anatomical fact 
readily explains the frequent occurrence of embolism in it. The result of 
cerebral embolism or thrombosis is to deprive the portion of the brain sup- 
plied by the obstructed vessel of its nutrition, in consequence of which it 
degenerates and softens. Softening of the brain is the usual result of embo- 
lism ; the name embolic softening has been applied to it, to distinguish it 
from inflammatory softening. 2 Niemeyer describes the initial result of em- 
bolism and thrombosis as partial anaemia of the brain, 3 and states that the 
subsequent softening is analogous to gangrene in the extremities induced 
by obstruction or obliteration of the vessels. But the difference is, that 
within the skull the absence of exposure to air precludes decomposition. 

If a large cerebral vessel, or a large number are obstructed suddenly, it 
may cause sudden death, and there will be no time for cerebral softening. 
Many writers include in the signs of cerebral embolism those of the first 
stage of softening. 

Symptoms. — The symptoms produced by the plugging of cerebral vessels, 
either by emboli or thrombi, are sudden in their advent. When an artery 
of considerable size is obstructed there is temporary loss of consciousness, 
the patient passing rapidly into coma, from which he gradually recovers 
with complete hemiplegia. If only a small branch of a cerebral artery is 
plugged there may be only a slight and transient loss of consciousness or 
confusion of mind, or there may be nothing to indicate its occurrence 
except sudden loss of speech. During- the period of loss of consciousness, 
if it occur, the face is pale and cold. 

Aphasia is common, but not a constant attendant. It may be complete 
or partial, the patient may be able to use only one or two words, as "no " 
or "table," and employs them to answer all questions. Again, his vocab- 
ulary may consist of a number of words, but he cannot use them aright ; 
he calls for his*boots when he intends to call for bread. 

Aphasia may be of two kinds, amnesic or ataxic. Amnesic aphasia is 
where the memory of words is lost, though the capability of uttering them 
may exist. Ataxic aphasia is where the muscles and parts that produce 

1 It is interesting to note that the vertebral was oftenest involved in the large number of cases seen by 
Nothnagel. 

2 Nothing can be definitely stated concerning embolism and thrombosis of the capillaries from pigment 
(in malaria), leucocytes (in leukaemia), and from fatty granules or salts. They are more pathological curi- 
osities than well-defined diseases. 

s The only other form of partial cerebral anaemia is from collateral oedema about spots of extravasa- 
tion. 



1000 



DISEASES OF THE NERVOUS SYSTEM. 



articulate speech cannot be co-ordinated ; the patient knows just the word 
he wants to speak but he cannot utter it. The ataxic form is commonly - 
associated with hemiplegia of the right side. 1 In ataxic aphasia a patient 
can read, write^ and listen intelligently to the speech of others. In amne- 
sic he only reads and understands what others say. After repeated attacks 
of embolism a patient may have both amnesic and ataxic aphasia. 

Within twenty-four hours after the occurrence of a cerebral embolism 
there may be convulsive movements in the muscles which are afterward to 
be paralyzed ; epileptiform convulsions frequently occur. If the patient 
pass into coma he may continue in a comatose state and die within a few 
days ; or he may recover from the coma with permanent hemiplegia 
and aphasia. There may be temporary improvement in the hemiplegia, 
but after the degenerative changes take place in the brain the hemi- 
plegia becomes permanent. In most of the cases where the hemiplegia is 
permanent the paralyzed muscles become contracted. When the hemi- 
plegia and aphasia are partial, and there has been no loss of consciousness, 
complete recovery generally takes place. A cerebral embolism may be so 
slight that there may be aphasia for a few days, and then the patient will 
completely recover without any other symptom. 

Hemiopia and unilateral amaurosis with alternate hemiplegia are symp- 
toms of cerebral embolism ; they are due to extravasations into the optic 
nerve and to embolism of the arteria centralis retinas on the corresponding 
side. Embolic amaurosis may precede cerebral embolism for a few days. 
The ophthalmoscope shows pallor of the papilla and absence of pulsation 
in the retinal arteries. Even when the middle cerebral is alone occluded 
collateral fluxion may cause arterial and venous hyperemia of the reti- 
nal vessels and congestion of the optic disc. If the patient does not begin 
to improve in twenty-four or forty-eight hours after embolism occurs, a 
fatal issue may be expected. In such cases the temperature rises to 104° 
F., remains at that point for a couple of days, and then rapidly declines. 2 
There are often evidences of embolism in other parts of the body, as the 
spleen, kidneys, extremities, etc., etc., which will aid in the diagnosis. 

Bilateral embolism usually results from separate attacks. These cases 
are marked by epileptiform convulsions, temporary aphasia, hemiplegia, or 
rarely double hemiplegia, accelerated and irregular — perhaps difficult — res- 
piration, unilateral anaesthesia of the conjunctiva, and normal sensibility 
of the cornea. 

Differential Diagnosis. — Cerebral embolism and thrombosis often cannot 
be positively distinguished from cerebral hemorrhage. The symptoms in 
some cases are the same. If the hemiplegia is upon the right side and 
there is aphasia the probabilities are in favor of embolism. If there is 
no aphasia, and the loss of consciousness is prolonged and the facial paraly- 
sis is marked, cerebral apoplexy has occurred. If the paralysis is rapidly 
recovered from, it indicates embolism and not apoplexy. 

Cerebral thrombi form in old age without cardiac or pulmonary disease, 



1 Ogle states that in left-handed individuals the centre for language is in the right island of Eeil. 
3 Bourneville. 



CEREBRAL SOFTENING. 



1001 



on account of rigid, calcified and atheromatous arteries ; the paralysis is 
less marked, and aphasia is usually incomplete. If the paralysis improves 
after a day or two and then gets worse, it indicates embolism. 

Prognosis. — The prognosis will depend upon the size of the artery plug- 
ged ; complete recovery is always possible, partial recovery is not infrequent. 
Still, cerebral embolism and thrombosis are serious conditions, on account 
of the danger that they will lead to cerebral softening. The prognosis is 
usually better in those cases where the hemiplegia is partial than when it is 
complete. In cases where the symptoms at first are mild, but gradually 
grow worse, the prognosis is unfavorable. It is impossible to determine the 
extent and duration of the paralysis which sometimes continues after its 
occurrence. Chronic visceral diseases, senility, and debility or ancemia ren- 
der the prognosis unfavorable. The occurrence of coma is very unfavorable. 
Even after rapid disappearance of the paralysis and aphasia there is great 
danger of another attack. 

Treatment. — The plan of treatment in cerebral embolism and thrombosis 
is a tonic and stimulant one. No depletory or revulsive measures are 
ever admissible. The action of the heart, and the constitutional appear- » 
ance of the patient must determine whether alcoholic stimulation is to be 
resorted to or not. In cases of coexistent cerebral hypersemia, local de- 
pletion may be of service. The hemiplegia is to be treated the same as in 
cerebral apoplexy. Iron, cod-liver oil, and a tonic plan of treatment 
should follow the disappearance of the paralysis. 

CEKEBEAL SOETEKENTG. 

Embolism and thrombosis are undoubtedly the most frequent causes of 
cerebral softening. But I shall adopt the view that there are several 
varieties of very different causation and anatomical changes, and shall 
follow the usual classification of red, yelloiv, and white softening, although 
this division is somewhat arbitrary and unsatisfactory. 

Morbid Anatomy. — Bed softening is marked by punctate redness or by 
numerous minute capillary apoplectic foci, with fatty degeneration of the 
nerve cells and fibres. The pultaceous spot is deep red, shading off into 
the neighboring brain-tissue with no distinct limit. There may be several 
of these red foci ; as many as twenty have been found in different stages 
of discoloration and softening. In all cases the centres show most marked 
changes. There is more or less ©edematous swelling of the adjacent brain- 
tissue, so that upon cutting into it the softened spot will rise above the plane 
of the section. The vessels are enlarged, often from proliferation of the en- 
dothelium, forming masses of varying sizes, frequently within the vascular 
lymph-sheaths, making a white rim visible on cross-section. There is pro- 
liferation of the cellular elements of the neuroglia, and the nerve-elements 
simultaneously undergo fatty changes. Few pathologists claim that any in- 
flammatory exudation accompanies these changes. There is a debris in and 
about the focus, consisting of fat granules, altered blood corpuscles, and free 
nuclei, a few pigment-granules, shreds of brain-tissue, and large granular 



1002 



DISEASES OF THE NERVOUS SYSTEM. 




corpuscles. 1 The nerve fibres become macerated, and their white substance 
is coagulated and broken up into large masses. There is varicose hypertrophy 

of the axis-cylinders. 
This condition is called, 
by Hayem, the cloudy 
swelling of VircJww. 
A spot of red soften- 
ing may become dry 
and shrunken, or cica- 
trization may occur. 
The phenomena of ab- 
sorption consist in fatty 
degeneration and casea- 
tion, or the formation 
of a cyst by a process 
analogous to that de- 
scribed under the head 
of Apoplexy. 

Yellow softening is 
usually the result of 
partial cerebral anaemia 
from obstruction of the 
cerebral vessels. It may 
occur in any portion of 
the brain, but most fre- 
quently has its seat in 
the middle or posterior 
lobes, and in the cortex 
or corpus striatum. Stasis is accompanied by all the changes described 
as occurring with an infarction which is followed by fatty degeneration, 
and it may proceed very slowly or with great rapidity should hemorrhage 
fail to occur. The coagulated blood in the vessels undergoes a retrogres- 
sive change, the fibrin becoming granular. Fatty and granular matter 
in large quantities surrounds the infarction, which becomes dry and slowly 
contracts. Corpora amylacea, blood-pigment, and crystals from the al- 
tered fatty material are found. A soft, yellow-white mass — often of a sul- 
phur color — is thus formed, varying in size from a hazel-nut to an orange. 
The consistence is variable, but in typical cases it is a gelatinous, moist, 
and tremulous pulp. A stream of water will readily wash out the focus of 
softening. These degenerative changes proceed until the focus of softening 
becomes changed into a mass of reticulated fibres, in whose meshes is a 
milky fluid. The vessels in the wall of this cyst are covered by fat granules, 
and are empty or contain a yellowish clot ; but their lymph-sheaths are 
irregularly dilated with pigment, fatty, granular and detached endothelial 

1 Gluge's corpuscles are large spherical cells, filled with fat ; they are abundant, dark by transmitted 
and bright by reflected light. The origin of Gluge's corpuscle, so prominent in yellow softening, is as 
various as that of pus-cells. 



Fig. 198. 

Cerebral Softening. Elements from an Apoplectic Focus in Red 
Softening. 

A. Shreds of nerve fibres. 

B. Altered blood co?^puscles. 

C. Fat spherules. 

D. Masses of myelim. 

E. Free nuclei from neuroglia. 



300. 



CEREBRAL SOFTENING. 



1003 




cells. In this form of softening there is usually a faint line of demarcation 
between the focus and healthy brain-tissue. The color of yellow softening is 
due to fatty changes and a deposit of blood-pigment. These foci may cica- 
trize similarly to apoplectic foci, or result in the formation of a cyst. This 
process may follow either 
an obstructive or hemor- 
rhagic infarction. Eed 
softening may also termi- 
nate in yellow softening/ 
from gradual absorption of 
the broken-down corpus- 
cles and pigment matter. 

White or atrophic soft- 
ening is the form met 
with so frequently in old 
age. 2 It is white or re- 
sembles healthy brain- 
tissue; the process is a slow 
one. Hemorrhage or hy- 
peremia is rarely present. 
It is usually met with 
in the white matter of the 
hemispheres, and the de- 
gree of change may be 
so slight as to render its 
detection difficult, or it 

£i -iTPfl i BBB. Irreqiilarly dilated lymph- sheath containing granulo- 

may De SOIt ana aimuent fatty rnatter and detached endothelia. x 300. 

The specific gravity of the softened mass is less than normal brain sub- 
stance. White softening is never distinctly limited, but shades off into the 
adjacent tissue. In chronic softening of the convolutions their form is 
preserved, but they are markedly atrophied ; over them the pia mater is 
more or less ©edematous, and fills up to a certain degree the space caused 
by the atrophy. Should the vessels in or near a white softened patch be 
examined, they will usually be found atheromatous or the seat of end- 
arteritis. Thus it is evident that the color has no relation to the patho- 
logical changes. Eed softening may come from embolism ; yellow, directly 
from thrombosis, embolism, or be a second stage of red ; white may be 
primary, or secondary to yellow. In every case the cause is the primary 
pathological feature — the color is secondary. 

Etiology. — Embolism and thrombosis are most frequently the causes of 
cerebral softening, especially in old age. It is essentially a disease of old 
age, for nearly all the predisposing causes of thrombosis are met with in 
advanced life. Thrombotic softening between thirty and fifty is rare. But 

1 Rokitansky described yellow softening as occurring in well-developed spots. The fluid is acid in re- 
action from liberation of fatty and phosphoric acids. He further says the same kind of softening occurs 
about adventitious products in the brain, tumors, clots, etc., etc.— Path. Anatomy. 

2 Durand-Fardcl and Lancereaux both describe ramollissement blanc as the last stage of red softening. 
Charcot speaks of its frequency in old people with cancer.— Mai. des Vieillards. 



Fig. 199. 

Cerebral Softening. Small Blood-vessel from a Focus of 
Yellow Softening. 

AA. Lumen of the vessel containing the remains of a clot. 
~tB. Irregidarly dilated lymph-sheath 
fatty matter and detached endothelia. 



1004 



DISEASES OF THE NERVOUS SYSTEM. 



embolic softening may occur at any period of life where the predisposing 
causes of emboli exist. Syphilis and chronic alcoholismus must be ranked 
next to embolism and age as causes. It has been shown that syphilitic 
disease of the arteries leads to softening. Although the embolus that in- 
duces cerebral softening is usually cardiac in origin, it may spring from an 
aneurismal clot, from thrombosis in the large arterial trunks, or originate 
in gangrenous or carcinomatous foci in the lungs. Cerebral hemorrhage 
is a frequent cause of softening, and it may follow blows on the head or ex- 
posure to intense cold or heat (sun-stroke). 

It is well established that any new growth in the brain is accompanied 
by a zone of peripheral yellow softening. Fevers, the exanthematous 
especially, ulcerative endocarditis, necrotic and ulcerative diseases in the 
lungs and bronchi and osteo-myelitis have led to softening, but are more 
frequently the cause of abscess. 1 Glanders, puerperal diseases, and the 
toxic action of mercury and lead are regarded by some as causes. 2 

Symptoms.— Inflammatory red softening is usually attended by well 
marked febrile symptoms ; the temperature may reach 102° or 103° F. 
The pulse is accelerated at first, but afterward it becomes slowed. The 
face is flushed and the pupils irregular. There is intense and persistent 
cephalalgia, accompanied by dizziness, vertigo, and somnolence, and fol- 
lowed by confusion of mind, delirium, convulsions and stupor or coma. 
The gait is tottering and speech embarrassed. At first there is hyperes- 
thesia, formication, itching, and neuralgic pains. Later — with the paral- 
ysis — there is anaesthesia. Vomiting is often severe and obstinate. Mus- 
cular twitchings, contractions, clonic convulsions, and hemiplegic symp- 
toms are present and precede coma. Aphasia may accompany these symp- 
toms. If meningitis complicate the softening, its diagnosis is difficult. 
The softening may take place rapidly and be accompanied by hemorrhage. 
In such a case apoplectic symptoms will be prominent. Sudden and deep 
coma, however, may occur in acute softening without hemorrhage. Death 
may result in from two to eight days ; or, recovery may rarely occur with 
more or less permanent paralysis. 

White softening is oftenest met with in old age, and is usually preceded 
by despondency, physical weakness, loss of memory, and inability for pro- 
longed mental labor. 3 It may come on with acute symptoms, or insid- 
iously. Even when sudden in its development prodromata may have ex- 
isted very like those of apoplexy. Diminution in the motor power is often 
an important precursor of softening. When such premonitions occur, the 
symptoms either gradually increase or advance by sudden exacerbations, 
with intervals of apparent improvement. The affected side becomes 
feeble, the hands, feet and fingers are moved awkwardly, there is an un- 
steady tottering gait, and finally complete paralysis. Death may result 
from implication of the respiratory centres. 

Many cases are ushered in by the symptoms of cerebral thrombosis oi 

1 Reynolds and Bastian state that red softening mny be caused by " prolonged mental exertion or ex 
citement." 

2 M. Rosenthal, Bis. of Nervous System, vol. i. 

1 Durand-Favdel lay stress upon monotony of word or gesture as a valuable diagnostic sign. 



CEREBRAL SOFTENING. 



1005 



embolism, and subsequently, as softening slowly progresses, its characteris- 
tic symptoms are developed. In the aged, prodromata may not be promi- 
nent, and with momentary or without loss of consciousness the patient 
becomes suddenly paralyzed and aphasic. This resembles an apoplectic 
seizure, and is accompanied by headache and vertigo. The features are 
symmetrical until attempts at expression are made. Again, convulsions 
may occur instead of an apoplectiform seizure, or delirium may be promi- 
nent with muscular rigidity, spasmodic twitchings, dysphagia, and suffu- 
sion of the eye. Stupor and paralysis seem to alternate. The urine and 
faeces are passed involuntarily, and the patient dies from exhaustion. Bed- 
sores are apt to form about the buttocks. 

In all forms of softening there is more or less complete hemiplegia at- 
tended either by anaesthesia or hyperesthesia. When convulsions occur 
they are followed by increasing stupor and paralysis. If the paralysis 
begins at the fingers or toes and extends toward the trunk (creeping 
palsy), it is the chief symptom aside from the failure of mind and mem- 
ory. After a time these patients have to be fed and watched like children ; 
after eating they sleep until they are aroused again, and they often in their 
actions and in their mental capacity appear like very young children. 

Differential Diagnosis. — Eed softening may be mistaken for acute men- 
ingitis. Acute meningitis is, however, attended by a higher temperature, a 
peculiar pulse, more intense headache and vomiting, and is marked by dis- 
tinct stages — headache, delirium and coma. 

Yellow and white softening may be confounded with chronic meningitis 
and cerebral tumor. 

In softening there is usually a history of cardiac valvular disease or of 
senile atheroma. There is well-defined local pain in cerebral tumor, 
while the headache in softening is dull and diffused. Speech and intel- 
lect are less affected in tumors; they are both markedly implicated in 
softening. Permanent facial paralysis is usually present with cerebral tu- 
mors, and absent in softening. The limbs are principally involved in soft- 
ening. Epileptiform convulsions occur far more frequently with tumors. 
The symptoms of softening are usually steadily progressive ; while those 
of tumors are irregular and of longer duration. 

The diagnosis between the varieties of softening can only be made by 
the previous history of the patient. 

Prognosis. — Acute red softening may lead to abscess, or be a rapidly 
fatal complication of a pre-existing cerebral disease ; death is rarely de- 
layed beyond the tenth day. Chronic softening is a slowly fatal disease. 
Death may be due to the softening, to meningitis, asphyxia, pulmonary 
complications, diarrhoea, acute bed-sores, hemorrhage into the softened 
spot, or to exhaustion and anaemia. 

Treatment.— In all varieties of cerebral softening the most important 
thing to be accomplished is to improve nutrition. In the acute variety the 
patient must be kept quietly in bed ; cold may be applied to the head, and 
mild revulsives to the extremities. 

In threatened chronic softening — in the aged especially — attention is to 



1006 



DISEASES OF THE NERVOUS SYSTEM. 



be paid to the diet. The food must be simple, supporting, and very easy 
of digestion ; the best article of diet is milk. Excitement, active and 
prolonged mental or physical exertion must be carefully guarded against, 
and the bowels gently moved each day. Zinc, phosphorus, and strychnia 
may be given in combination with iron and quinine. The constant current 
alternating with the Faradic should be employed on the paralyzed limbs. 
For the relief of insomnia and the nervous phenomena cannabis indica 
combined with the bromides and chloral may be given. Bed-sores demand 
prompt treatment, for they frequently hasten the fatal issue. Alcoholic 
stimulants are indicated in the feeble and aged. 1 



The term cerebral apoplexy, although often applied to a somewhat uni- 
form combination of symptoms of varied causation, will be confined to non- 
traumatic hemorrhage into the cerebral substance or meninges and the re- 
sulting symptomatic conditions. 



Morbid Anatomy.— Cerebral hemorrhages are of all sizes, from minute 
capillary extravasations 2 to large clots cont aining several ounces of blood, 

» Cautery blisters, etc.. have often been tried. In none of the cases did benefit ensue ; in some, actual 
increase in the severity of the symptoms followed. Dr. Reynolds regards cod-liver oil as "the most valu- 
able agent in the treatment of chronic cerebral softening." Reynolds' System, art. Softening, by Keynolds 



CEREBRAL APOPLEXY. 




Fig. 200. 
Cerebral Apo^xy. 
Horizontal Section of the Cerebrum through a Clot in the Left Optic Tract, 




and Bastian. 
2 Capillary apoplexy of Cruveilhier. 



CEKEBRAL APOPLEXY. 



1007 



the so-called hemorrhagic foci. Preceding the hemorrhage the rup- 
tured vessel is the seat of miliary aneurisms due 1 to arterial fibrosis which 
commences in the perivascular lymph-spaces, and extends to the tunica in- 
tima. Globular, saculated, or fusiform dilatations are developed in vary- 
ing numbers, which are generally microscopic in size, but may be as large 
as a pin-head, and through their ruptured walls hemorrhage occurs. Mi- 
nute extravasations, however, play an important part in the development 
of apoplexy. Such foci are sometimes the result of venous thrombosis, and 
are probably soon absorbed, or they may accompany cerebral softening, as 
well as occur in the neighborhood of large apoplectic spots. More rarely 
an aggregation of these pin-head extravasations forms an apojilectic focus. 
In capillary hemorrhage, the lymph-sheath may remain intact, or be filled 
and more or less distended with blood. Fatty degeneration of the walls of 
the central vessel usually follows. In the other form (hemorrhagic focus), 
there is found, on autopsy, a clot, varying in size from a pea to a hen's 
egg, imbedded in the cerebral substance, which is irregularly spherical in 
the hemispheres, but in the motor tracts it is elliptical or irregular. In 
some cases an entire hemisphere is ploughed up by a large irregular hem- 
orrhage, which when near the cortex may break through the brain sub- 
stance, dissecting up or even rupturing the pia mater. 

The most frequent locations of these extravasations are the intraven- 
tricular nucleus of the corpus striatum, the extraventricular nucleus, optic 
thalamus, cerebellum, and pons— in the order named. The corpus stria- 
tum is sometimes pushed up and surrounded by the extravasation ; this is 
made out most distinctly by looking into the ventricles. The ventricles 
themselves may also be filled by a hemorrhage, or their septa torn and blood 
escape upon the surface of the brain. In the aged, apoplectic foci are not 
infrequently found between the membranes, in the meshes of the pia, or 
even superficially. When extravasations are extensive the cerebral convo- 
lutions are flattened, the sulci more or less obliterated, the dura is tense, 
and sometimes there is visible bulging when the hemorrhages are super- 
ficial. The adjacent pia mater and uninjured brain substance are ansemic 
from pressure. 

A recent clot is a soft, grumous mass, composed of coagulated blood and 
brain substance in varying proportions, at whose centre is the opening into 
the ruptured vessel. 2 It has a ragged wall of cerebral pulp, more or less 
deeply stained, and covered with fibrinous material, the result of the hem- 
orrhage. Surrounding this is a zone of discolored oedematous brain sub- 
stance, studded, in many cases, with capillary hemorrhages. 

When the apoplectic stroke is not immediately fatal, the following changes 
may take place in the clot : (1) the fluid parts may be absorbed, leaving the 
solid elements to undergo secondary changes ; (2) the clot and the lacerated 
cerebral tissue surrounding it may undergo fatty metamorphosis and be 
absorbed ; (3) inflammation may occur in the surrounding brain substance. 



1 Charcot et Bouchard ; Nouvettes recherches sur V hemorrhagie cerebrate. Arch, de Phys. 

2 Rokitansky states that in one form of apoplectic clot the fibrin collects near the centre, and in another 
toward the periphery of the mass. Path. Anatomy. 



1008 



DISEASES OF THE NEttYOUS SYSTEM. 



The subsequent changes which follow the absorption of the fluid portion of 
the clot are a granular and fatty degeneration of its solid constituents. It may 
then go on to caseation and subsequent calcareous change, or it may become 
encysted by the development of new connectiye-tissue from the neuroglia, 
forming a firm, smooth, pigmented cyst wall, 1 in which granular and fatty 
corpuscles are mingled with haematoidin crystals. The contents of this 
cyst are at first a milky or dark chocolate fluid, according to the amount of 
red globules present, which later becomes thick and creamy, and finally 
forms a firm, hard caseous mass, or if entirely absorbed there remains a firm, 
or friable, pigmented cicatrix. Around spots of capillary hemorrhage, the 
brain is softened and stained ; the medullary substance of the nerve fibres 
is broken up and intermingled with pigment granules and red and white 
blood corpuscles. 

Whether a cyst must have existed previous to the formation of a cicatrix 
is a question still in dispute. It requires from six months to two years foj 
the cyst to be absorbed and cicatrix to form. There may be a number ol 
these in the same brain, corresponding to the number of apoplexies. 2 Gran- 
ules and crystals of haematoidin are found between the adjacent nerve ele- 
ments and in the perivascular lymph-spaces, when the deep layers of the 
cortex are involved. The nerves connected with the motor tracts undergo 
degeneration, and connective-tissue increase takes place between the 
atrophied nerve fibres. These degenerative changes after a time extend 
into the spinal cord, and general atrophy of the brain may follow. 3 

Etiology. — Apoplexy is rare before forty years of age ; and after this the 
tendency steadily increases. Thus age is the most powerful predisposing 
cause. When it is stated that after seventy the tendency ceases, the small 
number of those who live after seventy is not taken into account. 

It is now generally believed that miliary aneurism is the antecedent state 
of every vessel that spontaneously ruptures within the cranial cavity. Peri- 
arteritis is thus a powerful predisposing factor, causing arterio-sclerosis. 
Fatty, atheromatous, and fibroid degenerations of the walls of the vessels 
also predispose to apoplexy. Hence the importance of gout, rheumatism, 
syphilis, chronic Bright's, and chronic alcoholismus as predisposing causes. 
Aortic insufficiency, pulmonary emphysema, and left ventricular hyper- 
trophy are important etiological factors. 4 

I have already spoken of the liability to hemorrhage in leuksemia and 
progressive pernicious anaemia. Scorbutus, typhus, pyaemia, malignant 
jaundice and chlorosis are conditions in which the blood does not afford 
adequate nutrition to the vascular walls, and they are then easily ruptured. 
Men are more liable to apoplexy than women, on account of their active 
mode of life and greater liability to excitement. Apoplexy occurs more in 
winter than in summer. The so-called plethoric habit which causes so 
much anxiety has little significance, for the emaciated valetudinarian is 

1 Forster states that a connective-tissue wall is not always found, even when death does not occur. Path, 

Anatomy. 

2 Cruveilhier states that he found fifteen in one brain. They cause thickening of the brain. 

3 Diseases of Old Age ; Charcot and Loomis, N. Y. Wm. Wood & Co., 1881. 

4 Simple ventricular hypertrophy is a physiological condition in old age. 



CEREBEAL APOPLEXY. 



10G9 



just as liable to apoplexy as he of the opposite condition. 1 Whether 
atrophy of the brain can produce sufficient dilatation of the cerebral ves- 
sels to cause rupture is uncertain. Cerebral softening may, by affording 
less support to the vessels, predispose to hemorrhage ; but is far more fre- 
quently a result than a cause of apoplexy. 

The exciting cause of cerebral hemorrhage is usually sudden increase in 
the blood pressure, although apoplexy may occur without any such in- 
crease. Coughing, running, a fall, sudden mental excitement, straining at 
stool" or in passing urine, bending the head far over near the feet, a cold 
bath, the sexual act (especially in advanced life), large ingestions of alcohol, 
sudden stopping of bleeding piles, use of opium, and 'a too hearty and 
indigestible meal may all induce a stroke in one whose arteries or arterioles 
are diseased. 

Symptoms. — Preceding an apoplectic seizure there may be premonitory 
symptoms. Vertigo, dizziness, muscaB volitantes, double vision, temporary 
blindness due to retinal hemorrhages, tinnitus aurium, flushing or pallor of 
the face, nausea, an abnormally keen sense of smell, or a total loss of it, are, 
some of them, present in a certain proportion of cases. Epistaxis in one 
past middle life is an important and dangerous prodromal symptom. These, 
however, are unimportant compared with loss of memory, tremor, or neu- 
ralgic pains, irregular or retarded heart action, difficulty and thickness of 
speech, lethargy, stupor, change in temper and sense of weight, numbness 
or formication, which very often are present before an apoplectic seizure, 
and must always excite alarm whenever they occur in one past middle life. 
Partial facial palsy is, by some, regarded as a noteworthy precursor. 2 In 
many cases none of these premonitory symptoms are present, but the seiz- 
ure is sudden, the patient rapidly passing into a state of coma. In others 
the comatose state comes on gradually, and is preceded by pains in the head 
and a feeling of faintness. In rare instances hemiplegia and aphasia are 
the primary symptoms. Convulsions usher in the attack when large hemor- 
rhages occur into the meninges. With very small hemorrhages there may 
be only momentary insensibility ; the patient recollects everything, though 
not clearly, and those about him pronounce it a fainting fit, or bad attack 
of indigestion, as it frequently comes on after over-indulgence at the 
table. 

Usually the coma is sudden and complete, and lasts from a few hours to 
two or three days. 3 During this coma the respirations are deep, slow, 
stertorous, and accompanied by a puffing sound ; sometimes the face is pale, 
but more commonly it is red, swollen, and turgid, and as the coma deepens 
it assumes a dusky, livid hue. Pallor may continue throughout the attack 
when the hemorrhages are gradual. If the coma lasts from forty-eight to 
seventy-two hours the temperature is lowered on the second day in some 

1 If, as H. Jackson supposes, there is an hereditary tendency to apoplexy, it must be transmitted through 
arterial disease. 

2 Trousseau and Hughlings Jackson. 

3 Apoplectic coma, according to Niemeyer, Hutchinson, and others, is due to anaemia produced by 
pressure upon the capillary vessels. This only holds good for large hemorrhages ; and small hemorrhages 
sometimes produce coma. 

64 



1010 



DISEASES OF THE KERYOUS SYSTEM. 



instances to 96° R The third day it not infrequently rises. The pulse, 
at the onset of the attack, is slow and irregular ; later it becomes frequent 
and more regular. The pupils are seldom normal ; they may be dilated, 
or, in meningeal apoplexy, contracted. Inequality of the pupils is of much 
more serious import than equal dilatation or contraction. Sometimes when 
the pupils are small, they quickly enlarge upon rousing or disturbing the 
patient. The patient may be unable to swallow, the features become dis- 
torted, and, as the paralysis deepens, the pupils dilate ; the skin becomes 
cold and clammy, and the urine and fseces are passed involuntarily. An 
apoplectic patient may lie apparently dead, 1 yet even in such cases sudden 
death is rare. 2 Keflex movements* except at the very onset, may nearly 
always be excited, often more readily than during health. Convulsive 
movements during the coma are rare. Hemorrhages into the pons and me- 
dulla, implicating the roots of the pneumogastrics, are generally followed 
by death in a few hours. The side that is subsequently paralyzed may show 
convulsive movements from the commencement, and tetanic spasms in 
sets of muscles or in single muscles occasionally occur. In many cases 
the head and both eyes are turned toward the healthy side for a short 
time. 

After the coma, consciousness returns slowly ; and in from forty-eight to 
seventy-two hours headache, restlessness, wandering or delirium may come 
on. A slight febrile movement, increase of the pulse-rate and respiration, 
confusion of the mental faculties, and contraction of the flexor muscles, 
indicate the occurrence of inflammatory changes in and about the clot. 

Hemiplegia upon the side opposite to the hemorrhage is one of the most 
constant attendants of apoplexy, especially in the aged. It may be accom- 
panied by anaesthesia, but this is rarely present without hemiplegia. The 
hemiplegia is permanent or temporary, according to the extent and location 
of the clot. As recovery takes place, the thick speech, retracted mouth, 
deviation of the tongue, and other evidences of facial paralysis gradually 
disappear. The leg also gains more or less in strength, but the arm is 
permanently paralyzed. This is more favorable, 3 however, than when the 
arm recovers and the leg remains paralyzed. Sometimes the face remains 
semi-paralyzed after the other signs of paralysis have disappeared. 4 Mus- 
cular contractures, of varying intensity, which relax during sleep, are 
rarely absent. 

Diminution of electrical excitability is the rule ; and the temperature 
of the paralyzed limb is below normal. The muscles are either hard and 
rigid, or weak and flaccid. They always show reflex excitability. An- 
aesthesia soon passes away ; but it is claimed that sensation is never as 
perfect on the paralyzed as on the non-paralyzed side. Though anaes- 
thesia and paralysis are commonly distributed over the same region, the 

* Nothnagel. 

2 Wilks : Guy's IIosp. Reports, 178, 1866. 
s Trousseau. 

4 Total loss of motor power is called paralysis ; partial loss is called paresis. Gubler describes some 
interesting cases of crossed or alternate paralysis, where a left arm and a right leg, etc., were paralyzed. 
A few cases of paralysis of the facial alone and of the musculo-spiral alone have been recorded.— Union 
Medicate, 1854. 



CEREBRAL APOPLEXY. 



1011 



former is usually confined to the track of certain nerves. 1 Sometimes the 
paralyzed parts are hyperaesthetic, the pain being diffused. 2 The organs 
of special sense are rarely involved. Sight and hearing may be altered, 
upon increase of intracranial pressure. Hemiopia is not uncommon! 
Paralysis of the olfactory is rare ; but when the chorda tympani is alfected 
taste may be abolished on the fore part of one side of the tongue. 

On the second or fourth day after the apoplectic seizure erythematous 
patches may appear in the sacral region on the paralyzed side. Excoria- 
tion then occurs, and the acute bed-sore, the most important of the trophic 
changes, appears as a dry brown crust. The eschar may slowly extend to 
the sound side. 3 The intellect rarely remains as clear as before seizure, 
and the disposition changes. The memory, especially for recent events' 
is markedly impaired, and the will-power is greatly diminished. Some- 




Fig. 201. 



Vertical Transverse Section of the Brain through the Optic Thalamus. 

A, A. Motor tracts of th£ cortex cerebri. 

B. Optic thalamus. 

C. Badiation of internal capsule to tlte motor tracts of the cortex. 
B. Lenticular nucleus. 

E. Claustrum. 

F. Caudate nucleus. Charcot. 

times complete imbecility follows an apoplexy. In the very aged there is 
a form of apoplexy that is seemingly associated with hemorrhage into, or 
rupture of, the walls of the ventricles ; it is accompanied by a general 



1 Tiirck states that anaesthesia is permanent when the inner part of the lenticular nucleus, the super- 
ficial portions of the thalamus opticus anrl the adjoining portions of the corona radiata are involved. The 
anaesthesia is also permanent in lesions of the pons and peduncles. 

2 Charcot has laid stress on the arthritic pains that occur in the paralyzed limbs (spontaneous), and 
Brown-Sequard on the neuralgic pains that are so troublesome during clamp, cold weather. The joints 
are swollen, hot and moist, and there is pain on motion. 

3 Some claim that these eschars depend upon trophic influences due to local hypersemia. Charcot 
states that they are due to irritation of trophic centres in the brain. Most authorities, including Charcot 
and Nothnagel, ascribe little influence to vaso-motorial changes.— Charcot, Lecons sur les Maladies du 
System Nerveux. Paris, 1872. 



1012 



DISEASES OF THE NEKVOUS SYSTEM. 



epileptiform attack, lasting from fifteen to thirty minutes, during which 
the tongue is bitten and frothing at the mouth occurs. This is followed, 
apparently, by no serious results, other than the gradual development of 
extreme debility. Death, however, usually occurs after a longer or shorter 
period, which varies with the age and constitution of the patient. 
Localization of cerebral lesions. 

I. Hemorrhage into the motor ganglia — corpus striatum 1 and lenticular 
nucleus — occurs in nearly seventy per cent, of all apoplexies. It is attended 
by hemiplegia, partial paralysis of the face, some anaesthesia, and slight 
ocular disorders and perversions of the special senses. Intelligence is modi- 
fied, memory chiefly, and there may follow hemi-chorea and athetosis. 2 
The head is turned from the paralyzed side. To say whether the lenticu- 
lar nucleus or the nucleus caudatus is alone involved is impossible. 

II. When the thalamus opticus is alone involved there is anaesthesia 
and no motor paralysis. No points (yet) known are indicative of exclu- 
sive implication of this ganglion. 3 

III. Lesions of the cortex are most interesting from their diverse mani- 
festations, and from the study and experimentation that have been ex- 
pended upon this subject. 4 The motor zone of the cortex, however, em- 
braces the anterior and posterior central convolutions and the lobulus 
paracentral. Hemiplegia, in nowise differing from that due to lesions 
of the nucleus lenticularis, may arise from hemorrhage into this part. 
Aphasia, both ataxic and amnesic, follows destruction of the island of Eeil, 
or of the third left frontal convolution. Hemorrhage into the paracentral 
lobule is followed by paralysis of the arm and leg of the opposite side. 6 
Following cortical lesions there appear convulsive epileptiform movements 
in certain groups of muscles, or in single muscles called ft partial epilepsy 
of cortical origin." 

IV. Extensive cortical hemorrhage is usually associated with more or 
less meningeal apoplexy, and is to be distinguished from pachymeningitis. 
The seat of meningeal hemorrhage may be at the base or convexity, or 
spread over both hemispheres. The symptoms in children are somno- 
lence, spasms and tremor. Death usually occurs rapidly with convulsions, 
dyspnoea and sudden attacks of vomiting. 6 In the adult death often oc- 
curs very suddenly, and most cases of sudden death from apoplexy are at- 
tended by meningeal hemorrhage. Rupture of the posterior communica- 
ting artery is preceded by signs of compression of the third, fifth and 
sixth cranial nerves. 7 

V. Hemorrhage into the pons is commonly followed by coma and 
speedy death. Convulsions attend the passage of blood into the fourth 

1 The caudate nucleus. 

2 Top. Diagnos. d. Gehirnkt. Nothnagel, 1879. 

8 Hammond and Luys alone state that aberrations of the special senses follow lesions of this part of the 
brain. 

4 Charcot and Pietres state that destruction of the infr. parietal lobe, angular gyrus, of the anterior 
portion of the first, second and third frontal convolutions produces no motor paralysis. 

6 M. Rosenthal states that psychical disturbances play the chief part in cortical (hemorrhagic) lesions. 

6 Wtirt. Med. Corblatt Msasser. 

7 Gougoucnheim. 



CEREBRAL APOPLEXY. 



1013 



ventricle. Incomplete paraplegia, facial paralysis, at times on the same, 
at others on the opposite side to the lesion, contracted pupils that do not 
respond to light, disorders of taste, smell, or hearing, indicate apoplexy in 
the median portion of the pons. Sometimes hemorrhage into the pons 
attended by slight spasms is followed by partial hemiplegia, 1 or by irregu- 
lar and difficult breathing. Besides crossed paralysis, we may find hemi- 
plegia, paraplegia and paralysis of all the extremities, with or without 
facial paralysis ; or double facial paralysis with hemiplegic phenomena. 2 
The mental symptoms are few, if any. Anaesthesia is common ; and may 
be crossed also. All authorities note that articulation is more difficult 
and paralysis of the abducens is more likely to occur with this than with 
any other brain lesion. 

VI. Hemorrhages into the anterior lobe are commonly attended by hemi- 
plegia, incomplete paralysis of the face, and when on the left side by 
aphasia. 

VII. Hemorrhage into the middle lobe is attended by amblyopia, con- 
gestion of the retinal veins, and injection of the optic papilla. 3 Xausea, 
dizziness and headache often occur. 

VIII. Hemorrhage into the posterior lobe is marked by intellectual dis- 
turbances, and usually by the absence of motor and sensory disturbances. 
When hemiplegia occurs its tendency is to gradually disappear. Frequently 
no symptoms attend a hemorrhage into the substance of the cerebral 
lobes. 

IX. In hemorrhage into the cerebellum vomiting is a prominent symp- 
tom. 4 Although it is the great co-ordinating ganglion, clots in the cerebel- 
lum rarely produce disturbance of co-ordination. Sensibility is never dis- 
turbed, but there is pain in the back of the head. Sometimes the eyes are 
rolled about mcoordinately, and amaurosis and amblyopia occur. In 
hemiplegia 5 from hemorrhage into the cerebellum there is no lingual or 
facial paralysis, though there is loss of facial expression. The patients 
can, and do, lie only in one position ; when they are moved they immedi- 
ately return to it. 

X. Hemorrhage into the lateral cerebellar lobes is attended by obstinate 
headache, vertigo, vomiting, amblyopia, amaurosis, dilatation of the pupils, 
thick and difficult speech, and by hemiplegia on the opposite side. 6 Should 
the hemorrhage encroach upon any of the great centres, the symptoms will 
be more pronounced. Injury of the cardio-inhibitory centre would be in- 
dicated by irregular heart action, a condition that frequently occurs. 

XI. When the crura of the cerebellum are involved, the symptoms resem- 
ble those of hemorrhage into the cerebellum ; most modern pathologists, 
ascribe all the synrptoms of cerebellar hemorrhage to lesions of the crura. 

1 Gnbler and Lays state that crossed paralysis is always attended by apoplexy in the pons. Exceptions 
have occurred, however. — Trousseau, Clin. Med. 

2 Brown-Sequard. 

3 White spots in its centre were noted, in addition to the amaurosis, in Hughlings- Jackson's cases. 
—Reynolds? System of Med. 

4 Berliner Klinische Wochenschrift—Rexa&k, 1865. 

5 London Lancet, Nov. 2, 1861. 

5 Rosenthal, Bis. of yervous Sys. vol. i., p. 50-60. 



1014 



DISEASES OF THE NEKYOUS SYSTEM. 



The patients are sometimes forced to rotate about the long axis of the body, 
in some cases toward, in others from, the paralyzed side. 

XII. Hemorrhage into the cerebral peduncle is attended by hemiplegia 
and alternating facial paralysis, and by ptosis, mydriasis, and diverging 
strabismus on the same side. 

XIII. Destruction of the corpora quadrigemina leads to blindness and 
the pupils become fixed. 

XIV. When the medulla oblongata is involved, the symptoms are the 
same as those due to injury of the pons. In addition there is diabetes and 
albuminuria in many cases. Grlosso-pharyngeal and hypoglossal paralysis 
cause dysphagia and loss of power to protrude the tongue ; dyspnoea, ir- 
regular heart action, and gastric derangements arise from implication of the 
pneumogastric. 

XV. Finally, when hemorrhage occurs into the ventricles, death is usu- 
ally rapid. Recovery is possible, however. 1 Spasms and contractions of the 
paralyzed extremities occur in many of these cases. 

Differential Diagnosis. — Apoplexy may be mistaken for cerebral congestion, 
uraemia, alcoholic coma, cerebral embolism, opium poisoning, epileptic and 
hysterical coma. 

Stertorous breathing — a common symptom in apoplexy — is absent in cere- 
bral congestion. The pupils are alike in congestion; in apoplexy they are 
unequal. The coma is of short duration in congestion ; in apoplexy it 
persists for some time. Congestion has a long prodromal period; in apo- 
plexy this is short or absent. Should paralysis be present from congestion, 
it is usually bilateral; while in apoplexy hemiplegia is more or less complete. 

The mental faculties are rapidly and completely restored after an attack 
of apoplectiform congestion, while the reverse is the case in apoplexy. 

In urwmia the previous history of the patient is important, and there is 
more or less oedema. Hemiplegia is never present in uraemia ; it is rarely 
absent in apoplexy. Ursemic coma comes on gradually and is usually pre- 
ceded by convulsions; while the coma of apoplexy is more sudden in its ad- 
vent, and is followed rather than preceded by convulsions. Casts and al- 
bumen in the urine are strong presumptive evidences of ursemic coma. 

Profound alcoholic intoxication is often mistaken for apoplexy. A pa- 
tient can be roused from alcoholic coma, but not from apoplectic. There is 
no stertorous breathing in alcoholic coma ; while this is rarely absent in apo- 
plexy. The pulse, in alcoholic coma is feeble ; in apoplexy it is full, strong 
and slow. There is no hemiplegia in alcoholismus, and the urine as well 
as the contents of the stomach will contain alcohol. 

The diagnosis between apoplexy and cerebral embolism is often difficult. 
Both may be preceded by rheumatic endocarditis and valvular disease of 
the heart, although they are more frequent in embolism than in apo- 
plexy. In embolism there is rarely complete loss of consciousness ; and if 
it occur it is of short duration ; while loss of consciousness is the rule in 
apoplexy, and it usually continues for two or three days. The pulse in em- 
bolism is feeble and frequent, and the face is pallid ; while in apoplexy the 



1 Diseases of Old Age ; Charcot and Loomis, New York, 1881. 



CEREBRAL APOPLEXY. 



1015 



pulse is slow and full, and the face is suffused. Aphasia is the rule in em- 
bolism and the exception in apoplexy. The pupils are unchanged in em- 
bolism ; while in apoplexy they may be dilated, contracted, or unequal. 
The respiration is normal in embolism and stertorous in apoplexy. There 
is usually right-side hemiplegia in embolism; if left side hemiplegia exist, 
it is probably due to cerebral hemorrhage. Arterial degeneration is always 
present in apoplexy ; while in embolism the arteries may be normal. The 
paralysis is temporary in embolism and recovery is complete ; while in 
apoplexy it is delayed, and recovery is partial. Vomiting is a far more 
prominent symptom of apoplexy than of embolism. Embolism is probable 
when hemiplegia occurs suddenly in the young; apoplexy is a disease of 
middle and advanced life. Premonitory cerebral symptoms are never pres- 
ent in embolism ; they may be in apoplexy. 

Opium poisoning gives many of the symptoms of apoplexy. Apoplexy 
is usually accompanied by dilated or irregular pupils; opium always pro- 
duces regular and generally pin-head pupils. Convulsions may attend 
apoplexy ; they are absent in opium poisoning. The coma comes on more 
gradually, and is not usually as deep in opium poisoning as in apoplexy. 
An exceedingly slow pulse and respiration indicate narcotic poisoning. 
Stertor and hemiplegia attend apoplexy, and the pulse may be irregular. 

The coma of epilepsy may be confounded with that of apoplexy ; bat 
the blood-stained frothing at the mouth, the imprint of the teeth on the 
tongue, the history of previous convulsions, the rapid recovery, and the 
age of the patient are sufficient to distinguish epileptic from apoplectic 
coma. 

In hysteria the coma is not deep, and cold will restore to consciousness. 
Stertor is absent, the pupils are mobile or unchanged. In hysterical hemi- 
plegia the patient drags the limb like an inert mass, contractions develop 
more rapidly than in apoplexy, and the electro-muscular contractility 
diminishes after it has lasted for a short time. Hysteria is preceded by 
characteristic hysterical attacks which have been followed by abundant 
limpid urine. In spinal hemiplegia sensation is preserved. The electro- 
muscular contractility is diminished, and reflex excitability is increased. 
Sensation is lost on the opposite side, but motion and contractility are in- 
tact. 

Prognosis. — The prognosis of apoplexy is always grave. The greater the 
age the more unfavorable it is. 1 Death rarely occurs at the onset of the 
seizure ; but the hemiplegia, the loss of mental power, and the liability to 
recurring attacks render it, even when not at once fatal, a dreaded con- 
dition. It is a favorable sign if the hemiplegia begins to improve very soon 
after the attack ; but if the period of unconsciousness is prolonged, if the 
coma deepens, if reflex excitability is wholly lost, the sphincters relaxed, 
the breathing irregular, puffy, and noisy, if the pupils enlarge, or the 
temperature after having fallen rises rapidly, a fatal termination is in- 
dicated. Convulsions in the aged always indicate great danger. 



1 Durand-Fardel state that ventricular and meningeal hemorrhages are frequent after sixty ; hence an 
apoplexy in one who has passed that age must be regarded as very serious. 



1016 



DISEASES OF THE NERVOUS SYSTEM. 



The general condition of the patient and the extent and degree of paraly- 
sis are always important factors in the prognosis. Epileptic seizures may 
follow a partial recovery from apoplexy. Death may occur from the shock 
of a large extravasation, from interference with the medullary centres, 
from asphyxia, and sometimes from inanition. 

Treatment. — In one who has the prodromal symptoms of apoplexy, or 
whose age and condition are such as to favor its occurrence, prophylaxis 
may avert an attack. 

The principal prophylactic measures are the avoidance of sudden or 
violent physical exercise or strain, and of strong mental emotions. The 
diet should be most nutritious, but non-stimulating, and sleeping and 
living rooms should be large and well ventilated. Great care should be 
taken that the functions of the intestines, liver, and kidneys are kept at 
their normal standard ; and moderate exercise should be taken daily in the 
open air. Sudden extremes of temperature should be avoided ; therefore 
hot or cold baths are to be forbidden. The body should always be warmly 
clothed in flannels. 

In the advent of the premonitory symptoms, free purgation and the 
application of blisters to the neck with the bromide of lithium and oxide 
of zinc are indicated. 

When an apoplectic seizure has occurred, the patient's head is to be 
elevated, the clothing about the neck loosened, and he is to be put in bed 
in a cool, dark and absolutely quiet apartment, with cold applied to the 
head and heat to the feet. If the fit occur after a hearty meal, vomiting 
must be induced and a purge given. Blood-letting is to be the exception ; 
but if a very robust individual with high arterial tension is seized, and 
there is evidence of progressive hemorrhage, then six to eight ounces of 
blood may be taken. The condition of the heart and the arterial tension 
are the guides as to the propriety of blood-letting. In old age or in the 
weak, with a pale face and feeble pulse, venesection is never to be prac- 
tised. The condition of the bladder should be carefully examined, and the 
urine drawn if necessary. Much of the turgescence of the face is due to 
the falling back of the tongue, consequently the patient should be placed 
on his side. Sinapisms may be applied to the nape of the neck, calves, and 
over the stomach, when venesection is not practised. 

As the patient comes out of the coma the vital powers must be sustained, 
the most absolute rest and quiet enjoined, and the bowels kept freely open 
by mild salines. Milk and beef juice are to be freely administered, and if 
there is very great feebleness stimulants may be given. Stimulation is 
demanded very early in old and feeble subjects. Narcotics are indicated 
when there is great restlessness and insomnia, especially in the aged. 

The clot in the brain is now a foreign body : nothing external or internal 
can remove it ; hence blisters, ointments, drugs, etc., etc., are worse than 
useless. The galvanic current to the paralyzed limbs is indicated if the 
paralysis persists. It may be passed directly through the brain, and though 
the absorption of the clot may not be aided by it, it often benefits the 
paralyzed limbs. It should not be resorted to until three or four months 



ABSCESS OF THE BRAIN. 



1017 



after the seizure ; but passive motion, gentle friction, and the application 
of stimulating liniments to the surface may be practised early on the par- 
alyzed limb. Massage of the paralyzed limb should always form part of 
the treatment. When electricity is used, three or four seances a week, each 
lasting from five to eight minutes, are sufficient. 1 

ABSCESS OF THE BRAIN. 

Abscess of the brain or suppurative encephalitis may occur in any part 
of the brain. It may be simple or multiple, and may not differ in charac- 
ter from abscesses in the connective-tissue in any part of the body. 

Morbid Anatomy. — The white substance of the middle cerebral lobes is 
its most frequent site. About 16 per cent, of all cases are located in the 
cerebellum, and about 3 per cent, each in the pons, corpus striatum and 
thalamus opticus. 2 They may vary in size from a walnut to the involve- 
ment of an entire hemisphere. Usually they are from one to two inches 
in diameter. They are irregularly spherical in shape. 

Embolic abscesses are usually multiple. Their walls are irregular and 
made up of shreddy, disintegrated brain substance, with projections Avhich 
are found to surround blood-vessels. A limiting membrane may or may 
not exist. In recent abscesses it is either wanting or incomplete. Some 
abscesses have a membrane from their very onset ; they are encapsulated. 
Usually a zone of red softening surrounds the abscess, and around this is 
an envelope of oedematous brain substance. 3 

Their contents are usually inodorous and composed of a greenish, creamy 
pus, fatty and granular matter, the debris of necrosed brain-tissue. Py- 
emic abscesses may contain fetid pus. The pus is decidedly alkaline ; very 
rarely is it acid. When mucin is present the pus is ropy, viscid, or gela- 
tinous. As an abscess increases in size it causes pressure on the adjacent 
brain substance. In large abscesses the convolutions are compressed, so 
that their edges are sharpened and their surfaces flattened. On removing 
the brain a bulging with a boggy feel is sometimes noticed. 

Cerebral abscesses may rupture into the ventricles, or they may make 
their way to the surface of the brain and cause diffuse suppurative menin- 
gitis. In rare instances they discharge into the cavity of the tympanum, 
the nasal fossa?, or the orbit of the eye. 4 Multiple abscesses are small ; 
they are found scattered throughout the brain. The processes by which 
the formation of a cyst wall is effected in these abscesses have been de- 
scribed by Rindfleisch as follows : a fibrinous wall, sometimes a quarter of 

1 The subcutaneous injection of strychnia into the paralyzed limb has been recommended, and hypo- 
dermics of ergotin have been advocated during the attack and at, the commencement of the subsequent 
coma. Dr. Celborne reports a case whereafter an hour and a quarter's persistent practice of artificial 
respiration by the Sylvester Method, asphyxia was averted. -Jour. Med. Chirur. Pesth., Dr. Foster, iV. Y. 
Med. Rec, 1876. 

2 Hammond states that the gray matter is involved first, the white secondarily. Gull and Sutton state 
just the contrary. 

3 Rokitansky states that yellow (chronic) softening surrounds cerebral abscess in a large majority of 
cases. 

4 Niemeyer states that the pus, after reaching the surface of the brain, may perforate outwardly through 
the bones, provided extensive meningitis has not been excited.— Text-Book of Pract. Med.,\o\. ii., p. 227. 



1018 



DISEASES OF THE NERVOUS SYSTEM. 



an inch thick, may envelop the abscess. The innermost, lining membrane 
of this cyst-wall consists of a yellow, smooth layer of cells. Tortuous 
venous vessels traverse it ; it is sometimes called the pyogenic membrane. 
Next to it is a layer of germ-tissue, irregular in thickness. Externally is a 
stratiform, spindle-celled tissue, that forms a direct transition into the sur- 
rounding brain matter ; in spite of which, however, the abscess can be 
enucleated. A zone of fatty degeneration surrounds the outermost (fibrous) 
layer of the cyst-wall. The pus, Rindfleisch further states, is greasy, 
greenish-yellow, acid, and usually odorless. It is to be noted that Gull 
and Sutton state the pus to be decidedly alkaline and very fetid in old 
abscesses. 

Haematoidin crystals, margarin, and cholesterin are not infrequently 
found mingled with the pus, and the entire capsule is to be regarded as a 
neuroglia production. Absorption, cheesy degeneration, and the forma- 
tion of chalky masses are said to occur in cerebral abscesses. The cyst- 
wall retracts and finally disappears/ 

Etiology. — Cerebral abscess occurs at all ages. Males are more subject 
tc it than females. Among its chief causes are suppurative otitis and 
traumatism, especially blows on the head. It may result from suppurative 
inflammation of the face and scalp, and from suppuration about the orbit 
or nose. Syphilitic and other diseases of the bones of the skull, the tem- 
poral especially, are not infrequently followed by abscess. Pyaemia and 
glanders are among its frequent causes. Red inflammatory softening is the 
first stage of abscess. Ulcerative endocarditis and osteo-myelitis are espe- 
cially liable to give rise to it ; the embolus in these cases has a special 
character. There are cases in which no cause can be found for their de- 
velopment. 

Symptoms. — Headache is the most constant and prominent symptom of 
abscess of the brain. In some cases it is not severe but is constant, in 
others it is so severe that patients are not able to bear it without an anodyne. 
It may be so circumscribed as to localize the very site of the abscess. With 
the headache there is vomiting and dizziness. Delirium and disturbance 
of intellect may be marked but transitory ; it may alternate with stupor. 
Epileptiform convulsions, and signs of cerebral pressure may end in coma. 
Incontinence of urine and faeces is a prominent symptom in most cases. 

It is to be remembered that large abscesses have been found in the brain 
of those who during life, gave no cerebral symptoms. Otitic abscesses 
of the brain are preceded by all the signs of the (causative) local disease. 
Headache, vomiting, delirium, fever and irregular chills, spasmodic move- 
ments in the muscles of the face or limbs, then hemiplegia, coma and death 
— this is the usual course of such an abscess. But cases are reported where 
an artificial or spontaneous exit to the pus has been followed by recovery. 2 
In some cases optic neuritis has been found. 3 Rapid and progressive 
emaciation usually accompanies cerebral abscess. At times there will be 
hyperaesthesia and abnormal acuteness of the special senses at the onset ; 



1 Rosenthal, Diseases of Nervous System, vol. i. 

2 Schloz. 



3 Hughlings-Jackson. 



TUMORS OF THE BRAIN AND MENINGES. 



1019 



and this will be followed by sopor, anaesthesia, formication, numbness, etc., 
etc. If the abscess involves the motor tract, hemiplegia or local paralyses 
will occur. 

When pyaemic abscesses occur in the brain, they are chiefly diagnosticated 
by the constitutional symptoms. It will begin with rigors and run an 
acute course ; the temperature may reach 105° R Ague-like rigors and 
the initial signs of abscess coming on when the conditions of pyaemia exist 
must lead to the suspicion of multiple cerebral abscess. 

Sometimes in cbronic abscess of the brain there is a long latent period. 1 
During this time epileptiform convulsions, facial paralysis, and hemiplegia 
and aphasia accompanied by intermittent chills and headache may occur ; 
After which, acute symptoms may be present for a few days and end in 
death. The acute symptoms differ widely in different cases ; there may 
be localized headache over the abscess, delirium, nausea, vomiting, well- 
marked signs of cerebral irritation, ending by a fall in temperature and 
pulse, deep coma and death. 

Differential Diagnosis. — It is always difficult to distinguish cerebral ab- 
scesses from cerebral tumor. Abscess is accompanied by greater emacia- 
tion and is of shorter duration than tumor. Local paralyses of long 
standing are common in tumors, rare in abscess. Eigors and more or less 
fever usually attend abscess. An ozoenal or otorrhceal discharge, the his- 
tory of traumatism, or the fact of a latent period having existed, is in favor 
of abscess. Softening may be mistaken for abscess. The age of the 
patient, the condition of the blood-vessels, the slow development of the 
hemiplegia, the absence of constant or intense localized pains in the head 
and the gradual loss of mental power, distinguish softening from abscess. 

Prognosis. — Acute abscess of the brain is always fatal in from four to 
twenty days. Chronic abscess terminates fatally from its complications, 
the commonest of which are meningitis, cerebral hemorrhage, oedema, 
softening, thrombosis of the cerebral sinuses, serous effusions into the 
meshes of the pia mater and the ventricles, and pulmonary hypostasis. 
When abscesses are situated away from the motor tract and surface of the 
brain, they may exist for years and give rise to no symptoms. 

Treatment. — The treatment of cerebral abscess is altogether surgical. 
The operation of trephining for traumatic abscess, and the treatment of 
chronic aural disease, are fcund in modern surgery and in special works 
upon diseases of the ear. Eecently the withdrawal of pus from the brain 
has received much attention, and marked success has attended surgical 
operations for the accomplishment of this end. Anodynes are always indi- 
cated for the relief of the intense headache. 

TUMOKS OF THE BKAIN AND MENINGES. 

The most frequent intracranial growths are tubercle, cancer, gummata 
and gliomata. Apoplexy and abscess, which have much in common with 
tumors of the brain, are elsewhere described. Some intracranial growths 



1 Lebert says from one to two months. 



1020 



DISEASES OF THE NERVOUS SYSTEM. 



are peculiar to the brain, e. g., psammomata ; but the majority (cancer, 
tubercle, gummata, etc.) do not differ, in their anatomical characteristics 
from similar growths elsewhere in the body. 
Intracranial tumors may have their origin in the meninges, as sarcomata, 




myxomata, lipomata, cholesteatomata and psammomata ; in the blood-ves* 
sels as angiomata, aneurisms, and a peculiar tumor in rare instances found 
in the third ventricle — the epithelioma myxomatodes psammomum ;* and 
in the neuroglia, as gliomata, gummata and fibromata. 

Morbid Anatomy. — The commonest form of cerebral tumor is the tuber- 
culous. These growths vary in size from a pea to an orange. They are hard 
and compact, their exterior being gray, semi-transparent, and intimately 
blended with the surrounding brain-tissue. Their centres are soft and yel- 
low. They develop slowly and may calcify. The vessels going to them are 
dilated, and at the centre of the growth they are indistinguishable. Tu- 
bercular tumors occur in the hemispheres, cerebellum, optic thalami, cor- 
pora striata, peduncles, pons Varolii and ependyma of the ventricles f but 
the cerebellum 3 is their favorite seat. At times tubercular growths are 
encysted. 

Cancer of the brain may originate in the cranial bones, the dura mater, 
the pia mater, the cerebellum, the cerebrum, the pons, or the medulla oblon- 
gata. Encephaloid cancer is the commonest variety. The color depends on 
(1) their vascularity, (2) the kind of softening about them, and (3) on 



1 E. Long Fox, in Quoin's Dictionary, p. 157. 

2 Forster. 



Jenner. 



TUMORS OF THE BRAIN AND MENINGES. 



1021 



the amount of retrogressive degenerative changes that have occurred at 
their centres. When more than one tumor is present, they develop sym- 
metrically, and are liable to involve homonymous parts of the brain (Roki- 
tansky). 

Gummata, or syphilomata, may appear as soft, red-gray, jelly-like 
masses, irregular in form, and intimately blended with the adjacent brain 
substance. They are chiefly composed of round cells, but spindle and 
stellated cells are sometimes found. They may have an alveolar frame- 
work. Capillaries are not numerous in their substance. There may, how- 
ever, be small points of extravasation. There are rare forms of gummata 
which consist of a well-defined homogeneous mass, which is dry, friable 
and cheesy. Atrophied neuroglia and round and spindle cells in a state 
of fatty degeneration are often found throughout the gummy masses. 
Syphilomata are generally found at the circumference, and especially at 
the base of the brain. They may have their origin in the membranes, the 
vessels, or the neuroglia. The surrounding inflammation joins them to 
the meninges. If the latter be joined to the dura mater, granules are de- 
veloped in the pia, which vary in size from a pea to that of a small egg. 
Syphilitic tumors in the interior of the brain are very rare. 1 

So-called syphilis of the brain may appear, (1) as well-defined hard 
tumors, (2) as thickenings, adhesions, and contractions or puckerings of 
the meninges, (3) as disease of the walls of the vessels, and (4) as spots 
of softening or diffuse gelatinous accumulations. 2 

Gliomata 3 may develop either in the brain substance, or in the meninges 
along the course of the cephalic nerves, or in the retina. On account of 
its vaccularitv, hemorrhages are liable to take place into its substance. At 
times a light brown coagulum causes the tumor to resemble tuberculous or 
gummatous growths. It is often difficult to distinguish a glioma from nor- 
mal brain substance. These tumors may be either hard or soft ; soft gli- 
omata contain only a small quantity of intercellular substance. Hard 
gliomata have bundles of parallel or interlacing fibrillae as their fundamen- 
tal substance. They vary in size from minute masses to masses as large 
as an orange. They grow slowly and are usually solitary. There are fat 
granules, cholesterin crystals, neuroglia nuclei, a debris of nerve-tissue, 
and more or less redness and softening in the immediate neighborhood of 
gliomata. 4 Diffuse gliomatous masses were once thought to be infiltrated 
cancer of the brain. 

Psammomata, or Virchow's sandy tumor, are soft, juiceless sarcomata 
whose cells are thin, flat, irregular in outline but very large. The vessels 
are in direct connection with the cells. Psammomata usually develop 

1 Rindfleisch states that syphilomata develop in the brain substance along the lymphatic sheaths and 
the vessels, and that they produce spots of softening by compression of the vessels and arrest of the cir- 
culation. . _ m , 

2 Niemeyer states that gummata are more frequent as diffuse infiltrations. Virchow, Charcot and West- 
phal have found gummata in the white substance of the hemispheres, in the thai, opticus, the pituitary 
gland, the optic tracts, the cerebral peduncles, the pons, and in the cerebellum. 

3 The neuroglia-sarcomata of Cornil and Ranvier. 

* Ernest Wagner and Obermeier regard hyperplasia of the pineal gland as essentially the same as a glic 
matous neoplasm. 



1022 



DISEASES OF THE NERVOUS SYSTEM. 



from the dura. They may reach the size of a pea, and are hard, smooth, 
and spherical. These calcareous tumors often have a concentric or lami- 
nated structure. 

Cholesteatoma (called pearl tumors from their lustre) do not always 
contain cholesterin, but consist of concentric layers of epithelial cells 
that have partially undergone fatty degeneration. They may have an in- 
distinct fibrous envelope. They rarely exceed one and one-half inch 
in diameter. They are aggregations of crystalline, pearly masses, the 
size of a mustard-seed ; they grow slowly from the pia at the base of the 
brain, or in some depression of it. They are pathologically insignificant. 

Cysts (independent of cystic developments from echinococci, etc., etc.) 
are rare. They seldom exceed the size of a pin head, and are found on the 
walls of the lateral ventricle. They may occur singly or in groups. Trans- 
parent serous cysts developing from the vessels of the choroid plexus are 
not rare. 

Medullary or ganglionic neuromata — tumors of nerve-cells and ganglia 
— occur in, and on the brain ; they are seldom larger than a pea, and are 
found on the ventricular surface, in the white substance, or in the cor- 
pora striata. 1 A tumor to be a neuroma must contain a large number of 
nerve-cells. 

Sarcomata appear as well-defined, round or lobulated tumors, varying in 
consistency, and in size from that of a walnut to an apple. They may 
originate in the cerebral hemispheres, but more frequently they arise from 
the dura, especially at the base of the skull. There are two forms, the 
hard sarcoma with compact hard fundamental tissue and small cells, and 
the soft sarcoma with loose, scanty intercellular substance and numerous 
cells of large size. They are separated from the surrounding brain sub- 
stance by a very vascular zone. 

Myxomata appear either as well-defined tumors or as infiltrated masses 
whose seat and size resemble those of sarcomata. Indeed, to determine 
whether a tumor is a sarcoma that has undergone mucous transforma- 
tion, or a myxoma with patches of embryonic tissue, is always very diffi- 
cult. 

A true myxoma or sarcoma may result from a glioma (q. v.), the tran- 
sition being gradual ; these various sarcomatous tumors are found in the 
hemispheres, the anterior lobes, thalamus opticus, cerebral peduncles, or 
they may involve the pons and tubercular quadrigemina. 2 

Lipomata are rare, and are only found at the raphe of the corpus cal- 
losum and fornix. 3 

Osteomata, new formations of bone, independent of ossification or other 
neoplasia, are not frequent. Osteoma of the cerebellum has been found to 
follow encephalitis. Osseous new growths must not be confounded with 
syphilitic or other exostoses. 



1 Cornil and Ranvier, Pathol. Histologiqve. 

2 Transac. Pathol. Society, Dr. Cayley, vol. xvi., p. 23. 

3 Virchow. Benjamin reports a case where ossification had occurred ; Niemeyer describes lipomata as 
" small lobulated tumors starting from the dura." 



TUMORS OF THE BRAIN AND MENINGES. 



1023 



Papillomata are the rarest form of cerebral tumors. They are cauli- 
flower-like, budding growths, with abundant milky juice, very vascular, 
and surrounded by a zone of cerebral softening. A large one — situated on 
the ependyma of the third ventricle — is described by Cornil and Ranvier. 1 

Fibromata appear as hard, fibrillar tumors, small, and rarely peduncula- 
.ed. In one case seventeen fibrous tumors were found on the ependyma of 
the lateral ventricle. The pons and the cerebral peduncle are sometimes 
implicated by this tumor. 

Angiomata, or erectile tumors, are masses composed of vessels of new 
formation. They are found in the cerebral substance, corpus striatum, 
cerebellum, and floor of the fourth ventricle. They may be multiple. 2 

Aneurisms are not uncommon ; they do not attain a large size. They 
involve the basilar artery, the vessels in the Sylvian fossa and corpus cal- 
losum, the anterior communicating — rarely other than basic vessels ; from 
their position they are liable to compress some of the nerves at the base of 
the brain. Miliary aneurisms have been considered in the history of apo- 
plexy. 

Hydatids or echinococcus cysts usually exist as solitary tumors which may 
attain any size. They are generally located at the centre of the white matter 
of a hemisphere. The cyst-wall is always absent when the hydatid is in the 
ventricle. Some claim that it is absent even when located elsewhere in the 
brain. They grow slowly, producing atrophy of the brain. Five large hy- 
datid cysts have been found in various parts of the same brain. 

Cysticerci in the brain form small serous cysts that may occur in any jDart 
of the organ, and are rarely solitary. Cruveilhier describes a case where 
one hundred were found. When the cysticercus is lodged in cavities, it is 
non-encysted and tends to grow easily into the form of a tape- worm. These 
parasites may be found dead and changed to a chalky mass in which some 
of the hooklets are embedded. 

Etiology. — Tumors of the brain are twice as frequent in males as in fe- 
males. Tuberculous tumors are most frequent in children ; they usually 
do not develop until after the second year. Cancer is rare before forty ; it 
is primary in fifty per cent, of the cases. Syphilitic growths are a mani- 
festation of tertiary syphilis. Hydatids occur between the ages of ten and 
thirty-five ; while cysticerci are rarely found before forty. Aneurisms oc- 
cur in middle life, and are associated with evidences of arterial degenera- 
tion. 

Symptoms. — Cerebral tumors of large size may give rise to no symptoms, 
but in most cases their development is attended by more or less marked gen- 
eral or local symptoms. These, however, cannot be stated in any order 
that is applicable to all cases. I shall only consider the more important 
and constant of the general symptoms. The most characteristic are head- 
ache and disturbance of the intellectual faculties. The most constant local 
symptom is local paralysis. Headache is generally a prominent and per_ 



1 Path. Hist., p. 378. 

2 Obermeier gives the name pachymeningitis hemorrhagica bregmatica to angiomatous growths upon the 
Inner surface of the dura. 



1024 



DISEASES OF THE NERVOUS SYSTEM. 



sistent symptom. It is more severe than in any other cerebral disease, ex- 
cept meningitis ; it is constant, and is increased by light, sound, or move- 
ments of the head. With the headache there are tinnitus aurium, morbid 
acuteness of hearing, disturbance of vision, strabismus, with more or less 
perversion of the special senses, local hyperesthesia, anaesthesia, and im- 
pairment of the mental faculties. Vertigo, when the patient assumes the 
upright position, is almost always associated with the headache, and vom- 
iting occurs at irregular intervals without any apparent cause. There are 
rarely any febrile symptoms, except when inflammation occurs about the 
tumors. A slow irregular pulse is of frequent occurrence during the early 
stage of their development, and the respirations are often irregular and 
slowed. Spasm of single muscles or groups of muscles and general epilep- 
tiform or choreic seizures often follow severe attacks of vertigo. 

Hemiplegia is entirely absent in a large number of cases. If present it 
may come on slowly, or suddenly after an epileptiform seizure ; facial paral- 
ysis on the same side as the hemiplegia, is present in some cases, and rigid- 
ity of the affected muscles is common. Double hemiplegia is not infrequent ; 
one side being implicated some time after the other. If paraplegia exists 
it indicates a median tumor, usually at the base or in the cerebellum. 

If the tumor involves the island of Eeil or the posterior portion of the 
third convolution there will be aphasia. The intellectual disturbances are 
varied. Melancholia and paroxysms of grief or joy are frequent. Incoher- 
ence of speech, failure of memory, temporary loss of consciousness, and a 
gradual passage into a condition of imbecility and helplessness are a part of 
its history. This is especially liable to occur in cases where the tumors are 
rapidly developed. 

The choked disc or congested papilla, and the neuro-retinitis as revealed 
by the ophthalmoscope, are regarded by some as important in the diagnosis 
of cerebral tumors. Such conditions may cause amaurosis and amblyopia. 1 
If there is loss of sight from involvement of the optic nerves, the pupils 
will be dilated and they will not contract under the influence of light. If 
the tumor is situated above the corpora geniculata, although there is loss of 
sight, the pupils will respond to light. As the tumor increases in size, the 
paralysis advances from one set or group of muscles to another, and this ad- 
vancing paralysis is a most important diagnostic sign. Its course is usual- 
ly from above downward. 

On account of the local disturbances which result from the complicating 
encephalitis, abscess, softening, or oedema may occur and give rise to their 
own peculiar symptoms. The bowels are usually obstinately constipated. 
Clinically there may be recognized three classes of cases : (1) those which are 
attended by no symptoms, (2) those in which the symptoms are slowly de- 
veloped and intermittent and extend over a number of years, (3) those in 
which the symptoms come on suddenly and are rapidly fatal. 

Differential Diagnosis. — Tumors of the brain may be mistaken for abscess, 



1 Annuske (in v. Graefe's Archiv) states that optic neuritis occupies the first rank among the symptoms of 
intracranial neoplasia. 



TUMORS OF THE BRAIN AND MENINGES. 



1025 



cerebral softening, epilepsy and chronic meningitis. The points of diagnosis 
between the first two have already been considered. 

An apoplectic or hysterical seizure will hardly ever be mistaken for a cere- 
bral tumor. 

Epilepsy is a paroxysmal disease ; it usually occurs early in life and is 
rarely accompanied by any of the local phenomena of tumor. 

In chronic meningitis the pain is not so severe or as constant as in cere- 
bral tumor, the mind is perverted and weakened, epileptiform convulsions 
are rare, and the special senses and facial nerves are not implicated. 

The differential diagnosis of the different varieties of cerebral tumor 
may be briefly summarized as follows '.—tubercular growths are met with 
in early life ; they are accompanied by fever, have a tubercular history, or 
have the evidences of tuberculosis in other parts of the body. They are 
usually located either in the cerebellum or pons. 1 Cancer of the brain 
may be suspected w r hen the patient is over forty, when there is a marked 
cachexia with progressive emaciation, when there is an hereditary cancerous 
history, or when cancer exists in other organs, and when the development 
of the cerebral symptoms has been rapid. Implication of the cranial bones 
by the tumor always indicates cancer. 

Syphilomata are attended by nocturnal headache, by the constitutional 
signs of syphilis -or evidences of previous syphilitic disease. Their symp- 
toms remit and sometimes disappear under anti-syphilitic measures. Ptosis 
and dilatation of the pupil are more often met with in syphilitic tumors 
than w T ith any other. 

Gliomata follow traumatic injuries to the skull, and progress slowly with- 
out any interference with the general health. 

Aneurism may be suspected in the aged, with the signs of general arterial 
degeneration. 

Cysticerci occur after forty, and produce, at first, subacute epileptiform 
attacks, which become very frequent. One hundred epileptic seizures have 
occurred in a day with cysticerci in the brain. Paralysis of the limbs and 
hemiplegia are very rare, while the psychical disturbances are marked, and 
occur very early. 

The diagnosis of hydatids is exceedingly difficult. The tumor-symptoms 
are inconstant ; the intellect is unaffected, and there may be oedema of 
eyelids. 

The rules which will aid in the localization of cerebral tumors are as fol- 
lows : — tumors of the convexity, even when large, may give rise to no 
symptoms. Usually, however, they cause headache, motor disturbances, 
delirium, convulsions ; but rarely disturbances of sensation or paralysis. 

Tumors of the anterior lobes cause diffuse or circumscribed headache, 
convulsions, and epileptiform attacks, hemiplegia, and aphasia. The 
special senses are undisturbed, except the sense of smell. 

In tumors of the middle lobes the special senses (especially sight) are 
affected, and there is usually anaesthesia of the surface on the side opposite 
the tumor. 



05 



1 Hirscttberg. 



1026 



DISEASES OF THE HERYOTTS SYSTEM. 



Tumors in the posterior lobes cause greater psychical disturbances than 
those in any other position. Motion, sensation, and the special senses 
(sight excepted) are more or less disturbed. Vertigo and convulsions are 
common. 

Tumors in the corpus striatum and lenticular nucleus are accompanied 
by hemiplegia, convulsions, facial paralysis, difficulty in articulation, dis- 
turbance of intelligence ; but the special senses are not impaired. The 
symptoms correspond to those of apoplexy, but they are of slower develop- 
ment. 

Tumors in the tuber cula quadrigemina are attended by convulsive spasms, 
paralysis of the motor oculi, disorders of vision on both sides, slight paral- 
ysis of the face, and unilateral paralysis of the limbs. 

Tumors in the cerebral peduncles induce headache, vertigo, hemiplegia 
alternating with sensory disturbances, paralysis of the motor oculi on the 
same side, neuro retinitis, difficulty of micturition, but no intellectual dis- 
turbances. 

Tumors in the pons Varolii induce crossed paralysis of motion (and 
sometimes of sensation also), amblyopia, amaurosis, choked disc, dysphagia, 
strabismus, difficulty in articulation, but no convulsions. There is usually 
paralysis of the bladder. 

When the cerebellar peduncles are involved the gait is tottering and un- 
steady ; the patient tends to fall to one side, or rotate around the median 
line. 

In cerebellar tumors, there will be occipital headache, oscillatory move- 
ments, unsteady gait, intense vertigo, strabismus, amblyopia, and amaurosis; 
but there are no disturbances of the intellect or sensation. 

In tumors of the medulla, the symptoms not infrequently resemble 
glosso-labio-laryngeal paralysis. There is dysphagia, disturbances of sensa- 
tion, convulsions, occasionally saccharine urine, and difficulty in articula- 
tion. 

Prognosis. — The character of cerebral tumors varies with their structure. 
The prognosis is always unfavorable ; carcinomatous and tuberculous 
tumors are progressive and early fatal. In hydatids and aneurism, though 
life may be prolonged, death is a certain result. Ia syphiloma, life may 
be prolonged for years by judicious and timely treatment. The average 
duration of cancer is about one year. 1 Echinococci tumors have been 
cured. 2 In any case of cerebral tumor which is attended by intense pain 
and progressive emaciation, the course is rapid, and the prognosis un- 
favorable. Death may occur from continued convulsions, paralysis, 
cerebral softening, oedema or hemorrhage. Secondary inflammation with 
abscess, and meningitis, and pulmonary complication, may be the cause 
of death. Anaemia and exhaustion are common modes of death in specific 
tumors. 

Treatment. — In a case of cerebral tumor where syphilis can even be sus- 



1 Lebert states that three months and five years are the extremes. 

2 Mouline trephined, and Fletcher incised, a frontal tumor, withdrawing the hydatids. These are 
phenomenal cases. 



SCLEROSIS OF THE BEAIN. 



1027 



pected, mercury and iodide of potassium in large doses should be admin- 
istered. The diet and hygienic surroundings should be carefully regulated, 
the patient restricted in exercise, the pain and sleeplessness should be re- 
lieved by anodynes. 

SCLEEOSIS OF THE BRAES". 

Independent of cerebrospinal sclerosis, this is a comparatively rare con- 
dition. Cerebral sclerosis is a chronic interstitial inflammation, following 
hyperemia of the neuroglia. 1 It may be diffused or multiple. 

A 




Fig. 203. 

Diagram showing the Connective-tissues of Medullated Nerve Structure. 

AA. Two bundles of medullated nerves. 
BB. Epineurium. 
CC. Perineurium. 
DD. Endoneurium. 

E. Axis-cylinders. 

F. Neuroglia cells. 

Morbid Anatomy. — The medullary substance is the favorite seat of mul- 
tiple cerebral sclerosis. 

On section, masses of gray, hard, well-defined, transparent sclerotic tissue 
are found — sclerotic islands varying in size from one-fourth to one inch. 
They may be so numerous and small as to be scarcely discoverable. 8 

The cut surface of a sclerosed patch is moist with serum; and usually 
shows small blue or gray-red spots. 



1 The tissue forming the skeleton framework of the brain is called the neuroglia by Virchow. It is 
analogous to the connective-tissue framework between the liver-lobules and kidney tubules. 

2 Cornil and Ranvier describe cerebral sclerosis as almost exclusively involving the convolutions, and 
consisting of a first stage where hyperplasia of the neuroglia produces a vascular, pulpy, gelatinous mass ; 
and of a second stage where atrophy of the new elements is accompanied by development of a vascular 
structure, hard and resistant. 



1028 



DISEASES OF THE NERVOUS SYSTEM. 




A microscopical examination of the patch in its soft stage shows active 

hyperplasia of the neuro- 
glia-cells. Later, com- 
pression of nerve - sub- 
stance occurs from the 
pressure of the hyper- 
plastic neuroglia tissue, 
which, at this period, ex- 
ists as fibrillated connec- 
tive-tissue, whose fibrils — 
extremely fine and inter- 
lacing in all directions — 
form a network contain- 
ing atrophied nerve ele- 
ments and small round or 
oval nucleated cells. The 
axis - cylinders are pre- 
served, and are sometimes 
markedly hypertrophied 
at their periphery. At 
the centre of the mass 
are found numerous amy- 
loid corpuscles, a few 
atrophied axis-cylinders, 
fat granules, and new 
formed fibres that entirely 
replace the normal elements. The walls of the vessels are thickened. In 
the brain any portion of the white substance may exhibit this lesion. 

Etiology. — The causation of cerebral sclerosis is obscure. It unques- 
tionably is intimately connected with changes in the vascular system, for 
the localities in which it is developed are the terminal arteries, L e., ar- 
teries that do not anastomose, or anastomose slightly. Sclerosis is often 
found in epileptics and in the insane. It is occasionally met with in ad- 
vanced life. 

Symptoms. — The symptoms of cerebral sclerosis are a gradual enfeeble- 
ment of the mental powers, especially memory, muscular tremors, headache, 
dizziness and vertigo. Accompanying these, one group of muscles after 
another becomes paralyzed. There is no regular order in the development 
of the paralysis, first a lower, then an upper extremity, then some of the 
facial muscles are involved. Melancholia, pains in the extremities, and a 
sense of formication are common. The nutrition is rarely interfered with ; 
many patients gain flesh. Convulsions and disturbances of special sense 
are rare. Strabismus may be present. 

A peculiar symptom is / 'estimation, — the patient bends forward and trots 
along like one trying to run after he is tired out. Late symptoms are 
paralyses of the muscles of deglutition, speech and respiration. In rare 
instances the first and only symptoms are convulsions of an epileptiform 



Fig. 204. 
Sclerosis of the Brain. 

Section of Cerebrum through a patch of sclerosed tissue. 

The normal brain structure Jias entirely disappeared, and is re- 
placed by interlacing fibrils of connective-tissue, in the meshes of 
which are shown small nucleated cells, atrophied nerve fibres and 
fat granules, x 300. 



HYPERTROPHY OF THE BRAIN. 



1029 



character, followed by hemiplegia. 1 Labio-glosso-pharyngeal paralysis may 
exist in sclerosis. Electrical reactions are not changed, when the cord is 
uninvolved. Inanition, emaciation, muscular contractures, and, rarely, an 
unexplainable rise in temperature, precede death, which occurs in collapse 
with loss of consciousness. 

Differential Diagnosis. — Sclerosis of the brain may be mistaken for cen- 
tral softening, paralysis agitans, or tumors. 

Softening occurs in old age ; the paralysis is in one set or group of mus- 
cles, and if it extends, does so in an orderly manner. There is ancesthesia, 
and the symptoms develop more suddenly than in sclerosis. 

Paralysis agitans is marked by rhythmic tremor passing from one upper 
to the corresponding lower limb ; there is a peculiar deformity of the fingers 
and toes ; the facial muscles are not affected, and the patient inclines to 
the paralyzed side in walking. Paralysis agitans occurs only after the for- 
tieth year, and is accompanied by no cerebral symptoms. 

Cerebral tumors are attended by headache, convulsions, and signs of 
brain irritation without loss of mental power. 

Prognosis. — Sclerosis of the brain may continue from five to eight years, 
but it is progressive and always fatal. Death may occur from inanition, or 
complications such as pneumonia, bed-sores, pleurisy, tuberculosis, ma- 
rasmus, or cerebral paralysis. 

Treatment. — Little can be done for this disease except to improve the 
general health. Yet it should be mentioned that Yulpian recommends 
chloride of iron, Mitchell the bi-chloride of mercury, Hammond the chlo- 
ride of barium, and many the phosphite of zinc. Nitrate of silver and 
strychnia are said to relieve tremor. 

HYPERTROPHY OF THE BRAIN*. 

Cerebral central hypertrophy is an increase in the neuroglia (the nerve 
filaments and ganglia are uninvolved), and may be partial or general. The 
term cerebral hypertrophy is really a misnomer. 2 

Morbid Anatomy. — On removal of the skull-cap the brain protrudes be- 
yond the cranial bones. The skull-bones are thinned. If the disease be- 
gins very early in life, the head may become as large as in congenital hy- 
drocephalus, and the sutures will be separated. The convolutions and sulci 
are lessened by pressure, and the membranes are thin and dry. The dura 
mater may be adherent. The ventricular fluid is absent. Intense anaemia 
always exists ; the brain matter, both white and gray, is white, and tough 
and elastic. The brain is heavier than normal. The cerebrum is usually 
involved. But hypertrophy of the cerebellum, thalamus opticus, corpus 
striatum, pons Yarolii, and medulla oblongata may also occur. 

Etiology. — Hypertrophy of the brain may be congenital. It appears, 

1 Charcot states that cerebral sclerosis not infrequently commences with, nausea, headache, vertigo, syn- 
copal and apoplectiform attacks, followed by diplopia, amblyopia, nystagmus, disturbances of mind and 
of speech. 

2 Virchow in 1862 and 1867 published his article on hypertrophy of the brain ; his views were based on 
the results of autopsies, and to these we are indebted for our knowledge of this subject. 



103C 



DISEASES OF THE NERVOUS SYSTEM. 



when not congenital, in childhood before the third year. It may be hered- 
itary, i. e., it may occur in several members of tho same family. It may 
be the result of traumatism, lead poisoning, chronic alcoholismus, or epi- 
lepsy. It not infrequently accompanies idiocy and insanity. In children, 
swelling of the lymphatics and thymus gland, and the evidences of rickets 
precede or coexist with its development. Dwarfs are often the subjects of 
cerebral hypertrophy. 

Symptoms. — Virchow makes two forms, acute and chronic. In the former, 
headache, epileptiform convulsions, retardation or great acceleration of the 
pulse, vertigo, delirium, sympathetic vomiting, dyspnoea, and dysphagia 
occur. In children there is weakness, tremor, and a tottering gait, and 
the head inclines to one side. Convulsive movements of the eye or arm 
occur. There may be permanent strabismus. The child may be very pre- 
cocious at first ; later he becomes feeble-minded or idiotic. Periodical lar- 
yngeal spasm (thymic asthma) may occur. Bulimia is marked ; and the 
child is constantly somnolent. The tongue, often larger than normal, pro- 
trudes from the mouth, and children often persistently suck it, Headache 
is rarely absent. It is steadily progressive, and ends in coma, preceded by 
dilated pupils, slowed pulse, vomiting, and repeated convulsive attacks. 

Differential Diagnosis. — It is very often impossible to differentiate between 
chronic hydrocephalus and hypertrophy of the brain. In hypertrophy the 
child has been, or is, bright and precocious ; in hydrocephalus he is alioays 
stupid. The fontanelles pulsate in hydrocephalus ; they do not in hyper- 
trophy. The cerebral souffle may be heard in hypertrophy but not in hy- 
drocephalus. 

Prognosis. — It always terminates in death. It may end either by pro- 
gressive stupor or from complications. 

ATROPHY OF THE BRAIN". 

Atrophy of the brain may be either infantile or senile; it is never met 
with in adult life. 

Morbid Anatomy. — In children the disease begins in utero. The skull is 
oblique ; one-half is thick, smaller than normal, and misshapen. The cor- 
responding parts of the brain are atrophied, hard, altered in color, and are 
studded with collections of serum. (Rosenthal.) Atrophy, or absence, of 
the corpus callosum is the result of defective foetal development. It is 
generally accompanied by intra-uterine hydrocephalus. Physiologically, 
the brain begins to diminish in weight after the sixtieth year; at that 
time it is one-fifteenth lighter than during early adult life. Hence 
slight atrophy is physiological in old age. But in senile atrophy there 
is more or less marked diminution in the anatomical elements of the 
brain, and a loss in the interstitial connective-tissue. The cells of the 
cortex are swollen and pigmented ; and pigmentation also occurs in the 
walls of the vessels, which often undergo more or less fatty degeneration. 
The cortex is thinned, and in it are found corpora amylacea. The fat in 
the cerebral substance is lessened, the water increased. Senile atrophy is 



ATKOPHY OF THE BRAIDS'. 



1031 



usually general ; but when partial it affects the left hemisphere. There is 
unequal thinning of the convolutions, and the sulci are large and deep. 
The meninges are somewhat clouded. The brain is usually tougher than 
normal, and the ventricles contain from two to twelve drachms of fluid. 
This is a purely conservative process. The ependyma is granular and 
nodular. More or less serum distends the meshes of the pia mater. The 
medullary substance and the corpora striata are riddled with holes, etat 
crible. 1 

On section the brain lias a leathery toughness ; ifc may be corrugated. The 
cortex is of a dirty gray color; and the medullary substance is a dull white 
or drab color. Partial atrophy may extend to the cortex, or it may follow 
the fibres through the peduncles, pons Varolii, and pyramids. A crossed 
lesion may sometimes be met with, due to atrophy of one cerebral and of 
the opposite cerebellar hemisphere. There are remarkable instances of 
diminution of the cerebellum to one-half its normal size and weight. 

The loss in weight of the brain in the general paralysis of the insane is 
greater than in any other disease. The cerebellum and basal portions of 
the cerebrum are unaffected ; the most striking degree of atrophy being in 
the frontal lobes, the convolutions exhibiting it most of all. Of all the 
changes accompanying this form of atrophy those in the dura are most 
marked ; it is adherent to the bone, and hemorrhages into its substance are 
frequently met with. Pachymeningitis, haematoma, ruptures and foldings 
of the dura over the brain are often met with. Some regard these as the 
specific lesions of general paralysis. The pia mater is cedematous and 
thickened, either continuously or in patches. 

Etiology. — Cerebral atrophy may be congenital or occur as a part of 
senile change. It may follow cerebral hemorrhage or softening, and is 
occasionally caused by tumors, meningeal inflammation, and internal or 
external hydrocephalus. Injury or destruction of the peripheral nerves 
may induce secondary cerebral atrophy. Excess in venery, the opium 
habit, and alcoholismus are adduced as its causes. It is met with of tener in 
males than in females. Senile marasmus is its chief cause. 

Symptoms. — Senile cerebral atrophy is attended by gradual failure of the 
mental faculties. Memory is impaired, the special senses are markedly 
dulled ; and the movements, at first unsteady, are soon accompanied by 
tremor. The patient is somnolent ; indeed, he sleeps the greater part of the 
time. Soon the condition popularly known as "second childhood" is 
reached. There is often more or less complete loss of power over the 
sphincters. Atrophic degenerations of that half of the body on the same 
side as the atrophied cerebellum, or on the opposite side to the atrophied 
cerebrum are apt to occur. Incomplete paralysis accompanies these atrophic 
changes. Epileptiform attacks are quite frequent ; choreic attacks occa- 
sionally occur. 

Only a brief mention can here be made of the symptoms of the extensive 
atrophy which occurs in general paralysis of the insane. Headache, dizzi- 
ness, irritability of temper, weakness of memory pre-eminently, thickness 



i Durand-Fardel and Parchappe. 



1032 



DISEASES OF THE NEKYOUS SYSTEM. 



of speech, change in the character of the voice, a feeling of self-importance, 
grandeur and great riches, — these are very common. Sudden and uncalled- 
for outbursts of rage are common. It is very much like senile dementia. 

Atrophy of the brain ultimately involves the medulla, implicates the 
great life-centres situate therein, and deglutition or respiration is so much 
interfered with that death results. In general paralysis of both sides of the 
body there is usually complete imbecility. 

Differential Diagnosis. — Senile cerebral atrophy may be mistaken for 
cerebral hemorrhage and softening. The history of the case is essential in 
its differential diagnosis. Atrophy of the cerebellum may be mistaken for 
tabes clorsalis and multiple sclerosis. From the former it is diagnosticated 
by the absence of vesical symptoms and by more intense pains ; the anaes- 
thesia about the dorsal vertebras is a valuable point, as it is always present 
in tabes and not in atrophy. The intra-uterine variety of cerebral atrophy 
is easily recognized by the paralyses and spasmodic seizures that occur 
directly after the birth of the child. 

Prognosis. — Congenital atrophies, or those occurring in the early life, 
usually terminate during the fourth year. Senile atrophy is steadily pro- 
gressive to a fatal termination. No estimate of its duration can be made. 
It may be complicated by hypostasis in the lungs, bronchitis, pulmonary 
oedema, pneumonia, acute bed-sores, or by disease of the bladder or kidneys. 
In the general paralysis of the insane its duration is rarely more than a year. 
Death is reached by intercurrent apoplexies, exhaustion from large bed- 
sores, anaemia or pulmonary complications. 

Treatment. — Improvement of the general health is regarded as the most 
important indication. Some advocate exercise and massage of the para- 
lyzed limbs. Niemeyer recommends cold douches. In atrophy in general 
paralysis, galvanism, iodide of potash, calabar bean, morphia, and chloral, 
alone or together, prolonged tepid baths, and attention to the bowels and 
bladder have been recommended. 



DISEASES OF THE SPINAL COED. 



Diseases pi the spinal cord and its membranes will be considered under 



the following heads 



Spinal Hyperemia. 
Spinal Meningitis. 
Acute Myelitis. 
Chronic Myelitis. 
Non- Inflammatory Soften- 
ing. 

Acute Bulbar Paralysis. 
Progressive BuTbo-Nuclear XVI. 
Paralysis. XVII. 
VIII. Infantile Spinal Paralysis. 



1. 
II. 
III. 
IV. 

V. 

VI. 
VII. 



IX. 
X. 
XL 
XII. 
XIII. 
XIV. 
XV. 



Acute Spinal Paralysis of Adults. 
Chronic Anterior Myelitis. 
Progressive Muscular Atrophy. 
Cerebro- Spinal Sclerosis. 
Locomotor Ataxia. 
Spasmodic Tabes Dorsalis. 
Amyotrophic Lateral Sclerosis. 
Pseu do-Hypertrophic Paralysis, 
Spinal Apoplexy. 



HYPEKiEHIA OF THE SPIRAL CORD AND MENINGES. 



1033 



HYPEREMIA OF THE SPINAL COED AND MENINGES. 

Hyperemia of the spinal cord may be active or passive. 

Morbid Anatomy. — The most intense active or passive hyperemia of the 
spinal meninges may disappear between death and the time of a post-mortem, 
and a gravitation from position may induce a congestion which is decidedly 
misleading. In active hyperaemia the arterioles are injected and the parts 
assume a rosy color marked possibly by numerous points of extravasation. 
In passive hyperaemia the veins of the cord and membranes are distended 
with dark blood. Chronic congestion results in thickenings, pigmentation 
and opacities of the membranes, attended by development of new con- 
nective-tissue which may be the starting-point of a general sclerosis. 

Etiology. — Active hyperemia may result from muscular exertion, or ex- 
cesses in venery, from vaso-motor paralysis due to exposure to cold and wet, 
concussion, and suppression of menstrual or hemorrhoidal fluxes. Hy- 
peraemia is always an attendant of general or local myelitis. It occurs with 
acute infectious diseases, typhoid, small-pox, scarlet fever, and measles, 
with chronic malarial infection, and in some cases of rheumatism and 
puerperal fever. It may also result from poisoning by carbonic oxide, 
strychnia, nitrite of amyl, alcohol, etc. 1 Intense active hyperaemia has 
been found in those who have died of spasmodic affections, or who have 
worked in compressed air, as in caissons. 2 

Passive hyper cemia is caused by any obstructive disease of heart, liver, or 
lungs, and by mechanical pressure upon venous trunks, by tumors, fluid 
effusion, etc. 

Symptoms. — The onset of active hyperaemia may be sudden, while pas- 
sive hyperaemia generally comes on slowly and often insidiously. In most 
instances there is pain along the spine, especially in the lumbar region, 
which radiates down the thighs and is increased by movement and pressure. 
There is hyperaesthesia of the lower limbs associated with itching, burn- 
ing, or formication, and reflex irritability is augmented. 

Hyperaesthesia, sharp pains, spasms, and symptoms of irritation would 
rather point to active hyperaemia, while numbness, anaesthesia, heaviness of 
the limbs and vesical paresis are more commonly associated with congestion. 3 
In rare cases the disease is so sudden in its onset that the patient may 
awake to find himself in a state of incomplete paraplegia. During the 
whole course there is no fever and little, if any, change in the pulse. 
Dyspnoea occurs when the nerve roots are involved high up in the cord. 4 
Quite often during attacks of spinal congestion, persistent priapism occurs 
and the iron-band sensation about the waist is a frequent symptom. 5 

1 Magnan has experimented with absinthe on animals, and found it to produce intense hyperemia when 
given in large doses., 

2 St. Loins Med. and Surg. Jour.— Dr. Clark. 

3 Rosenthal states that violent emotions and sometimes the dorsal decubitus increase the rachialagia. 

4 Steiner reports a case where facial paralysis occurred.— Archiv der Heilk. 11, 1870, p. 233. 

5 Fabra has observed pain, anesthesia, hyperesthesia, slight paresis, and, rarely, convulsive phenom- 
ena occurring in the last stages of heart disease, which seemed to be due to passive hyperemia of the 
cord.— Gaz. desHop., 1876, No. 147. 



1034 



DISEASES OF THE NERVOUS SYSTEM. 



When convulsions occur in such diseases as tetanus there is intense Irj . 
peraemia of the gray matter of the cord. 1 

Differential Diagnosis. — Hyperaemia of the cord may be mistaken for 
spinal anaemia, meningitis, myelitis or apoplexy. 

In anosmia the symptoms are relieved by the recumbent posture, while 
they are increased in hyperemia. Anaemia occurs suddenly, as from em- 
bolism and thrombosis. Women suffer most frequently from anaemia, 
men from hyperaemia. Vesical complications follow congestion, but not 
anaemia. 

In inflammation of the cord there will be fever, paraplegia, paralysis of 
the sphincters, loss of electro-contractility, with bed-sores and subsequently 
wasting of the muscles. 

The onset of spinal apoplexy is sudden, paraplegia is complete within a 
few hours, and accompanied by anaesthesia, paralysis of the bladder and 
rectum, the early development of gangrenous bed-sores, and in most cases 
by the symptoms of cystitis and myelitis. 

Prognosis. — The prognosis is favorable, although the condition is one 
which has a marked tendency to become chronic. Complete recovery is 
slowly reached, except in those cases where the cause is permanent. 

Treatment. — If its cause can be reached, it should at once be removed. 
Severe and sudden congestion demands local abstraction of blood by wet 
cups along the spine or leeching about the anus. The patient should be 
kept quiet on his side. In recent cases ice-bags to the spine, hot foot baths, 
and a brisk purge will relieve the pain. Ergot and belladonna and hot 
douches along the spine are highly advocated in chronic passive hyperaemia. 
In reflex hyperaemia, or hyperaemia due to vaso-motor disturbances, elec- 
tricity may afford relief. 

SPINAL MENINGITIS. 
Spinal meningitis may be acute or chronic. 

Morbid Anatomy. — Acute inflammation of the spinal meninges is gener- 
ally diffuse, and runs a course similar to acute cerebral meningitis. The 
pia mater is hyperaemic, swollen and studded with ecchymoses. The ex- 
udation takes place into the meshes of the membrane, and the effusion may 
be sero-fibrinous, or purulent. The pia mater is thickened, opaque, and 
oedematous, and a turbid fluid fills more or less completely the spinal 
canal. Although the exudation is more abundant upon the posterior sur- 
face, it usually envelops more or less completely the whole cord, whose 
substance may either be pale and anaemic, or exhibit changes of com- 
mencing myelitis and softening. The roots of the nerves are embedded in 
the exudation, and present changes similar to those in the cord. The 
exudation may be wholly absorbed, and the membranes and the cord return 
to their normal condition ; but more frequently the inflammation becomes 
chronic. 

In chronic spinal meningitis there are found the opacity, thickening, 
adhesions, and puckerings so characteristic of chronic interstitial inflam- 



1 Weinberg. 



SPIRAL MENINGITIS. 



1035 



mation in similar membranes. The membrane is tough, dark, bluish-gray 
in color, pigmented, and contains calcareous plates. It is adherent at 
various points to the thickened dura mater (pachymeningitis spinalis). 
The fluid in the spinal canal is always increased in amount ; it may be clear 
serum, or contain lymph flocculi, blood, or pus. The irregular and local- 
ized adhesions and retractions produce sclerosis of the cord, and also induce 
anaemia, atrophy, and degeneration of the nerve roots. 

Etiology. — Spinal meningitis is a disease of youth and early adult life, 
and may follow a traumatism, as in a fall, blow, dislocation, fracture, or 
other injury to the vertebras, or concussion, which is thought to be a fre- 
quent cause. It may arise from extension of inflammation from the 
cerebral meninges, from any disease of the spine, such as caries, cancer, 
etc. Prolonged exposure to cold — especially damp cold — or brief exposure 
to intense cold when the body is heated, as well as exposure to intense heat, 
will induce spinal meningitis. Operations for spina bifida have been fol- 
lowed by rapid and fatal spinal meningitis. 

Rheumatism is said to be an occasional cause, and some authors regard 
all febrile and infectious diseases as liable to be complicated by it. 1 Syph- 
ilis, venereal excesses, alcoholismus, chorea, tetanus, and hydrophobia may 
each, in rare instances, induce spinal meningitis ; 2 and scrofulosis, tuber- 
culosis and wasting diseases are very apt to be complicated by it. 

The chronic form is often a sequel of the acute, and is very apt to accom- 
pany alcoholismus, syphilis, impeded venous return, and diseases of the 
cord. The latter are the most frequent of all causes. Chronic or acute 
inflammation of the cord, or any neoplasm that encroaches upon the spinal 
canal, will lead to localized chronic meningitis. Excessive use of tobacco 
or narcotics, and anti-hygienic surroundings are predisposing causes. 

Symptoms. — When spinal meningitis is associated with cerebral inflamma- 
tion its symptoms are less distinct than when it is uncomplicated. Severe 
pain in the back is the earliest and most prominent symptom. The -pain 
at first is localized about the seat of the inflammation, but later becomes 
diffused and shoots down the legs and arms. It is constant, and is made 
sharp and lancinating by motion, so that the patient holds himself in a 
fixed position with rigidly contracted muscles ; pressure along the spine 
may increase the pain. A chill or distinct rigor accompanies the pain, and 
is followed by rise in temperature, nausea, vomiting, and a sense of general 
malaise. The fever is never high and the pulse-rate is frequently below the 
normal. The muscles along the spine become rigid, and if the cervical re- 
gion is involved there is opisthotonos. Convulsive twitching of groups of 
muscles is attended by the most excruciating pain. The surface of the body 
becomes hypersesthetic in the area of motor derangement, and reflex activ- 
ity is increased. In a few instances all the extremities are involved, but 
usually there is only incomplete paraplegia. There is constipation, and 
the abdomen has the well-known boat-shaped appearance. 



1 C. B. Radcliffe, in Reynold's System. 

2 Koehler states that any pulmonary or cardiac disease 
marked predisposition to spinal meningitis. 



that impedes proper venous return affords a 



1036 



DISEASES OF THE NERVOUS SYSTEM. 



Afc the commencement of the attack there is a constant desire to mictu- 
rate. Later, paralysis of the bladder and retention of urine accompany the 
para-paresis, so that catheterization must be resorted to. If the paralysis 
involves the respiratory muscles there will be dyspnoea, and the temperature 
will rise to 106° or 107° F., and be followed by coma and death. If the 
meningitis is limited to the lower portion of the cord, the case will be pro- 
tracted, but marked by periods of slight improvement. In such cases bed- 
sores may develop, with incontinence of urine, and death finally occur from 
exhaustion. Sudden and profuse sweats may result from vaso-motor impli- 
cation. 

Chronic spinal meningitis is generally a sequel of acute, although it may 
develop without any acute symptoms. When the acute passes into the 
chronic form, pain and rigidity of the spine remain after the other symp- 
toms have subsided. The limbs are hyperaesthetic, and the seat of burning, 
formication, or itching. There may be a sensation as of a tight band about 
the waist, accompanied by weight and uneasiness in the limbs, which may 
develop into incomplete paraplegia. The bowels, at first, are constipated, 
but later the passages may be involuntary. The bladder is frequently par- 
alyzed, incontinence of urine occurs, bed-sores form, and a well-marked 
marasmus is developed. Finally the paralysis will vary in degree with the 
posture of the patient — and also from day to day. 

Differential Diagnosis. — Acute spinal meningitis may be confounded with 
myelitis, tetanus, and muscular rheumatism,. In tetanus the locked jaw, 
the peculiar implication of the facial muscles causing the risus sardonicus, 
and the intense cutaneous hyperesthesia, with recurring paroxysms with- 
out paralysis, are in marked contrast to the symptoms of spinal meningitis. 
In the latter disease there is great pain on motion, little or none on pres- 
sure, and muscular spasm is produced by attempts at movement rather than 
by irritation. There is, usually, a traumatic history in tetanus. 

Rheumatism in the muscles of the hacJc is accompanied by local pain only 
when movements are made : but there is nover that rigidity of the spine 
which is present in meningitis, nor the cutaneous hyperesthesia, paralysis, 
spasms, or febrile phenomena. 

Spinal irritation may be mistaken for meningitis, but the pain on press- 
ure confined to one spot, the absence of pain upon ordinary or slight mo- 
tion, and the disposition to a sudden transference of the diseased action 
from one organ or part to another, with possibly the occurrence of hyster- 
ical symptoms, will be sufficient to distinguish between them. 

Chronic meningitis may be mistaken f chronic myelitis. In meningitis 
pain is a far more prominent symptom than in myelitis; and it is increased 
by motion but not by pressure, the reverse of which occurs in myelitis. 
Paralysis is never complete in meningitis, and anaesthesia and muscular 
atrophy are rare as compared with myelitis. 

Prognosis. — Acute spinal meningitis runs a variable course ; should 
death occur within twenty-four or thirty-six hours the case is to be re- 
garded as epidemic. The usual duration of the acute form is from seven 
to ten days. The majority of cases are fatal, more especially those in which 



ACUTE MYELITIS. 



1037 



the membranes of the cervical cord are involved. In these cases, death re- 
salts from paralysis of the muscles of respiration, and will be preceded by 
intense dyspnoea and cyanosis. Even when recovery occurs, convalescence 
is tedious ; and though the general health is restored, pain, paralysis, 
and stiffness or atrophy of muscles are apt to continue for many months. 
Barely is convalescence rapid. In many acute cases death occurs from 
simple asthenia. 

Chronic spinal meningitis runs a very protracted course, and may ter- 
minate in death from exhaustion, anaemia or marasmus. It progresses by 
stages ; and although the prognosis is not so unfavorable as in the acute 
form, complete recovery is rare. Both acute and chronic are most severe 
in the very young or the very old and enfeebled. 

Treatment.— The same principles guide the treatment -of acute spinal 
meningitis as were advised in acute cerebral meningitis. The patient 
should be placed in bed in a cool room and a brisk purge administered. 
Ice or counter-irritation may be applied along the spine, and from the on- 
set the patient should be kept in a condition of semi-narcotism. Ergotin 
and belladonna hypodermically are said to produce contraction of the 
arterioles and restrain the inflammatory process. The internal ad- 
ministration of the iodide of potash with mercury is advocated. Warm 
baths are grateful to the patient, and produce a sedative effect, and have 
seemed to me to be of greater service than all other measures. The nour- 
ishment should be highly nutritious but never stimulating. When symp- 
toms of heart failure or asthenia come on, stimulants are indicated. 
Careful attention to the condition of the bladder should never be ne- 
glected. 

In chronic spinal meningitis counter-irritation over the spine, and de- 
rivatives to the surface are to be employed as long as the inflammatory pro- 
cesses are in progress, 1 Warm douches are excellent adjuvants, and in 
some cases are followed by marked benefit. Iodide of potash and mercury 
— the latter both internally and by inunction — are more clearly indicated 
in chronic than in acute cases. The galvanic current is often of service 
in preventing the muscular atrophy and contractions which are sequelae 
of the paralyses. 

ACUTE MYELITIS. 

Myelitis is an inflammation of the substance of the spinal cord, and 
may be limited to the gray or white matter ; it runs an acute or chronic 
course, and involves the whole or isolated portions of the cord. 

When the gray matter alone is involved, it is called central myelitis ; 
when the white matter and the meninges are involved it is called cortical 
myelitis. 

When once established the disease may be ascending, descending, or trans- 
verse in its extension. 



1 Brown-Sequard advises sinapisms, stimulating ointments, and oils, moxa, and in severe cases, white' 
not irons to the spino. 



1038 



DISEASES OF THE NERVOUS SYSTEM. 



Morbid Anatomy. 




-In acute myelitis the portion involved is softened and 

discolored to an extent 
corresponding to the 
amount of vascular dila- 
tation and transudation 
of red blood cells. 
Hemorrhage takes place 
into the softened spots, 
although in many cases 
it is doubtful whether 
the hemorrhage prece- 
ded or followed the soft- 
ening. In most cases 
the cord is enlarged, and 
on section, blood points 
and spots of ecchymoses 
are seen. The veins 
especially are distended 
and surrounded by a 
layer of red and white 
blood corpuscles. 

Microscopically there 
will be found swelling 
of the cells of the neu- 
roglia, ampullae-like di- 
latations of the axis-cyl- 
inders, hypertrophy of 
the cells in the anterior horn of the gray substance, and an albuminoid gran- 
ular degeneration of the nerve fibres. The nerve cells not infrequently 
show pigment degeneration, and the ganglion cells are clouded and swollen. 

These morbid processes result in entire disappearance of the normal ana- 
tomical elements of the cord. The adjacent membranes will be congested, 
thickened, opaque, and adherent to the Ci>rd, while collections of blood or 
pus underneath the membrane may cause it to present a nodulated appear- 
ance. These changes are most marked in the gray matter of the dorsal and 
lumbar regions. Acute red softening soon becomes yellow from fatty de- 
generation, from changes in the coloring matter of the blood, and from 
diminution in vascularity. Later, as its consistence diminishes, a pale 
yellow or white diffluent mass is left. 1 

Etiology. — Acute myelitis is a disease of children and young adults. In 
children it takes the form of acute anterior polio-myelitis or spinal paral- 
ysis. Exposure to excessive heat or cold, intense and prolonged muscular 
exertion, and excessive venery are said to predispose to it ; and in children, 
dentition is regarded as a predisposing cause. Myelitis may be excited by 
traumatism, lying on the damp ground, and exposure to sudden chilling 
of the surface when overheated. Whether suppression of the menses, check- 

1 Erb states that this softening is due to fluid exudation from the vessels, and destruction of the nerve 
fibre-. 



Fig. 205. 
Acute Myelitis. 

From a Section through the Dorsal Spinal Cord, including portion of 
the Anterior Gray Cornu. 

A . Patch of ecchymotic tissue. 

B. Nerve fibres with swollen axis-cylinder. 

C. Hypertrophied and pigmented ganglion cells, with ampullar 

dilatation of nerve fibrils. 



ACUTE MYELITIS. 



1039 



ing hemorrhoidal fluxes, or profuse perspiration of the feet cau cause it is 
uncertain. Pressure on the cord, from tumors or displacements of the 
bony parts, whether occurring suddenly or developing slowly, will induce 
myelitis, or it may be excited by extension of inflammation, especially from 
spinal meningitis. 

Myelitis also arises during the course of small-pox, measles, scarlet and 
typhoid fevers, acute articular rheumatism, malignant pustule, puerperal 
fever, and syphilis. Continued jarring of the spine from travel on rail- 
ways will induce it. 1 Visceral disturbances— especially of the genito-uri- 
nary and digestive organs — and diseases of the joints are said to act as reflex 
causes. In many cases the myelitis comes on without any assignable cause. 

Symptoms. — Acute myelitis usually commences with slight febrile symp- 
toms, pain in the back, a peculiar sensation of an iron band around the waist, 
and the pulse is frequently feeble and irregular. Anorexia, headache and 
general malaise usually precede the attack. The power of motion in the 
lower extremities is rapidly lost, and soon complete paralysis occurs, which 
is usually both sensory and motor. Patients will complain of a sense of 
numbness in the feet ; they cannot feel the ground under their feet, and 
they have a sensation as if something was crawling over their legs. Re- 
tention of urine and fasces, which marks the onset, gives place to inconti- 
nence, from paralysis of the sphincters. Tremulous and spasmodic move- 
ments often occur in the limbs that are subsequently paralyzed ; and at the 
commencement of the paralysis their temperature is elevated. Electro- 
muscular contractility is diminished. 

The pains in the back are increased by pressure, and localized at certain 
vertebras. The application of heat or cold over the sensitive spot produces 
pain ; and a warm or cold sponge at the junction of the normal and anaes- 
thetic parts produces a burning sensation, felt in a line around the body. 
When the paraplegia is sudden and complete, hemorrhage into the softened 
focus may be suspected. The paralysis frequently extends rapidly upward, 
and wdien the cervical cord is involved paresis and anaesthesia of the arms, 
irregularities of the pupils, dyspnoea and dysphagia will be present ; the 
pain in these cases is located in the neck. The itching, burning, or boring 
pains in the limbs and the sense of formication that precede the paraplegic 
symptoms are rarely influenced either by pressure or motion. Keflex 
action is diminished or lost, and its abolition is an indication of the extent 
to which the gray matter is involved. 

Trophic or vaso-motor disturbances appear early, causing acute bed-sores, 
oedema of the paralyzed limbs, effusions into the joints, and more or less 
muscular atrophy. The urine becomes alkaline and often bloody. Reten- 
tion is of frequent occurrence and results in cystitis and pyelitis ; uraemic 
symptoms may appear, and sepsis often occurs from the bed-sores and 
gangrenous inflammation. Among the later manifestations are darting 
pains, spasmodic twitchings and contractions, either of isolated groups or 
of all the muscles in the paralyzed part. 2 This marks its passage into the 



1 Ollivier, Hine, and Leyden regard mental shock, especially from fright, or anger, as a cause. 

2 The spinal epilepsy of Brown-Sequard is a spasm of all the muscles of the lower extremities generally 
following transverse myelitis. 



1C40 



DISEASES OF THE NERVOUS SYSTEM. 



chronic stage. In some few cases hemi-paraplegia is induced by myelitis. 
The disease is always progressive. In some classes the paraplegia may be 
so rapidly developed that in forty-eight hours the patient will be unable to 
lift or move his legs. 

Differential Diagnosis. — Acute myelitis may be confounded with acute 
spinal meningitis, hysterical paraplegia and paraplegia from reflex urinary 
irritation. 

In meningitis there is acute pain on motion, with rigidity of the muscles 
of the back ; in myelitis there is no pain on motion and the muscles are 
flaccid and relaxed. Paralysis in spinal meningitis is incomplete, but para- 
plegia or hemi-paraplegia is always present in acute myelitis. Cutaneous 
and muscular hyperesthesia, with febrile and cerebral symptoms, exists in 
meningitis, but is absent in myelitis. 

Hysterical paraplegia is diagnosticated by the attendant hysterical symp- 
toms, globus hystericus, large flow of limpid urine, jactitation, etc. It is 
not a true paraplegia, and generally occurs in young women. 

In paraplegia from reflex irritation, genito-urinary troubles will precede 
the paraplegia ; in myelitis the urinary symptoms follow the paraplegia. 
In reflex urinary irritation the paraplegia is incomplete and does not 
extend upwards ; in myelitis it is complete and increasing. There is no 
paralysis of the sphincters in reflex irritation ; in myelitis it is an early 
and marked symptom. There is no girdle sensation, no formication, or 
sense of swelling and heat in reflex paraplegia ; while these symptoms are 
always present in myelitis. The urine is acid in reflex, and alkaline in 
myelitic paraplegia. The muscles are atrophied in myelitis ; and nor- 
mal in reflex paraplegia. Myelitis of the cervical portion of the cord is 
attended by paralysis of all the extremities, increase in reflex irritability, 
dysphagia, dyspnoea, vomiting and impaired speech. When the whole 
cervical region is involved the upper extremities are first implicated, and 
they lose their reflex irritability. The pharyngeal, thoracic, and ocular 
symptoms are also marked. The pulse is rapid and irregular. 

Prognosis. — In acute myelitis death may occur in twelve to thirty hours, 
or be delayed two or three weeks. When the disease is protracted a month 
it becomes chronic. Complete recovery is rare ; incomplete recovery oc- 
curs quite often. Cervical myelitis is the most, dorsal the least unfavor- 
able. Bed-sores, cystitis, nephritis, and pyelitis, or high fever and sud- 
den and complete paralysis, render the prognosis exceedingly unfavorable. 

Treatment. — The most important thing in the treatment of acute mye- 
litis is absolute rest. Ergot and belladonna have been highly recommended, 
but I have never obtained any positive results from their use. Blisters and 
other counter-irritants, electricity and strychnia are contraindicated. Spinal 
bags filled with hot water have seemed to me to give the greatest relief to 
this class of patients. Diuretics and mild cathartics should be given ; and 
catheterization practised from the outset. If the myelitis is of syphilitic 
origin, iodide of potassium may be of service, but not otherwise. A sup- 
porting, nourishing plan of treatment is to be adopted from the onset. To 
prolong life, complications must be prevented as far as possible. Bed-sores 
must be prevented by great cleanliness and the daily use of the galvanic 



CHRONIC MYELITIS. 



1041 



current ; cystitis may be avoided by the frequent use of the catheter and 
the washing out of the bladder. 

CHEONIC MYELITIS. 

Under this term are included a variety of changes in the cord, of which 
white softening is perhaps the most frequent. 

Morbid Anatomy. — When chronic myelitis is the sequela of acute, the 
change to white softening marks the entrance into the chronic stage. In 
this stage, by a process precisely similar to that which occurs in the brain, 
a cyst is formed. It is divided by numerous septa of connective-tissue, and 
contains fluid resembling chalk and water. After absorption the cicatrix 
is gray, shrivelled, and pigmented. Less commonly, though by no means 
infrequently, there is hyperplasia of the neuroglia, and a dense, gray, scle- 
rosed focus remains. Large cells with numerous processes, called Deiter's 
cells, are seen in this sclerosed tissue, and the ganglion cells are found at- 
rophied. Large quantities of corpora amylacea are formed. Usually the 
cord is hard and gray, but in many cases it appears to the naked eye per- 
fectly normal, while the microscope reveals chronic myelitis. 1 It is slightly 
diminished in volume, and the atrophy may be uniform, or irregular, and ab 
scattered points. 

Chronic inflammation of the meninges with progressive atrophy of the 
roots and trunks of the peripheral nerves is met with in chronic myelitis. 
There is increase in the connective-tissue of the neuroglia, and degeneration 
of the nerve fibres. The ganglion cells are hard and pigmented, and large 
Deiter's cells are abundant. The axis cylinder remains intact for a long 
time. 2 Fat cells are everywhere present, and in cases of very long standing 
large excavations in the substance of the cord may occur. 

It is impossible to distinguish interstitial from parenchymatous my- 
elitis. 3 

Etiology. — All the constitutional causes that were enumerated as causes 
of acute may be included under the remote causes of chronic myelitis, and 
of these chronic alcoholismus, sexual excesses, and reflex disturbances are 
more liable to result in chronic than acute myelitis. 

Symptoms. — The symptoms of chronic myelitis are so complex that Char- 
cot calls it a " polymorphous " disease. It is usually insidious in its onset ; 
and in its development disorders of sensation precede motor disturbances. 
Pains in the limbs simulating rheumatism are gradually associated with 
muscular weakness ; and tingling, formication, numbness of the limbs, with 
the girdle sensation, are followed by an unsteady gait. Local anaesthesia 
alternates with hyperesthesia. Weakness of the bladder and constipation 
are both the result of muscular weakness. These symptoms are followed 

1 So-called gray degeneration. 

2 Charcot and Ley den. 

3 Leyden, in the Zeitschr.f. Klin. Med., Berlin, 1879, No. 1, p. 1-26, recites a most interesting case, where 
numerous large round nucleated cells were found pushing npart nerve fibres in the posterior dorsal region 
of the cord of a man who had been poisoned in a caisson. Recently " syste?ns " have been described in 
the cord, and some pathologists have classified diseases of the cord on this physiological basis. Leyden 
describes two forms of system disease of the cord, where chronic myelitis is the sole lesion, i. e., tabes dor- 
salis, and atrophy of the motor parts of the cord. These two combined give a combined system disease. Re- 
generation of destroyed nerve fibres in the cord is possible though very rare. 

66 



1042 



DISEASES OF THE NERVOUS SYSTEM. 



by paraplegia, muscular atrophy, cystitis, and chronic bed-sores. Slight 
tremors and twi tellings of the muscles are not uncommon. Patients with 
chronic myelitis always complain of cold feet. 1 

There is usually progressive emaciation and cachexia. Some cases remain 
stationary for months and even years ; but the majority reach a fatal ter- 
mination through successive exacerbations and remissions. 

Differential Diagnosis. — Chronic myelitis may be confounded with spinal 
apoplexy, spinal meningitis, or locomotor ataxia. 

It is distinguished from hemorrhage by the sudden advent of the hemor- 
rhage, and from meningitis by the absence of pain. 

In locomotor ataxia the double heel-and-toe tread, the neuralgic pains, 
the preservation of motor power, of control of the sphincters and sexual 
force, all stand in contrast to the signs of chronic myelitis. 

Prognosis. — The prognosis in chronic myelitis is always unfavorable. It 
may continue from two to ten years, but in no case can there be complete re- 
covery. It may remain stationary also ; but the functions are never restored. 
Death results from cystitis and pyelitis, bed-sores, and other complications. 

Treatment. — Eest is the most important remedial agent. When a cause — 
such as lead poisoning, disease of bladder, uterus, etc. — can be reached it 
must be removed. Dry cups daily to the spine are usually of service. 
Ergot, belladonna, nitrate of silver, iodide of potash, arsenic, phosphorus, 
and strychnia have all been recommended and benefit claimed for them, 
as may be said of hot or cold baths at natural springs. 2 The bladder must 
be emptied twice or three times daily and the bowels kept freely open. 
The galvanic current is considered beneficial, or at least harmless. Fric- 
tion, shampooing, and massage of the paralyzed limbs prevent wasting of 
the muscles. 

NON-INFLAMMATORY softening. 

Our knowledge of this rare condition is vague. Indeed, until recently, 
its existence was denied. 

Morbid Anatomy. — The site, extent and limitation of non-inflammatory 
softening are the same as in myelitic patches. Myeline, broken-down nerve- 
tubes, large granulation corpuscles, are all found in the patch. Kadcliffe 
describes white softening as non-inflammatory and due to anaemia. 

Etiology. — Slowed blood-current, a tendency of the blood to spontaneous 
coagulation, and disease of the walls of the blood-vessels are regarded as 
causes of non-inflammatory spinal softening. 3 It is sometimes met with 
within the month after childbirth, in the late stages of syphilis, after great 
bodily exertion, sexual excess, and exposure. 

Symptoms. — The symptoms of non-inflammatory softening do not differ 
essentially from those of chronic myelitis, spinal hemorrhage, and spinal 
tumors. Its invasion is generally gradual, and the complexity of symp- 
toms varies according as the foci are circumscribed or diffuse, central, lat- 
eral, or completely transverse. If the softening extends completely across 

1 Erb states that catheterization and dressing the bed-sores produces varied movements in the paralyzed 
limbs. 2 Erb, Rosenthal and others. 

3 Dr. Moxon calls attention to the fact that the blood supply at the lower end of the cord— where soft- 
anings are most frequent— is peculiar and easily interfered with.— Brit. Med. Jour., vol. i. 1881. 



ACUTE BULBAR PARALYSIS. 



1043 



the cord, there is complete paralysis of the lower extremities and of the 
abdominal muscles. The limbs are cold to the touch and their tempera- 
ture is sub-normal. The toes are turned inward, so that as the patient 
lies in bed the feet form a cross. The skin becomes dry and rough, and 
the muscles are flabby although not wasted. There is almost complete abo- 
lition of reflex movement. Early in the disease there is retention of urine, 
which is followed by incontinence and partial retention, and the usual 
sequelae of cystitis and possibly pyelitis or arnmonaemia ; the kidney may 
become studded with minute abscesses. 

Differential Diagnosis. — Its slow onset and the previous history enable us 
to differentiate between non-inflammatory softening and spinal hemorrhage, 
it is not difficult to determine the extent of the lesion ; but to determine 
whether it is central or peripheral, anterior or posterior, is always difficult 
and often impossible. 

Prognosis. — The prognosis is always unfavorable. There is great danger 
of intercurrent diseases, especially pneumonia, local or general meningitis, 
and inflammation of the genito-urinary tract, or septicaemia. In rare in- 
stances the paralysis may gradually disappear and partial recovery take place. 

Treatment. — No plan of treatment is successful. The bowels and blad- 
der must be attended to, and the latter is best washed out with a one-half 
per cent, solution of chlorate of potash. The galvanic and Earadic currents 
may be used. 

ACUTE BULBAR PARALYSIS. 

While acute bulbar paralysis involves a nervous distribution similar to 
that of the chronic form, its morbid anatomy is very different. 

Morbid Anatomy. — At the autopsy there will be foci of softening and ex- 
travasation from thrombosis and embolism. Erb states that there is an 
acute bulbar paralysis not due to these causes, but which is in reality a 
primary acute myelitis lulbi. 

Etiology. — The etiology of acute bulbar myelitis is unknown, aside from 
the causes of apoplexy, embolism, and thrombosis elsewhere in the cerebro- 
spinal system. 

Symptoms. — Its onset is very sudden; the prominent symptoms are head- 
ache, dizziness, and sometimes loss of consciousness (apoplectiform variety). 
Cough, dyspnoea, and hiccough are often present, and sometimes there are 
convulsions and weakness in the limbs accompanied by tingling sensations. 
In other cases coma and asphyxia precede the rapidly fatal issue. Paraly- 
sis is often best marked in the distributions of the bulbar nerves. This 
may affect the facial, trigeminus, accessorius, or glossopharyngeal. In 
many cases the paralysis is "crossed/' the hemiplegia being on the oppo- 
site side from the paralysis of the bulbar nerves. Very rarely the hemi- 
plegia is crossed, the arm of one side and the leg of the other suffering. 
In occlusion of the basilar artery the carotid pulse is unusually full. The 
paralysis is usually paraplegic, but may be hemiplegic. Occasionally it 
will begin severely on one side, and after a few days pass to the other one 
as the primary paralysis improves. 

Paralyses of the muscles of the pharynx and fauces are common in 



1044 



DISEASES OF THE 2STERVOUS SYSTEM. 



all forms of bulbar disease. Eosenthal states that, in addition to dyspnoea, 
Cheyne-Stokes respiration often appears as a characteristic symptom of 
medullary hemorrhage. 1 When the extravasations extend into the fourth 
ventricle, polyuria and albuminuria are observed. 2 In embolism, improve- 
ment is common, but in hemorrhage it is rare ; thrombosis of the vertebral 
arteries pursues a more chronic course, but with similar results. 

Prognosis. — If the patient recovers from the primary effects of the lesion, 
the prognosis of the paralysis is better than in the chronic form. The 
prognosis is better when the disease is associated with or due to syphilitic 
infection. In a few acute cases the paralysis is permanent, although it has 
no tendency to increase. In sudden and complete obstruction of the basilar 
or both vertebrals the prognosis is exceedingly bad. Limited or capillary 
hemorrhages render the prognosis unfavorable. 

Treatment. — This does not differ from the treatment of similar conditions 
elsewhere in the brain, which has been considered under apoplexy and cere- 
bral softening. 

CHRONIC BULBAR PARALYSIS. 



(Glosso-ldbio-laryngeal Paralysis. ) 

This is a progressive, symmetrical paralysis of the lips, adjacent facial 

muscles, tongue, pharynx, 
and sometimes of the 
larynx. 

Morbid Anatomy. — The 
medulla may be atrophied 
and show spots of gray 
discoloration which have a 
sclerotic feel. There is 
degenerative atrophy of 
the gray nuclei in the floor 
of the fourth ventricle ; 
with atrophy and gray dis- 
coloration of the nerve 
roots from the medulla, 
especially of the facial and 
hypoglossal nerves. 3 The 
ganglion cells and the 
nerve-nuclei lose their stel- 
late form and become 
shrunken, smaller, and of 
Morbid condition on the & dull ochre color. The 
prolongations and nuclei 
are rudimentary or even 
completely atrophied. The 




Fig. 206. 

Chronic Bulbar Paralysis. 

Transverse section of the bulbus on a level with the 
the nucleus of the hypoglossus. 



of 



AA'. Line dividing the section centrally, 
left hand. 

B. Ganglion cells forming nucleus of ftypoglossus. 

C. A vessel forming front and inner boundary of B. 

D. Floor of fourth ventricle. 

E. Nucleus 'of pneumogastric. 
On the left the nucleus of the hypoglossus is nearly obliterated, 

while that of 'the pneumogastric is'unaltered. Charcot. cells are filled With pig- 



1 See also accounts by Traube in the Berlin. Klin. Wochen., 1869 to 1874. 

2 Gazette des Hopitaux, 1862. 

8 Recent physiological investigations show that the lower facial nucleus and the hypoglossal nucleus 
are closely connected. 



CHRONIC BULBAR PARALYSIS. 



1045 



ment and granular matter, the nucleus and nucleolus present a vitreous, 
shining appearance/ and are separated from each other by large spaces. 
Atrophy and disappearance of the motor ganglion cells is always to be 
noted. It may be the sole lesion or be accompanied by increase in the 
neurolgia, when fat and granular corpuscles, numerous corpora amylacea, 
G-luge's corpuscles, and spider-cells will be found in the newly-developed 
tissue. The walls of the vessels are thick, and show more or less fatty 
change. The decrease in size of the gray nuclei is a measure of the inten- 
sity of the symptoms that existed during life. 

Similar bilateral lesions may be found in the nuclei of the pneumogas- 
tric, spinal-accessory, glosso-pharyngeal, facial, trifacial, motor oculi, and, 
very rarely, of the trigeminus. 2 

The muscles are pale and the fibres frequently show granular degenera- 
tion ; but sometimes fatty tissue is in excess. The fibres may be thin, and 
the tissue between them contain the pigment products of degeneration, so 
that the muscles, though degenerated, will preserve their normal bulk. 




Fig. 207. 
Chronic Bulbar Paralysis. 

A. Microscopical appearance of normal muscle from the tongue. 

B. Same muscle taken from a case of Glosso-ldbio-laryngeal Paralysis. 

C. Fasciculi of muscular fibres in transverse section. 

D. Atrophied fibres seen longitudinally, x 300. 

The muscular fibres show increase in their nuclei and changes precisely 
similar to those in progressive muscular atrophy. 

The nerves going to the muscles exhibit sclerosis of the neurilemma, 
slight traces only of the axis-cylinders remaining. The same degenerative 
atrophy is found in the nerve roots coming from the bulb. This disease 
is rare before the fortieth year of life ; it is essentially a disease of old age. 
Males are more subject to it than females. 



1 Yellow degeneration of Charcot. 



2 Duchenne. 



1046 



DISEASES OF THE NEEVOUS SYSTEM. 



Etiology. — Its etiology is always obscure. The neuropathic tendency 
seems fc> exercise some influence in certain cases. It is said to occur with 
syphilis and rheumatism. Bad hygiene, exposure to cold, excessive anxi- 
ety, close mental application, and prolonged physical exertion are all ad- 
duced as causes. 

Symptoms. — The earliest symptoms of bulbar paralysis are imperfect move- 
ments of the tongue ; the speech is indistinct, and enunciation of the pal- 
atal and dental sounds is imperfect. Often the tongue cannot be protruded 
as far as normal, nor the lips brought together as perfectly or separated as 
promptly as in health. Whistling and whispering are impossible. The 
lower part of the face becomes expressionless. The lips remain separated 
and the saliva is either tenacious or dribbles from the mouth, which is so 
drawn as to give the face a woe-begone expression. Speech may be entirely 
lost. 

When the palate muscles are involved, deglutition becomes difficult, 
and as the soft palate hangs motionless, not closing the posterior nares, the 
food regurgitates through the nose, or lodges in the upper part of the phar- 
ynx and collects between the cheeks and the alveolar arches ; portions are 
also apt to fall into the larynx. Another effect of palatal paresis is to give 
a nasal twang to the voice. 

If the laryngeal muscles become weakened and closure of the glottis im- 
perfect, coughing becomes ineffective and phonation is interfered with. The 
muscles of mastication are rarely involved until late in the disease, but ex- 
haustion and emaciation from insufficient food are developed early. The 
muscles atrophy, and tremblings and fibrillar twitchings occur. When the 
respiratory centres are involved there is a sense of fulness and constriction 
in the chest accompanied by attacks of dyspnoea. 

Lesions in the cardio-inhibitory centres are followed by attacks of syn- 
cope and a pulse of 140 or 160 per minute. There is an abnormal amount 
of saliva secreted, either as paralytic saliva 1 or from irritation in the me- 
dulla. 2 The laryngoscope reveals paralysis of the vocal cords. Should 
bronchitis occur expectoration is difficult, and if pneumonia or any other 
severe pulmonary affection develops it almost always terminates fatally. 
The muscles show the reaction of degeneration ; sensibility is unchanged, 
but reflex actions are greatly diminished or destroyed. Atrophy of the 
muscles at the back of the neck — the trapezii especially — is not infrequent. 
In some few cases the paralytic symptoms may be preceded by dull pains 
in the back of the head and neck, giddiness, queer sensations in speaking, 
and loss of reflex irritability in the pharynx and larynx. 3 

1 See M. Foster's Physiology. Art. Sub-maxillary Gland. 2 Pfliiger's Archiv, Bd. 7. 

3 Kirchoff reports a case where bulbar paralysis was produced by a unilateral lesion, and from the autop- 
sical results in this case the symptoms must be attributed to a lesion of the lenticular nucleus. A new and 
peculiar variety of bulbar paralysis has recently been described by Erb. An analysis of the symptoms 
shows that the parts chiefly involved are the motor oculi communis, the motor portion of the trigeminus, 
the spinal-accessory, and the upper cervical nerves ; and those more slightly affected are the facial (the 
upper branches to the face), the hypoglossal, and probably also the glossopharyngeal nerves. The nuclei 
of origin of these nerves are all situated in the floor of the fourth ventricle and in its immediate neighbor- 
hood in the pons Varolii. Erb supposes that, in the affection under consideration, the lesion is situated in 
the upper half of the fourth ventricle and spreads more deeply into the substance of the medulla, affecting 
nerve fibres as they pass upward from the nuclei of origin in the fourth ventricle. 



CHRONIC BULBAR PARALYSIS. 



1047 



Differential Diagnosis. — Progressive bulbar paralysis may be mistaken for 
tumors in the medulla, double facial palsy, embolism and thrombosis of the 
medulla, medullary apoplexy, embolism of one of the vertebral arteries, 
progressive muscular atrophy attacking the face, and general paralysis of 
the insane. 

In tumors of the medulla, we find neuralgia, clonic convulsions of the 
muscles of the face and tongue, disturbances of the smell and hearing, 
headache, vomiting, dizziness, and epileptiform attacks, the disease being 
either unilateral or decidedly marked only on one side. 

In double facial palsy, all the branches of the facial nerve are involved ; 
movements of the tongue and deglutition are normal. 

In embolism or thrombosis of the medulla, the sudden onset of the symp- 
toms with either hemiplegia or paraplegia, taken in connection with the 
age of the patient and the condition of the arteries, will be the chief points 
of diagnosis. In embolism improvement is possible. 

In bulbar hemorrhage, loss of consciousness, epileptiform convulsions, 
vomiting, prominence of unilateral symptoms are combined with bulbar 
paralysis of sudden advent. The previous history will aid in the diagnosis. 

Embolism of the vertebral arteries is accompanied by sudden (apoplec- 
tiform) onset of the symptoms of bulbar paralysis, hemiplegia, anaesthesia, 
variations in the paralyses, and co-existing disorders of sight and hearing. 

In progressive muscular atrophy, paralysis follows the atrophy ; in bulbar 
paralysis it is the reverse. Moreover, the thenar and hypothenar eminences 
are involved early, even should muscular atrophy first attack the tongue, 
lips and palate. 1 

In general paralysis of the insane, the cerebral disturbances and the fact 
that other muscles are involved besides those in the region of the mouth 
and palate, will establish the diagnosis. 

Prognosis. — The prognosis is grave ; although a temporary arrest may 
occur, genuine bulbar paralysis invariably terminates in death. The 
amount of dysphagia and dyspnoea and the rapidity of development will 
determine the relative gravity of the case. Its average duration is about 
two years. Bulbar paralysis may be complicated by progressive muscular 
atrophy, amyotrophic lateral sclerosis and disseminated sclerosis. Death 
occurs from starvation, paralysis of the heart or respiratory organs, or inter- 
current pulmonary diseases. Sometimes coma ends the scene, and there 
is a slight rise of temperature. 

Treatment. — A nutritious diet and the best hygienic surroundings, with 
quinine, arsenic and nitrate of silver are the means which have been most 
extensively employed. The German physicians condemn, and the English 
advocate, the use of strychnine and phosphorus. Ergot, belladonna, and 
iodide of potash may be given. Direct galvanic or Faradic currents ap- 
plied to the paralyzed parts have been recommended. In some cases a 
stomach tube may be used to prolong life, and perhaps gastrostomy may 
be demanded. 



1 Duchenne. 



1048 



DISEASES OF THE NERVOUS SYSTEM. 



INFANTILE SPINAL PAEALYSIS. 



Infantile spinal paralysis or acute anterior polio-myelitis is an inflam- 
mation of the anterior cornua of gray matter of the cord. It may occur in 
adults, but is almost always exclusively confined to children. 1 

Morbid Anatomy. — The early changes are those of inflammatory soften- 




Fig. 208. 

Anterior Gray Cornu of Spinal Cord in 
Early Stage of Infantile Spinal Paral- 
ysis. 

A. Large multipolar ganglion cells. 

B. Neuroglia cells in a state of active pro- 

liferation, x 300. 




Fig. 209. 

Anterior Gray Cornu of Spina Cord 
after establishment of the Sclerotic 
Process in Infantile Spinal Paralysis. 

A. Dense nucleated connective-tissue. 

B. Large masses of pigment— the re- 

mains of ganglion cells. 
O. Corpora dmylacea. x 300. 



ing ; medullary hyperemia and vascular exudations are the incidental 
occurrences. 2 Extensive changes may exist, and yet the gross appearance 
of the cord be unchanged. 

Microscopically there will be seen, in its early stage, all the changes of acute 
interstitial inflammation, and the neuroglia nuclei are in active prolifera- 
tion. Later a sclerotic process is established, and new connective-tissue 
developed, in which are multitudes of nuclei and corpora amylacea. Pig- 
mentation is more or less marked, and the ganglion cells, that have lost 
their processes, may remain only as irregular spherical masses of pigment. 
Thickening and increase of neuroglia in the anterior columns result in 
more or less atrophy of the nerve fibres. The anterolateral columns of the 
cord may be invaded, but the posterior usually escape. 3 The anterior roots 

1 Niemeyer calls it essential palsy. Erb describes it as a more or less diffuse myelitis of the anterior 
gray substance, which reaches its greatest intensity in the lumbar and cervical enlargements of the cord, 
and, as a rule, leaves no permanent and irremediable alteration except at those two points. 

2 Rosenthal. 

3 The most careful microscopical examination fails to decide what modern- pathology is still earnestly 
discussing, viz. : whether acute polio-myelitis is an interstitial or a parenchymatous inflammation. The 
majority favor the latter view, the ganglion cells being its supposed starting-point. 



INFANTILE SPINAL PARALYSIS. 



1049 



of the spinal nerve are shrunken, atrophied, and degenerated. They are 
gray and translucent. The vessels undergo considerable enlargement, and 
their walls are thickened. The motor nerves are involved secondarily to 
the cord at an advanced period of the disease. The muscles which are im- 
plicated rapidly undergo fibroid changes and atrophy. Their transverse 
striae are indistinct, and the nuclei become abundant ; the muscular fibres 
may wholly disappear. 1 The muscular fibres do not always suffer this 
degeneration, but sometimes they undergo fatty degeneration, or the mus- 
cles are so infiltrated with oil globules that they retain their normal size, 
and may even exceed it ; this is a pseudo-hypertrophy. 2 The hones are 
retarded in development, somewhat flexible, and contain more fat than 
usual. The tendons become atrophied, and the joints lose their com- 
pactness. 

Etiology. — This is essentially a disease of the first three years of life, the 
usual time of occurrence being between the sixth and fourteenth months. 
It attacks equally children of both sexes, the robust as well as those of 
feeble and cachectic constitutions. Cold, dentition, and traumatism are 
among its doubtful causes. It has occurred in two or more offspring of the 
same parents, and once in twins 3 after an attack of measles. Many regard 
acute febrile diseases as an important factor in its causation. It is devel- 
oped, if at all, during convalescence from such fevers. 

Symptoms. — The onset of infantile spinal paralysis is sudden. A child 
has well-marked febrile movement attended by dizziness, headache, restless- 
ness, nausea, vomiting, and sometimes delirium, convulsions and coma. 
Accompanying these symptoms there is more or less pain in the back. In 
many cases the febrile symptoms only last a few hours. Following a con- 
vulsion or attack of unconsciousness the child becomes paralyzed, or in 
some cases paralysis may come on suddenly without a single premonitory 
symptom ; the child goes to bed perfectly well and wakes with paraplegia. 
If only one lower limb is involved at first, the other soon becomes so ; and 
it is not unusual for all four extremities to be affected simultaneously. The 
arms alone are rarely involved. The paralysis is not accompanied by loss 
of sensibility. It reaches its maximum in from ten hours to six or seven 
days, and begins to diminish in about two weeks after its commencement. 
The paralyzed muscles become flaccid, relaxed, and attenuated, and if the 
paralysis is persistent they atrophy and undergo degeneration. The 
surface of the body is cold and of a purplish color. The limbs may pre- 
serve their normal contour ; but they are soft and often tender to pressure. 
The tendon-reflexes and reflex action in the muscles of the paralyzed part 
are entirely lost, and they fail to respond to the Faradic current. These 
alterations in electrical excitability are results of the reactions of degener- 
ation. 

Paralysis at the onset is general, but later it is localized in one group 01 
in single muscles. The muscles on the back of the forearm and front of the 
leg, in the foot, and the extensors of the leg, are more apt to be affected, 

1 Erb lays great stress upon the replacement of muscle tissue, in this disease, by fat, so that the 
muscles have the faded-leaf appearance of a typhoid heart. 

2 Erb. 3 Moritz Meyer. 



1050 



DISEASES OF THE NERVOUS SYSTEM. 



but the paralysis may involve only the deltoid, tibialis anticus, sterno-clei- 
do-mastoid, or the extensor longus digitorum. The joints are loosened, and 
the bones, especially the long ones, are smaller and shorter than those in the 
unaffected limb. The temperature of the paralyzed parts is often 5° or 8° F. 
lower than normal. The deformities and unnatural attitudes that result 
may simulate talipes ; and all varieties of contracture occur as late man- 
ifestations. The epiphyses atrophy and subluxations sometimes occur. 
The general health of the patient is usually good, and there is nothing that 
interferes with long life, except the paralysis and deformity. In severe 
cases there is at the onset loss of control of bladder and rectum. In such 
cases slight vesical weakness usually continues during life. The normal 
sensibility of the skin is preserved throughout. 

Differential Diagnosis.— Infantile spinal paralysis may be mistaken for 
progressive muscular atrophy , pseudo-muscular hypertrophy, rachitis, tem- 
porary infantile paralysis, myelitis, and hemiplegia. 

Progressive muscular atrophy begins insidiously and is slowly progres- 
sive ; spinal infantile paralysis begins suddenly, and after a time a certain 
amount of improvement occurs. Progressive muscular atrophy is rare in 
children before the fifth or seventh year of age. It commences by palsy 
about the lips and mouth, and the electro-contractility of the affected 
muscles is lost only in proportion to their atrophy and degeneration, the 
uninvolved fibres . responding to the current. This fact taken in connec- 
tion with the age of the patient will usually enable one to make a diag- 
nosis. 

Pseudo-muscular hypertrophy begins ivithout fever ; the motor power at 
first is only weakened, and the trunk and extremities are involved late 
in the disease. The electro-muscular contractility is preserved, and there 
is always increase in the volume of the muscles. In walking the patient 
spreads the feet far apart, and there is a peculiar incurvation of the verte- 
bral column not seen in infantile spinal paralysis. 

Rickets is attended by no change in electro-muscular contractility, is 
preceded by no cerebral or pyretic phenomena, and there coexist develop- 
mental and other changes that cannot fail to determine the character of the 
deformity. 

In temporary paralysis there are no signs of softening or atrophy of 
muscles, there is no change in electro-muscular contractility, and the pa- 
ralysis is recovered from in twenty to thirty days. 

In myelitis, trophic disturbances and genito-urinary complications are 
sufficient to distinguish it from infantile spinal paralysis. 

Hemiplegia from acute cerebral affections in childhood can generally be 
distinguished from acute anterior polio-myelitis by loss of intelligence and 
speech, strabismus, paralysis of half the face, dilated pupils, and normal 
electrical contractility in connection with disturbances in sensation, stiff- 
ness of the joints, spasmodic contractures with absence of fever, and mus- 
cular atrophy. 

Prognosis. — There is little or no danger to life in acute anterior polio- 
myelitis, even when the attack commences with very active symptoms. A 



ACUTE SPIRAL PAEALYSIS OF ADULTS. 



1051 



mild, or even a severe, onset may be followed by complete restoration of the 
function and power of the paralyzed muscles : — so-called temporary spinal 
palsy. Usually the improvement is such that the function of the few mus- 
cles that remain permanently paralyzed, and atrophied is performed by the 
muscles not involved. All the paralyzed muscles in which Faradic irrita- 
bility is not completely lost are restored. 1 

Treatment. — In the acute stage rest in the recumbent posture is the most 
important element of treatment. Beyond this the treatment is the same 
as for acute myelitis. After the febrile symptoms have subsided — usually 
by the fourth week — measures must be adopted to restore the function of 
the paralyzed muscles. The early and persistent use of the galvanic current 
hastens the recovery in those muscles whose electric contractility is but 
slightly diminished, and will often arrest the wasting and restore them to 
a normal condition. When electric contractility is entirely lost little bene- 
fit can be expected. The longer the use of electricity is delayed the less 
the chances of recovery. Even if it fails to cure it has a tendency to pre- 
vent deformity. Saline and thermal baths and the water treatment of 
various kinds are recommended. Massage, friction, shampooing, inunc- 
tions, etc., are to be combined with the electric and hydropathic plans of 
treatment. The diet must be such as to bring nutrition to its highest 
point. Minute quantities of strychnia injected hypodermically have been 
found beneficial. Iron, arsenic, quinine and phosphorus are indicated — 
as tonics — in nearly every case. 



ACUTE SPINAL PAEALYSIS OF ADULTS. 

Duchenne and Moritz Meyer first observed that this disease not infre- 
quently occurred during adult life, with pathological changes identical 
with those of the disease in infancy. 

The etiology is obscure ; cold, wet, and the debility found in conva- 
lescence from fevers, jmeumonia, malarial poisoning, etc., have been sug- 
gested as causes. 

The symptoms at the onset are modified by the greater stability of the 
adult nervous system, and there is less restlessness, delirium, fever, etc. 
The cerebral symptoms may be very slight, transient, and easily overlooked 
and followed by paralyses, which go on to partial recovery as m the infantile 
form. There are no bone deformities or arrested developments ; and the 
joints do not become lax. Tingling, numbness, and formication occur in 
adults at the onset, and gastric symptoms are more frequent. 

Differential Diagnosis. — Absence of spasms and of trophic disturbances, 
diminution of reflexes, normal sensibility, non-interference with the sphinc- 
ters, the sudden onset and the subsequent improvements suffice to distin- 
guish this disease from all other affections of the cord. 

Chronic atrophic spinal paralysis resembles it, but the abrupt invasion 



1 Seeligmuller records two cases where progressive muscular atrophy occurred late in life in those who 
In infancy suffered from acute anterior polio-myelitis. 



1052 



DISEASES OE THE NERVOUS SYSTEM. 



of anterior polio-myelitis is absent in the former malady. If this point in 
the history be wanting a differential diagnosis may be impossible. 
The prognosis and treatment are the same as in children. 

CHRONIC ANTERIOR POLIO-MYELITIS. 

Duchenne was the first to describe (1853) this disease under the above 
name. It has since been called subacute and chronic inflammation of the 
gray anterior horns, chronic atrophic spinal paralysis, and subacute spinal 
paralysis. 

Morbid Anatomy. — The morbid anatomy of this disease is still obscure. 
So far as can be stated from the few recorded autopsies it is simply a 
chronic myelitis of the anterior cornua ; ^the neuroglia is increased ; the 
blood-vessels are thickened, the anterior nerve-roots are atrophied, and 
there is an abundance of granular and fat cells in the diseased district. 
Recently vacuoles have been found in the ganglion cells of the anterior 
horns. Almost entire disappearance of these cells was the chief lesion in 
one case. 1 

Etiology. — It is a disease of adult life from thirty to fifty, and excesses of 
any kind, or exposure to cold and wet, are said to exert an influence on its 
development similar to that in other spinal affections. 2 

Symptoms. — In some subacute cases slight fever and shooting pains in 
the back accompany the development of paralysis of the lower limbs. In 
others the patient first notices weakness and heaviness in his legs, followed 
by paralysis either of groups of muscles or of the whole limb. The mus- 
cles become flabby and progressively waste away. They are sensitive to the 
galvanic current, but respond little, if at all, to the Faradic. The irreg- 
ular distribution of the paralysis is characteristic. As the muscles are 
undergoing atrophy, fibrillary twitchings are often noticed. Tendon- 
reflexes and skin-reflexes are both abolished ; but sensibility is unaffected. 
There is vaso-motorial disturbance, indicated by cold and blue extremities. 
The temperature of the affected limbs is lo vered. Later, the upper limbs 
are involved. The paralysis first attacks the flexors or extensors on the 
forearm, and gradually involves isolated groups of muscles, or the whole 
limb. The fingers and hand, however, suffer most. When the disease has 
reached this stage the wasted muscles will no longer respond to the galvanic 
current. The rectum, bladder, and sexual power are undisturbed. When 
the process extends to the cervical region dyspnoea is present, and if the me- 
dulla becomes involved deglutition and articulation are affected, and great 
exhaustion is induced, asphyxia closing the scene. The general health re- 
mains good, and the mental faculties are unimpaired. 

Differential Diagnosis. — Chronic atrophic spinal paralysis may be mis- 
taken for progressive muscular atrophy, amyotrophic lateral sclerosis, acute 
ascending paralysis, and the acute spinal paralysis of adults. 

In progressive muscular atrophy paralysis follows the wasting ; the re- 

1 Arch, de Physiologie, 1876. 

2 Erb suggests that its co-existence with chronic lead poisoning is the result of an inflammatory 
action called forth by the saturnismus. 



PROGRESSIVE MUSCULAR ATROPHY. 



1053 



verse is the case in polio-myelitis. Portions of the muscles only are in- 
volved in progressive muscular atrophy, and it begins in the muscles of the 
thumb. Keflex action is retained, and the progress is much slower than in 
chronic polio-myelitis. Moreover, the susceptibility to the electrical cur- 
rents is never wholly lost in progressive muscular atrophy. 

In amyotrophic lateral sclerosis, though the upper extremities may be 
wasted, there is a characteristically different combination of paralysis with- 
out wasting, and with more or less rigidity in the lower extremities. The 
reaction of degeneration is far more marked in chronic anterior polio- 
myelitis. Keflex clonus and exaggerated tendon-reflexes are absent in 
chronic polio-myelitis, and present in amyotrophic lateral sclerosis. 

In acute ascending paralysis the atrophy is not marked ; electrical re- 
actions of nerves and muscles are normal, reflex action is preserved for a 
long time, and bulbar symptoms with vesical disturbances are not uncom- 
mon. Acute ascending paralysis is of short duration compared with chronic 
anterior polio-myelitis. 

In acute spinal paralysis of adults the paralysis, which is sudden in its 
onset, is more extensive, and after a short time there is improvement in 
motor power ; while in chronic atrophic spinal paralysis there is a dis- 
tinctly progressive unremitting spread of the disease from part to part. 

Prognosis. — In rapidly progressive cases the prognosis is bad, but in those 
that are slowly developed and partial the prognosis is better, and sometimes 
complete recovery may take place, or certain muscles or groups remain 
paralyzed and atrophied while others improve. After a long time the dis- 
ease may be spontaneously arrested and the patient remain paralyzed the 
remainder of life. The most unfavorable cases are those in which the 
cervical region and the medulla become involved, death occurring with 
symptoms of bulbar paralysis. The usual duration is from a few months 
to three or four years. 

Treatment. — Electricity and a nourishing diet, with rest, give the best re- 
sults. Dr. Bastian suggests that counter-irritation may do good in the 
early stages. Sulphur, mineral, and brine baths and the cold water treat- 
ment are advocated. It is a question whether either iodide of potassium 
or ergot is beneficial. Modern literature, though extremely rich in theories, 
is devoid of facts which can aid in the treatment. 

PROGRESSIVE MUSCULAR ATROPHY. 

As the name indicates, this disease is a progressive and chronic wasting 
and atrophy of the muscles, and results from trophic changes due to a cen- 
tral nerve-lesion. 

Morbid Anatomy. — The morbid anatomy of this affection differs little 
from that in spinal paralysis of children. Its essential lesion is atrophy of 
certain groups of nerve-cells in the anterior cornua of the cord. Some- 
times atrophy of the anterior horns is associated with a sclerotic condition 
of the lateral columns. The general changes are the same as in the late 
stage of anterior polio-myelitis. The central canal of the cord is some- 



1054 



DISEASES OF THE NEKVOUS SYSTEM. 




times dilated and filled with fluid. On microscopic examination the 
ganglion cells show pigmentation to a marked degree, with more or less 
atrophy. They are surrounded by indurated tissue. The blood-vessels 

are often dilated, and sur- 
rounding them is a zone 
of granular disintegrated 
or diffluent material, the 
so-called mixed exuda- 
tion. All these changes 
may be found in both 
gray and white matter. 
The anterior roots of the 
spinal nerves are atro- 
phied, and show more or 
less gray degeneration. 
Sometimes all except the 
neurilemma has disap- 
peared. The muscles over 
the body are not equally 
involved ; indeed, bundles 
of fibrillar in the same 
muscle are affected in dif- 
ferent degrees. This un- 

Teased Fibres from the Abductor Pollicis in a case of Progressive even character of the atro- 

a , Muscular Atrophy. h {g pecuUar U tMg 

A. Fibres from a normal bundle. . 1 

B. Fibres from a fasciculus adjoining A, atrophied and showing disease. The muscles 

fatty degeneration, x 300. . 

simply waste, and become 
pale or of a faintly yellow hue. They are harder and firmer than normal. 
The striae disappear only after great reduction in size. The interstitial 
structure is increased and filled with numerous lymphoid cells. Fatty and 
granular degeneration may occur later, with fatty infiltration, and if the 
fat-globules are present in large quantity the muscle may not be reduced 
in size. Granular disintegration is soon followed by transformation of the 
muscular tissue into fine fat-granules. 

In some cases progressive muscular atrophy has occurred without ap- 
preciable changes in the cord, and given rise to the belief tha t such changes 
were secondary to the muscular atrophy. It is very generally accepted, 
however, that the central lesion is the primary and characteristic change. 1 

Etiology. — Progressive muscular atrophy is chiefly met with in adult 
males in middle life. Heredity and consanguinous influence can no longer 
be doubted. 2 Excessive physical labor, exposure to cold and wet, are said 
to excite it. Those who habitually use one set of muscles are perhaps pre- 
disposed to the disease. Injury to the spine is an important causative factor. 

1 Virchow calls fat in the fibres parenchymatous, and fat in the interfibrillary tissue the interstitial 
form of degeneration. 

a Leyden states that in hereditary cases the lumbar muscles and those of the lower limbs are first at- 
tacked ; that it may appear in childhood, and that several members of the same family may be simulta- 
neously affected. 



PROGRESSIVE MUSCULAR ATEOPHT. 



1055 




Symptoms. — The invasion of progressive muscular atrophy is irregular 
and variable. It usually comes on insidiously, the first indication of its 
presence being a wasting and loss of power of some muscles or group of 
muscles. When regular in its course the wasting begins in the muscles of 
the hand ; first the ball of the thumb of 
the right hand, then the hypothenar 
eminence and the interossei are at- 
tacked, in the order named. Marked 
atrophy of the interossei causes the hand 
to have the characteristic bird-claw look. 
The left hand is soon involved, and the 
wasting then slowly ascends, attacking the 
muscles of forearms, arms, shoulders, the 
pectorals, and latissimus dorsi, with sym- 
metrical alternation. The arms may be 
reduced to skeletons of limbs, and the 
wing-shoulder is not uncommonly seen. 

"When the muscles of the trunk are in- 
volved, those of respiration and deglu- 
tition are very likely to become implica- 
ted early. Sometimes the starting-point 
is in the thoracic muscles. Although the 
legs become extensively involved later, 
the wasting seldom begins there. These 
atrophic changes advance very slowly, 
and the patient will remember that he had for weeks or months a feeling of 
slight numbness or formication, and that his fingers have seemed clumsy. 
They also may complain — just before atrophy begins— of a sensation of 
cold air being blown on them ; the hand and arm are very easily fatigued, 
and wandering pains not infrequently precede the wasting of the muscles. 
The parts to be attacked or those just involved are colder than normal. A 
peculiar fibrillary tremor — transient oscillatory movements in the fibres 
of the affected muscles — is present early. It occurs unknown to the 
patient, and may be excited by gently blowing or tapping on the skin. 
When the atrophy becomes extensive this ceases. The muscles respond 
promptly to the Faradic and voltaic currents, with a force in proportion 
to their bulk. The wasting in the muscles produces very different ap- 
pearances according to the group involved ; should those of the face be- 
come implicated, as frequently happens in children, the expression is 
stolid, grave, and unchangeable. Often, the head falls forward, and the 
saliva dribbles from the mouth. The speech may be faltering ; and the 
tongue small and shrivelled. Mastication and deglutition may become 
difficult, and as the muscles of respiration are involved dyspnoea is urgent 
and asphyxia or pulmonary complications result fatally. Many state that 
the pupil on the affected side is much smaller than its fellow, and re- 
acts to light but slightly. 1 

1 Rosenthal, Schneemann, Voisin, Menjaud and Bergmann. 



% " 
Fig 

Sketch of a Hand in 



211. 

Progressive Muscular 



Atrophy. — Charcot. 



1056 



DISEASES OF THE NERVOUS SYSTEM. 



In a certain number of cases agonizing pain along the nerves leading to 
the affected muscles occurs and is a prominent symptom throughout. 
Late in the disease atrophy of muscles proceeds so far that absolute im- 
mobility of a member is the result. 1 The general health is unimpaired, 
and the intellect is clear. 

Differential Diagnosis.— Progressive muscular atrophy may be mistaken 
for acute anterior polio-myelitis, for palsy due to injury of a nerve, lead 
palsy, malarial paralysis, post-paralytic atrophy of muscles, and sclerosis 
of the lateral columns. 

In injury of a nerve the atrophy is confined to the muscles supplied by 
that nerve, and is not progressive. In injuries of mixed nerves, sensation 
will also be lost. 

In lead palsy the history of exposure, the blue line about the gums, and 
the colic, with the fact that the extensor muscles of the hand, rather than 
those of the thenar and hypothenar eminences, are first atrophied, caus- 
ing the drop-wrist instead of a claw hand, and that their electric con- 
tractility is greatly diminished, are sufficient for a differential diagnosis. 

In malarial palsy there is no muscular wasting, no tremor, and there 
are the attendant well-known malarial symptoms. 

Muscular atrophy sometimes ioViows paralysis. But this fact alone, when 
the muscles do not respond to Faradization, excludes progressive muscular 
atrophy. 

Symmetrical sclerosis of the lateral columns — amyotrophic lateral 
sclerosis — is, according to Charcot, distinguished by its rapid course, the 
ultimate affection of all the limbs, and the almost constant extension to the 
bulbar nuclei, by the prolonged preservation of electro-muscular contrac- 
tility, and by permanent spasmodic contractures of the paralyzed and 
atrophied limbs. The symptoms of muscular atrophy are preceded in 
amyotrophic sclerosis by paralysis, and accompanied by rigidity ; this does 
not occur in muscular atrophy. 

Prognosis. — Progressive muscular atrophy is always a grave disease. Its 
course is slow and irregular ; it may appear in the muscles of the hand, and 
years elapse before it extends. There is little hope of checking its advance, 
even if the treatment is commenced at its onset. The disease is arrested 
spontaneously in a few instances within two or three years. Complete re- 
covery is rare. One year is the average duration, when recovery takes 
place. Its average duration is five years. 2 An hereditary element in the 
etiology renders the prognosis unfavorable, and when the disease is pro- 
longed several years, or the muscles of respiration and deglutition become 
involved, a fatal termination is rarely long delayed. Inanition, bronchitis, 
pneumonia, and hypostatic congestion are the causes of death. 

Treatment. — In the cases that have come under my observation no plan 
of treatment has had any beneficial effect. If an exciting or predisposing 
cause can be reached it should at once be removed. Damp, cold, and over- 

1 Herpes has been observed along the line of a nerve going to an atrophied muscle, and Rosenthal 
mentions hypertrophy of the bones with concentric osseous atrophy, arthropathies, and bed-sores as rare 
trophic disturbances. 

2 Roberts, in Reynolds System of Medicine. 



CEEEB RO-SPIiTA I j SCLEEOSIS. 



1057 



exertion should be avoided, and if syphilis be suspected, an anti-syphilitic 
treatment is indicated ; and cod-liver oil, phosphorus, arsenic, and the 
mineral tonics are to be given with a highly nutritions diet. The body is 
to be warmly clothed in flannel ; friction, moderate exercise, shampooing, 
massage, and inunctions are undoubtedly beneficial, if persevered in. 
Warm baths at natural springs are strongly recommended. Galvanism, 
however, is probably the most efficient remedy. The current should be 
applied along the spine, especially in the cervical region, and directly to 
the affected muscles. Faradization alternating with the constant current 
often leads to improvement and a temporary arrest of the disease. 1 The 
cramps and neuralgic pains are best controlled by hypodermic injections of 
morphine. 2 

CEREBROSPINAL SCLEROSIS. 

Morbid Anatomy. — On opening the spinal canal the cord is seen to be 
studded with well-defined nodules of sclerotic tissue which have given it 
the name of nodular sclerosis. 
These nodules are distributed ir- 
regularly throughout both the 
gray and white matter. They 
vary in number, and range in size 
from minute microscopical objects 
to the size of a walnut. They 
present a yellowish red, glistening 
appearance, are slightly elevated, 
semi-transparent, of a jelly-like or 
cartilaginous feel, and are marked 
by fine white lines. The meninges 
over the nodules are thickened and 
opaque, but seldom adherent to 
the substance of the cord. The 
sclerosed patches are well defined 
and easily distinguished from the 
normal tissue in which they are 
imbedded ; still there is no ab- 
rupt transition from healthy to 
diseased tissue. 

A microscopical examination 
shows the centre of the nodujes to 
be a dense mass of very fine fibril- 
lated connective-tissue, containing 
fat granules, corpora amylacea, Dei- 
ter's cells and small axis-cylinders 
which are glossy and brittle. The 
persistence of the axis-cylinders is regarded by Charcot as peculiar to dissem- 

1 Remak recommends galvanization of the fibres of the sympathetic nerve. 

2 Lockhart Clark hints that blistering and other forms of counter-irritation to the spine, late in the dis~ 
erne, deserve further trial. 

67 




Fig. 212. 
Cerebro-Spinal Sclerosis. 
Nodules of sclerotic tisme on the surface of the cord. 

A. Dura mater divided. 

B. Pia mater showing sclerotic patches. 

C. Pia mater reflected. 

D. Sclerotic nodules on the cord. 



1058 



DISEASES OF THE NERVOUS SYSTEM. 



inated sclerosis. Near the periphery the nerve tubes are surrounded by 
connective-tissue fibrillar running parallel with the inclosed nerves, and 
there is commencing hyperplasia of the neuroglia, proliferation advancing 
more or less rapidly according to the age of the nodule. The walls of the 
vessels are thickened and infiltrated with numerous fat and lymphoid cells, 
but their lumen is notably diminished. 1 The nerve cells in the gray cor- 
nua are either primarily or secondarily involved and undergo cloudy swell- 
ing, followed by pigmentation or granulo-fatty degeneration, — the yellow 
degeneration. 

Thus it appears that sclerosis is a primary, and multilocular chronic in- 
terstitial myelitis or encephalitis a secondary condition. 

Etiology. — The recognized exciting causes of multiple cerebro-spinal 
sclerosis are damp and cold, sudden chilling of the body, traumatism, and 
severe, long-continued brain work or physical exercise. Continued jar- 
ring of the body is also thought to produce the disease, and it is said to oc- 
cur in nervous people, with hysteria and after acute febrile diseases. It is 
essentially a disease of early life, few cases occurring outside the limits of 
fifteen and thirty-five. Heredity is said to play an important part in its 
etiology. Quite recently cases are reported as occurring in very young chil- 
dren. 

Symptoms. — Charcot makes three varieties of this disease, according as it 
is confined to the brain, or cord, or involves both. The latter is the more 
common ; it may come on insidiously or be sudden in its development. If it 
is insidious in its advent the patient complains vaguely of headache, ver- 
tigo, muscular weakness, mental disturbances, and queer feelings as for- 
mications, itchings, burnings, etc., in the limbs. The symptoms which 
are referable to the sympathetic system are nausea, vomiting, and cardial- 
gia. The patient notices very soon a loss of co-ordinating power ; he can- 
not control his hands in writing or his feet and limbs in walking. There 
is also impairment of the special senses. If the spinal element is promi- 
nent, there is more or less paresis of all the extremities, with contractures 
of the muscles. As soon as an attempt is made to use the paretic limbs, 
they become tremulous and contracted. This tremor is peculiar in not oc- 
curring until an attempt is made at voluntary motions, and at once ceas- 
ing when the parts are allowed to rest. It is called the shaking tremor. 
The more powerful the mental effort the more marked is the tremor. Even 
the head participates in it. 

In some cases the patient becomes childish or morose, and the cerebral 
symptoms in such cases are identical with those of cerebral softening. Dur- 
ing prolonged fits of yawning, sobbing, or laughing the respirations he- 
come stridulous, and in the advanced stages the voice is changed. The 
patient talks in a low monotone or whisper, dividing his words into sylla- 
bles, and emphasizing them as when scanning a line of poetry. If the 
sensory nerves are involved there are pains in the course of the affected 
nerves, and a girdle pain is felt about the abdomen. Amblyopia, nys- 



1 Charcot, Cornil and Ranvier maintain that in the sclerotic islands nerve-elements are always present, 
frommann and Erb hold the reverse. — Ziem. C'ycl., vol. xiii. 



CEREBRO-SPIKAL SCLEROSIS. 



1059 



tagmus, diplopia, and inequality of the pupils evidence invasion of the 
base of the brain and optic tracts. In the advanced stage vesical symp- 
toms, acute bed-sores, and loss of sexual power and control of the sphinc- 
ters become marked symptoms. Sometimes a sudden apoplectiform attack 
followed by paretic symptoms ushers in the disease. The course of the 
disease is peculiar. As its development is by stages, it may gradually 
progress for several years, and then remain stationary for a long period. 

Differential Diagnosis. — Disseminated sclerosis of the brain and cord may 
be mistaken for paralysis agitans, or locomotor ataxia, and when ushered 
in by apoplectiform symptoms may be mistaken for cerebral hemorrhage. 

In paralysis agitans the fine tremor exists when the patient is at rest, 
and is not accompanied by shaking of the head ; while in the shaking of 
disseminated sclerosis the head is always involved, the symptom ceasing as 
soon as the patient is at rest. Paralysis agitans is rare before forty ; mul- 
tiple sclerosis is rare after thirty-five. Changes in the voice and speech and 
ocular symptoms are present in disseminated sclerosis and absent in paraly- 
sis agitans. 

In locomotor ataxia the peculiar tremor, impairment of voice and speech, 
and nystagmus that belong to disseminated sclerosis are absent. In the 
former disease we notice the peculiar iron-band sensation, vesical symptoms, 
the Meniere's vertigo, the very slow and late appearance of paretic symp- 
toms, the lightning-like and agonizing neuralgic pains, and the peculiar 
double beat in walking, the heel being put down first, all of which are in 
marked contrast to the symptoms of multiple cerebro-spinal sclerosis. 

When disseminated multiple sclerosis is ushered in by loss of conscious- 
ness which rapidly deepens into coma, with marked hemiplegic symptoms, 
it may be mistaken for cerebral hemorrhage ; but in sclerosis the tempera- 
ture is very high during these peculiar attacks — 104° or 105° F. — the hemi- 
plegia passes off as the patient returns to consciousness or in a few days 
after, and the temperature rapidly falls to normal. 

Prognosis. — This disease is usually of long duration, five to ten years be- 
ing its average. It is rare for death to occur in coma. There is no well- 
authenticated instance where recovery has occurred. During the stage of 
its development and greatest activity deceptive remissions occur ; but after 
six or seven years emaciation sets in, a marasmus is developed, and the pa- 
tient is apt to die from intercurrent disease. 

Treatment. — The best method of treatment yet proposed is the restora- 
tive ; the object is to improve nutrition. Among the drugs that have been 
used, especially by Charcot and his followers, are chloride of gold, phos- 
phate of zinc, nitrate of silver, chloride of barium, potassium iodide and 
bromide, arsenic, belladonna, calabar bean, and ergot. The galvanic cur- 
rent is the best means of administering electricity. Opinion is divided as 
to the benefit obtained from hot or cold baths and thermal springs, or in- 
unctions and massage. Pain not infrequently becomes so severe as to de- 
mand hypodermic injections of morphine. 1 



1 Leyden reports a case of almost complete cure from galvanism and the baths of Rehme.— Beit. z. acute 
u. chron. Myelitis. Zeitsch.fiir Tclin. Med. Berlin, 1879, L, p. 126. 



1060 



DISEASES OF THE NERVOUS SYSTEM. 



LOCOMOTOR ATAXIA. 

Locomotor ataxia 1 is one of the most frequent diseases of the spinal 
cord. 

Morbid Anatomy. — Its principal pathological lesion is an increase in the 




posterior. 
Pig. 213. 



Diagram illustrating the Regions of Degenerative Changes in the Spinal Cord. 

A. Pyramidal tracts. 

B. Anterior columns. 

C. Haddon and Sower's lateral sensory tract. 

D. Mixed zone of lateral columns. 

E. Processus reticularis. 

F. Crossed pyramidal tracts. 

G. Direct cerebellar tracts. 

H. Postero-external columns. 

I. Postero-internal columns. Columns of Goll. After Flechsig. 

interstitial connective-tissue of the spinal cord. As the cord is removed 
from the spinal canal there will be noticed a grayish discoloration on both 
sides of the posterior median fissure. The pia and dura mater will be 
more or less firmly adherent to each other ; and the dura mater may be 
thickened, pigmented, opaque and studded with osseous plaques ; the pia 
mater may be congested and there may be an exudation into its meshes. 
The posterior aspect of the cord may appear atrophied, and have a firm, 
hard feel. In advanced cases the whole cord is smaller than normal. 

A cross section will show an increase in the cephalo-rachidian fluid, and 
the posterior columns will be shrunken, gray, cartilaginous and shining in 
appearance. Not infrequently the sclerosis will extend to the lateral 
columns and forward to the margin of the anterior columns. These 
changes usually begin in the lateral part of the posterior column in the 

i Duchenne was the first to give an accurate description of this disease. Trousseau and others have 
called it Duchenne's Disease. It is also known as posterior spinal sclerosis, tabes dorsalis, gray degeneration 
of the posterior columns and leuko-myelitis posterior chronica. It is often called progressive locomotor 
ataxia. 



LOCOMOTOR ATAXIA. 



1061 



upper lumbar and lower dorsal regions, and extend upward and down- 
ward. It is possible in long stand- 
ing cases for the medulla and the 
second, third, sixth and eighth cra- 
nial nerves to be involved, and for 
the entire cross section of the cord, 
at various points, to be shrunken, 
hard and gray. 

As a rale, the sclerosis ceases at 
the restiform bodies. 1 If (roll's 
columns are involved it is a second- 
ary degeneration. The posterior 
roots of the spmal nerves show gray 
degeneration and atrophy to the 
naked eye. 2 Ou microscopical ex- 
amination there will be found evi- 
dences of a large amount Of dense Locomotor Ataxia, 
and delicate connective-tissue COn- Section of Spinal Cord in the Cervical Region. 

taming nuclei, granular and amy- aa. Sclerosis of tu columns of GoU. 

loid corpuscles, in which are very 

few atrophied nerve fibres, which have lost their medullary sheaths. 3 
Large branching cells are found throughout the sclerotic tissue. The pos- 
terior columns are seen fused together by connective-tissue in the pia mater, 
which dips down into the fissure. The walls of the capillaries and small 
vessels are thickened and rigid, and their calibre is diminished. Their 
sheaths are filled with oil globules. They are also markedly pigmented. 4 
The sclerosis travels from the cord to the posterior roots of the spmal 
nerves, which show atrophy. The sciatic, crural, and brachial nerves have 
been found sclerosed and atrophied. 5 

Etiology. — Locomotor ataxia is more frequently met with in men than 
in women, the proportion being six to one. It occurs oftenest between 
the ages of twenty and fifty. In a neuropathic predisposition it may be 
induced by anything that seriously depresses the nervous system. Cold 
and wet, bad hygienic surroundings, excessive mental or bodily exertions, 
— onanism, and excesses in venery, especially, — depression of spirits, an 
insufficient or improper diet, the impoverished blood states that occur with 
or follow wasting acute or chronic maladies, prolonged lactation, syphilis, 6 
and, according to some, excessive use of tobacco, — are among its predis- 
posing causes. Blows on the spine, the suppression of menses or old 

1 Charcot describes the external bands :— two bands near the posterior cornua in the outer part of the 
posterior columns. They run parallel •with the posterior horns of gray matter. 

2 Charcot has drawn attention to the condition of the joints in some cases of locomotor ataxia. " Sur 
quelqnes arthropathies," etc. — Archiv. de Physiologie, i., 1868, p. 161. 

3 Cornil and Ranvi^r 'nsist that the axis-cylinder ahvays exists, but that it requires a peculiar mode of 
preparation to demonstrate this. 

4 Lockhart Clark states that he has sometimes found the extremities of the posterior cornua, and even 
the central gray substance, more or less damaged by disintegration. The question has been raised whether 
the initial lesion may not be in these cornua. 

5 Friedreich. — Yirchow's Archiv., T^de 26. 27. 

6 Erb found a syphilitic history in twenty-seven out of forty-four cases. 




1062 



DISEASES OF THE NERVOUS SYSTEM. 



hemorrhoidal fluxes may excite it. It is a question, when it follows pneu- 
monia, rheumatic fever, or diphtheria, if there is any causal relationship 
between them. 1 Its hereditary tendency is shown by its attacking two or 
more members of the same family, other members suffering from some 
other form of nervous disease. This is an example of the " neuropathic 
tendency.'' 2 In a large proportion of cases there is no assignable cause. 

Symptoms. — The symptoms of locomotor ataxia may be divided into three 
periods : a period characterized by disturbances of sensation, a period in 
which there is loss of coordinating power, and a period of paralysis. Dur- 
ing the first period there are sharp, tearing, lightning pains in the lower 
limbs, dysuria, incontinence, spermatorrhoea, nocturnal pollutions, excite- 
ment of, or loss of sexual desire, a sense of weariness in the limbs, and nausea 
and vomiting attended by severe and paroxysmal aching in the stomach. 
A sense of numbness and formication in the limbs is not uncommon in this 
period. There may be a girdle sensation, not only about the waist, but also 
in the limbs — chiefly about the knee and ankle. In some cases there will 
be evidence of arthropathies and symptoms much resembling those of active 
cerebral hypersemia. Eectal and urethral colics, bronchial spasms, and 
nephritic symptoms resembling those of renal colic, are not infrequent. The 
pains during this period are usually in the feet and legs ; but they may 
have their seat in the back, stomach, intestines, or bladder. If they are 
situated in the internal viscera, the functions of those viscera are disturbed. 
Wherever they may be seated, at first they do not come on often, and are 
of short duration ; but as the disease advances, the attacks become more 
frequent and are of longer duration. The muscles of the eyes may be af- 
fected, causing double vision or strabismus, which may last a few days or 
weeks and then disappear ; or changes may occur in other nerves which 
lead to loss of sight. There may be temporary or permanent dilatation of 
one or both pupils. 

The disturbances of surface sensation are manifold ; sometimes the pa- 
tient will complain of a sense of numbness in the hips, sometimes a prick- 
ing sensation, or a sensation of some soft substance between the feet and 
the ground ; one portion of the surface may be anaesthetic, another hyper- 
sesthetic. After a varying period, the ataxic symptoms appear, and the 
muscles are no longer moved in their natural way. The gait becomes un- 
steady, the patient walks like one intoxicated ; there is a sense of heaviness 
in the limbs, and if the feet are brought close together, and the eyes closed, 
the body sways to and fro and sometimes falls. After a time the patient is 
compelled to watch his feet while walking. Later on he throws out his 
feet and legs in the most grotesque manner ; for when the will acts the 
muscles contract far more than the patient intends. If the upper extrem- 
ities are involved, he is unable to dress himself ; he cannot pick up a pin, 
button his garments, or hold anything in his fingers. The movements of 
his hands and arms are forcible, irregular, and jerking. The gait during 

1 The most recent theory of its causation is that of Kahler and Pick, who regard those cases which fol- 
low acute infectious diseases as the result of the accumulation of fungi in the central nervous system, 
producing nutritive disturbances. 

2 Carre records eighteen cases of tabes in the same family in three generations M. Carre, These. 

Paris. 1862. 



LOCOMOTOR ATAXIA. 



1063 



this period is peculiar ; the heel is brought down first, then the toe : there • 
is a double beat to the step. Quiet or steady movements are impossible. 
At times the loss of coordination is so great that for days the patient is 
unable to walk, and then the coordinating power is partially restored. One 
extremity may be involved after the other, or both be attacked at the same 
time. During this period there is a marked loss of sensation, especially in 
the feet and legs ; these patients are often unable to tell when their feet 
touch the floor. Sensitiveness to pain is diminished, and it may be several 
minutes before the prick of a pin is felt. The sensory disturbances of the 
first period are increased, and the sight is more impaired. In this period 
there is loss of the reflex action of the muscles of the lower extremities, 
especially the muscles of the calf of the leg. The abolition of the patellar 
tendon-reflex is one of the diagnostic signs of the disease. It occurs very 
early in the disease, and it is often impossible to say when it first occurred. 
Cessation of reflex mobility of the pupil (Argyll Eobertson) is also an early 
symptom. Loss of the sense of temperature, a greater or less loss in electro- 
muscular contractility, and, in the irritative forms, increase in galvanic excit- 
ability, are not uncommon. During this period there may be developed a 
peculiar affection of the joints ; the joints most frequently affected are the 
knee, hip, shoulder, and elbow. The joint rapidly swells, and the synovial sac 
fills with fluid ; after a time disorganization of the articular surfaces takes 
place and may be followed by destruction of the ends of the bones. In some 
instances the swelling suddenly disappears and the joint is not disabled. 1 
Degenerative changes in the anterior horns are thought to be the cause of 
these joint symptoms. In a few cases skin eruptions of various kinds make 
their appearance. 2 In the last period paralysis occurs, and then are devel- 
oped muscular atrophy, bed-sores, and those vesical and renal symptoms that 
are so apt to lead to death. 

Nearly all the symptoms of locomotor ataxia appear intermittently, and 
the progress of the disease is rarely continuous. During the third period 
there is always complete impotence. In some cases the face has a pale 
yellow color, which is most marked during cold weather. 3 During this 
last period sensation about the rectum is lost ; hence the patient is apt to 
become exceedingly filthy unless great care is exercised. This condition is 
accompanied by almost constant dribbling of the urine. Intelligence, 
memory, and the higher cerebral functions are rarely, if at all, impaired. 
In a few cases of locomotor ataxia the patients become color-blind. Loco- 
motor ataxia is a non-febrile disease, but during the initial period febrile 
symptoms may occur, and are then especially important as indicating a 
rapid progress in the disease. 4 The former is neither an early nor a late 
symptom. Pierret says that all possible nervous disturbances of hearing 
may precede ataxia. After reaching the second period, the disease may for 

1 Blum states that the great friability of the bone? that results in spontaneous fracture is due to rarefy- 
ing ostitis.— Des. Arth. (Fori. nerv. Thhe. Paris, 1875. 

2 Charcot says that they follow the track of nerves that have been the seat of pain. 

3 Eulenberg attributes dicrotism of the pulse in ataxics to loss of vascular tone of spinal origin.— Ber* 
lin. Klin. Wochen. 

4 Among the most recent contributions to this disease is Erb's paper, wherein he ascribes great im- 
portance as a symptom to spinal myosis, i. e., reflex immobility of the pupil. 



10C.4 



DISEASES OF THE NEKYOUS SYSTEM. 



a long time remain stationary, or it may temporarily improve, but com- 
plete recovery is rarely, if ever, reached. In the long and slowly progres- 
sive cases fluctuations always occur, with improvement in summer and 
exacerbations in winter. 

Differential Diagnosis. — Locomotor ataxia may be confounded with para- 
plegia, multiple cerebrospinal sclerosis, cerebellar lesions, chronic myelitis, 
hysterical ataxia, and chronic spinal meningitis. 

Paraplegia is a true paralysis ; ataxia is not, and it is readily proved that 
in the latter disease muscular force is not diminished. In paraplegia the 
limbs are not thrown about in walking,— they are merely dragged. In 
paraplegia there is little or no resistance to artificial movement, while in 
ataxia there is great resistance in bending the limbs against the will of the 
patient. The nutrition of the muscles is markedly impaired in paraplegia, 
and normal in ataxia. Neuralgic pains are absent in paraplegia and present 
in ataxia. Strabismus, ptosis, etc., are present in ataxia and absent in 
paraplegia. 

The differential diagnosis between multiple sclerosis and ataxia has been 
given. 

Cerebellar disease has for its characteristic symptom vertigo ; this is rare 
in ataxia. A patient with cerebellar disease can stand and walk better with 
his eyes shut than open, has unimpaired cutaneous sensibility, and the* 
movements, while uncertain, are not so abrupt, vehement, and jerky as in 
ataxia ; they resemble rather the stupid movements of a drunken man. 
The absence of neuralgic pains, of vesical and sexual weakness, and the 
prominence of headache, vomiting, and convulsions in cerebellar disease 
will be sufficient for the diagnosis. 

In chronic myelitis there are no disorders of coordination. The patient 
suffers paresis, or even complete paralysis of the lower extremities, while 
in ataxia there is no paralysis, muscular power being undiminished. The 
limbs are dragged simply in chronic myelitis ; they are thrown forcibly 
about in ataxia. Ocular symptoms are absent in chronic myelitis, present 
in ataxia. Contractures, spasms, paralysis of the bladder, cystitis, and the 
early formation of bed-sores, together with the absence of intense neuralgic 
pains, will also serve to distinguish chronic myelitis from ataxia. 

In hysterical ataxia the history, and the occurrence of the disease in a 
female, with the subsequent course of the disease, will enable one to dis- 
tinguish it from ataxia. 

In meningitis there is pain, — increased on pressure, — slight paralysis but 
no incoordination, no flinging of the limbs in walking or moving, no aboli- 
tion of tendon reflexes, and no ocular symptoms such as are present in 
ataxia. 

Prognosis. — The usual course of locomotor ataxia is progressive. 

The prognosis as to its duration is uncertain. The disease sometimes 
ceases of itself, leaving the patient in a disabled condition, but still giving 
him years of life. The slower the development the longer the duration. 
The prognosis is more unfavorable when it occurs with a history of nervous 
disease in the family, when the early symptoms are serious and constant, 



SPASMODIC TABES DORSALIS. 



1065 



and when constitutional symptoms (especially emaciation) become marked. 
Complications likewise render the prognosis unfavorable. Complete re- 
covery is possible but not probable. The duration of the disease varies 
from six months to as many years. 

Treatment. — The efficacy of treatment depends upon the stage at which it 
is commenced. Undoubtedly, if the disease can be early recognized, its 
advance can in many cases be checked. 

Of the drugs recommended, nitrate of silver is perhaps the one most ex- 
tensively used. It should be given cautiously ; about one grain a day in 
divided doses. The galvanic current is nearly always of service. Some 
cases will be benefited by the iodides, others by the bromides. Strychnia, 
phosphorus, arsenic, the chlorides of gold, sodium, and barium, the phos- 
phide of zinc, belladonna and ergot all have been recommended. 1 The 
diet and mode of life should be such as to conduce to the highest degree of 
health and nutrition. Cod-liver oil and phosphorus may be given as ad- 
juvants to a nutritious diet. 

The patient should remain at rest as much as possible. Under no cir- 
cumstances should he be allowed to expose himself to cold or w T et or to sud- 
den changes in temperature. Flannel should be constantly worn next the 
skin. Simple thermal baths seem to do harm, but saline thermal baths 
sometimes give good results. Sulphur, chalybeate and mud baths have 
been recommended. Erb recommends, as better than all, the cold water 
cure. He advocates the wet pack for the neuralgic pains. Bleeding or 
depletion of any sort is contraindicated, even in the initial stages. For the 
gastric derangement bismuth will generally be found efficacious. Consti- 
pation must be overcome by mild cathartics. For the vesical weakness or 
for incontinence, Faradization of the bladder, bromide of potash, camphor, 
and lupulin are advocated. In order to preserve the nerve force and pre- 
vent exhaustion, crutches are very useful, as they prevent the muscles from 
being constantly overtaxed. 

SPASMODIC TABES DORSALIS. 

Under this name Charcot has described what Erb calls spastic spinal 
paralysis. It has also been called tetanoid pseudo-paraplegia. 

Morbid Anatomy. — As far as can be stated there is symmetrical sclerosis 
of the lateral columns, chiefly of their posterior portions. The induration 
shades off imperceptibly into the normal tissue of the columns. 

This degeneration does not differ microscopically from that seen in scle- 
rosis of the cord ; it often extends in varying degrees the entire length of 
the cord. Anterior polio-myelitis and posterior sclerosis are frequently 
associated. 

Etiology. — Spasmodic spinal paralysis is more common in males than in 
females, and is rare except between the ages of twenty and fifty ; it rarely 



1 Lockhart Clark recommend* morphine, cannabis indica and belladonna with, silver nitrate when the lat 
ter irritates the bowels or bladder. 



1066 



DISEASES OF THE NERVOUS SYSTEM. 



occurs in children. Traumatism and exposure to wet and cold are named 
as its causes. 

Beyond this its etiology is obscure. 

Symptoms. — Beginning very insidiously, the first symptoms noticed are 
weakness and paresis of the lower — rarely of the upper — extremities. 
These patients drag their limbs. This is followed by twitchings and stiff- 
ness of the muscles, and later there is so much muscular rigidity that loco- 
motion is embarrassed or rendered impossible. Exaggeration of the tendon- 
reflexes is an early and important symptom, and is associated with marked 
ankle-clonus, in which the muscles of the calf or the whole limb are put in 
a state of tremor when the foot is flexed, or when the patient puts his toes 
to the ground. As the muscular rigidity increases these signs diminish. 
Later, general muscular tremors or shiverings unaccompanied by tempera- 
ture changes may occur, in which all the muscles partake. They may be 
excited by cold or follow excitation of ankle-clonus when they do not occur 
spontaneously. If the patient is able to walk, he has the typical spastic 
gait ; the adductors keep the thighs close together, the toes are dragged, 
and as the heel is brought down the extensors of the foot contract spas- 
modically and may throw the patient forward, lifting him on his toes. 
Sensibility and skin-reflexes remain normal. 

Electric reaction of the muscles is unchanged ; while that of the nerves 
is lowered to both currents. In the advanced stage of the disease the 
muscles of the abdomen, back, or upper limbs may become involved. In 
the latter case the fingers and hand are strongly flexed ; the forearm is pro- 
nated and semiflexed, and the arm is fixed to the side. After a varying 
period paralysis of the affected parts occurs, and the contractures become 
more marked ; the legs are permanently extended, and the foot assumes 
an equino-varus position. Pain rarely accompanies the contractures, 1 and 
the nutrition of the affected muscles is not impaired. 2 

Differential Diagnosis. — Spastic paralysis may be confounded with tabes 
dorsalis, chronic anterior polio-myelitis, multiple sclerosis, peripheral paral- 
ysis, and transverse myelitis. 

In locomotor ataxia the ataxic symptoms, the double beat and stamp 
of the walk, the absence of tendon-reflexes, the general pains, the bladder 
symptoms, and the absence of paralysis and contractures are in direct con- 
trast to the symptoms of primary lateral sclerosis. 

In chronic anterior polio-myelitis atrophy follows the paresis and the 
muscles lose electric excitability. Tendon-reflexes are absent. In spastic 
paralysis rigidity follows paresis, and tendon-reflex and electric excitability 
are exaggerated. 

Multiple sclerosis, when it is located in the lateral column at the onset, 
is practically spastic tabes. When the sclerotic process attacks other 
portions of the cord, or when cerebral disturbances occur, it assumes its 
distinctive characteristics. 

J Erb states that pain in the back and limbs attended by formication and other paresthesia not un- 
commonly precedes the motor weakness at the beginning of the disease.— Virchoiv's Archiv., b. 70. 1877. 

2 Recently, Stumpell calls attention to the relaxation of the muscles which occurs in spastic paralysis 
when the legs are not irritated by their own weight. 



AMYOTROPHIC LATERAL SCLEROSIS. 



106? 



In peripheral paralysis there are disturbances of sensation and nu- 
trition ; the disease develops unsymmetrically, and reflex excitability and 
electro-muscular contractility are rapidly lost. 

In tranverse myelitis trophic disturbances, vesical derangements, and 
alterations in sensation are early and marked symptoms. They do not oc- 
cur in spastic paralysis. 

Prognosis. — In uncomplicated spastic paralysis the prognosis is good. 
Some claim that complete recovery is possible, and in most instances the 
symptoms can be ameliorated. The disease may progress slowly for years, 
and then remain stationary indefinitely ; or it may become complicated by 
bulbar or glosso-labio-laryngeal paralysis, and prove rapidly fatal. 

Treatment. — In addition to the treatment proposed for chronic myelitis the 
galvanic current is most useful. Iodide of potash, arsenic and cod-liver oil 
in small doses, with careful attention to rest and diet, are to be recommended. 
Shampooing, rubbing and massage afford great comfort, and calabar beaa 
may be given for the cramps. Nerve stretching has also been employed. 

AMYOTROPHIC LATERAL SCLEROSIS. 

(Spastic Paralysis.) 

Charcot calls this disease the deuteropathic form of progressive muscular 
atrophy. Pathologically and clinically it is a complex of progressive mus- 
cular atrophy and spasmodic spinal paralysis. 

Morbid Anatomy. — The sclerotic process begins in the cervical region, 
and although at first it is limited to the lateral columns, it soon attacks the 
anterior cornua and leads to destruction and atrophy of the large ganglion 
cells. It also extends downwards into the dorsal and lumbar lateral columns, 
and almost invariably upwards so as to involve the medulla, when the sigas 
of bulbar paralysis are induced and followed by a fatal issue. This process 
has its seat in the same portions of the cord as the secondary descending 
degeneration of Ttirck, and new bands of dense connective-tissue join the 
degenerated lateral columns with those portions of the anterior horns that 
are involved. 1 In the floor of the fourth ventricle the cells of the nucleus 
of the spinal-accessory, facial, and hypoglossal nerves are degenerated. The 
anterior roots and peripheral nerves are atrophied. Trophic changes in the 
muscles are identical with those of progressive muscular atrophy. 2 

It is stated that interstitial growth of neuroglia is sometimes found with- 
out marked degeneration or atrophy of the nerve fibres, but that the whole 
system of fibres and ganglion cells which unite the motor centres in the 
cortex with the muscles is involved. 3 

Etiology. — Nothing more can be said regarding its etiology than has al- 
ready been stated concerning the origin of the two diseases of which it is 
a compound. 

1 Archir. de Phys. Nor. et Path. 1879. 

2 Rosenthal stntes that their inflammatory character is more marked in amyotrophic lateral sclerosis, 
and thar hyperplasia of the perimysinm is more pronounced. 

3 Flichsig and Pick state that the whole system of nerve fibres and ganglion cells which unite the motor 
centres in tiie centres of the brain with the muscles are affected in amyotrophic lateral sclerosis. 



1068 



DISEASES OF THE NERVOUS SYSTEM. 



Symptoms. — The disease begins with weakness, paresis, and then actual 
paralysis in the upper extremities, associated with muscular atrophy, which 
is usually diffuse and rapidly progressive. Fibrillary spasms and twitch- 
ings of the affected muscles are well marked ; but electrical contractility 
is preserved. Sensibility is not impaired, but the muscles become rigid 
and contracted with the arms flexed. 1 In a few months the lower limbs are 
involved in the paralysis and rigidity, with exaggerated tendon-reflexes and 
contractures. Subsequently the muscles atrophy and show the reaction 
of degeneration and fibrillary spasm, while the contractures diminish. 
This is followed by the symptoms of bulbar paralysis. 

Differential Diagnosis. — Amyotrophic lateral sclerosis may be mistaken for 
progressive muscular atrophy. Bat in the latter disease the slow course, 
absence of bulbar paralysis, and partial affection of certain groups of 
muscles, are in marked contrast to the symptoms of the former. More- 
over, in amyotrophic lateral sclerosis the atrophy is preceded by paralysis. 

Prognosis. — The prognosis is decidedly unfavorable ; death results in from 
one to three years from bulbar paralysis. It is not, however, preceded by 
paralyzed sphincters, vesical troubles, bed-sores, or other trophic lesions. 

Treatment. — Eesidence in the open air at a high altitude and strict at- 
tention to the general health are of first importance. Beyond this the 
treatment is identical with that of other forms of spinal sclerosis. 

Mitchell recommends cod-liver oil, iron, strychnia, and dry cupping 
along the spine, with massage. 

PSEUDOHYPERTROPHIC PARALYSIS. 

This is a progressive muscular paralysis occurring chiefly in boys. 

Morbid Anatomy. — The German pathologists generally regard this dis- 
ease as a chronic myositis with hyperplasia of interstitial connective-tissue. 
Gowers, however, in a recent monograph, describes the substance with 
which the muscle is filled and its fibres replaced as a new growth. Fat 
accumulates in the new growth to such an extent as to induce atrophy, and 
the muscles undergo granular and fatty metamorphosis. 

As a final stage Charcot mentions waxy degeneration of the muscular 
elements. If a portion of the affected muscle is examined it will be 
found of a pale red or yellow color, according to the date of the disease. 2 
No lesions of the spinal cord have been demonstrated in this disease, 
although it is always described with diseases of the cord. 

Etiology. — Age and sex are the most constant predisposing causes, over 
eighty-eight per cent, of the recorded cases occurring before the tenth 
year. Hereditary influence appears most powerfully on the mother's side. 
The neuropathic tendency is more marked than in any other nervous dis- 
ease. The recognized exciting causes are cold, falls, and convalescence 
from acute febrile disorders. 

1 Erb states that as atrophy of the muscles progresses they may undergo simultaneous lipomatous 
hypertrophy. 

2 Charcot, Cohnheim and Eulenberg found no changes in the cord. Others have found spots of sclerosig 
and atrophy of the ganglion cells in the anterior horns. Lockhart Clark and Gowers have discovered ex- 
tensive disintegration of the gray matter at the centre of each lateral half of the cord and of the anterior 
commissui-e. 



PSEUDOHYPERTROPHIC PARALYSIS. 



1069 



Symptoms. — M. Duchenne makes three stages : first, a stage of weakness 
without increase in the size of the muscles ; the muscles chiefly affected are 
those of the legs, especially the gastrocnemii, lower part of the back, and 
the erectores spinae. Second, a stage in which hypertrophy appears and 
weakness extends to the upper extremities. During this stage for a year 
or more the child may evince no symptoms beyond a progressive weakness. 
He is easily and quickly tired, raises himself with increasing difficulty, and 
when erect does not stand firmly. He soon begins to show a peculiarity of 
gait and attitude. He walks with a swaying, unsteady step, and as he 
stands the shoulders are thrown backward and the spine is sharply bent in 
the lumbar region. The hyperplastic and degenerative changes in this stage 
produce the pseudo-hypertrophy of the muscles, which become firm and 
hard with increased loss of function. When the child is placed in an 
erect position the increase in size becomes very marked. In the supine 
position the soles of the feet are approximated and the joints of the lower 
extremities are flexed. Similar hypertrophy sometimes affects the muscles 
of the upper half of the body ; but more commonly they are wasted, and 
thus the protuberant belly and the thick, firm calf and thigh afford a strik- 
ing contrast to the emaciated muscles above the diaphragm. The children 
walk only with the greatest difficulty, or possibly they cannot stand without 
support, and the act of sitting or rising becomes difficult. Sometimes it is 
impossible for them to maintain even a sitting posture. The anteropos- 
terior curvature of the spine and the displacement of the shoulders are much 
exaggerated, and the toes often undergo a claw-like deformity. 

Gradually some muscles become soft and fatty while others remain firm 
and hard, and the child passes into a stage of complete paralysis of the 
trunk and upper extremities in which all the muscles that were hypertro- 
phied atrophy, and the patient becomes completely helpless. Formication 
is not uncommon at first, but neither anaesthesia nor hyperesthesia is pres- 
ent at any time. Electro-contractility of the muscles is unimpaired until 
the advanced stages of the disease. The upper extremities seldom surfer 
pseudo-hypertrophy, but may exhibit true progressive muscular atrophy. 
The deltoid and triceps are usually the only muscles enlarged. In nearly 
all cases the disease progresses symmetrically. The skin of the affected 
parts is sometimes bluish, dry, and thinned. The tongue and the muscles 
of the face may become enlarged, and some consider the cardiac hyper- 
trophy that is often present as of similar origin. 

In a number of cases the mental faculties have been impaired, but the 
general health is usually good, and the sphincters are never involved. 

Prognosis. — The prognosis is unfavorable, and when progressive muscular 
atrophy is superadded it is especially so. Cases of recovery have been re- 
ported. Its duration varies from a few months to several years. Intercur- 
rent disease is generally the direct cause of death. 

Treatment. — Duchenne's treatment is regarded as the most efficient. Lo- 
cal electricity, shampooing, and massage, if employed before the hyper- 
trophic changes occur, may arrest its development. 



1070 DISEASES OF THE NERVOUS SYSTEM. 



ACUTE ASCENDING PARALYSIS. 

This peculiar disease has no well-recognized anatomical lesions, but is 
regarded by most observers as a purely functional disease. 1 Many authori- 
ties have recently regarded it as an acute infectious disease, iu which the 
infectious element causes functional rather than organic changes, and may, 
in different cases, affect different parts of the nervous system. Some cases 
closely resemble forms of peripheral neuritis. 

Etiology. — Acute ascending paralysis is a disease of adult life, more com- 
mon in men than in women. Exposure to cold, emotional influences, 
venereal excesses, syphilis, acute febrile disease, and poisoning from corro- 
sive sublimate 2 have each been followed by it. 

Symptoms. — For the first few days there is possibly a slight fever, accom- 
panied by a sense of weariness and numbness and darting pains in the 
limbs, chiefly in the feet and in the tips of the fingers. This is followed by 
paresis, then actual paralysis of the distal portions of the lower extremities. 
The paralysis gradually extends upward, until in a few days paralysis of 
the lower extremities is complete. Soon the trunk muscles are implica- 
ted ; the patient can neither turn nor sit up in bed. The upper extrem- 
ities are then involved, the paralysis extending from the finger tips to the 
shoulder joint. Sometimes there is a distinct interval between the paraly- 
sis of the trunk and the upper extremities. In about seventy per cent, of 
cases the muscles of the neck and the diaphragm are involved, and finally 
bulbar paralysis is superadded. 

In some cases the disease pursues a reverse course, palsy of the extremities 
following the symptoms of bulbar paralysis. The paralyzed limbs are lax 
and the muscles flaccid ; but they do not undergo atrophy, and the electri- 
cal reactions of nerves and muscles continue perfectly normal. Sensibility 
is little if at all affected, the sphincters are not involved, cutaneous nu- 
trition is unimpaired, and there are few, if any, vaso-motor or trophic dis- 
turbances. Keflex action diminishes after the first two or three days. There 
is usually constipation and difficult defecation, on account of the paralysis 
of the abdominal muscles. The intellect is never disturbed. In over thirty 
per cent, of the cases, when, or before, the arms are implicated, the disease 
is arrested, and soon recovery of power begins to manifest itself, the parts 
first paralyzed being last restored. It is said that recovery has taken place 
even after the paralysis has reached the nerves of the bulb. As a rule there 
are no pains complained of in the paralyzed parts. 

Differental Diagnosis. — Acute ascending paralysis may be confounded with 
acute myelitis, acute spinal paralysis of adults, and, when slowly evolved, 
with chronic spinal paralysis. 

Acute ascending paralysis is differentiated from acute ascending mye- 
litis by the slight disturbances of sensation which attend it, by the preser- 

1 Dejerine claims to have found in two cases an alteration in certain fibres of the anterior roots (parenchy- 
matous neuritis';. The myeline was broken up into fragments. Multiplication of the nuclei in the white 
substance of Schwann, and disappearance of the axis-cylinders were noted. The majority of the fibres 
were unaltered. The same lesions were found in the intramuscular nerves of the affected members. 

2 Ketly in the Pester Med. Chir. Pres. Nos. 8-9. 1878. 



SPINAL APOPLEXY. 



1071 



yation of electrical excitability, and by the absence of motor irritation and 
trophic disturbances. 

Acute ascending paralysis differs from acute spinal paralysis of adults 
in the absence of atrophy of the paralyzed muscles ; the electrical reactions 
remain normal, and it is more rapidly progressive. The medulla is not 
involved in acute spinal paralysis, whereas about seventy per cent, of cases 
of ascending paralysis end in bulbar symptoms. 

Rapid atrophy of the muscles and the reaction of degeneration are promi- 
nent symptoms of chronic spinal paralysis, which are absent in acute ascend- 
ing paralysis. In the latter disease there is a far greater tendency to extend 
to the medulla. 

Prognosis. — Acute ascending paralysis is generally fatal. It may last 
several weeks ; but its average duration is from ten to fifteen days. The 
more rapid its progress, and the earlier the medulla is involved, the more 
unfavorable the prognosis. Improvement may take place even in the most 
acute cases. Death occurs from the same causes as in bulbar paralysis. 

Treatment. — All that can be done in this disease is to maintain the 
nutrition. Electrical currents may be applied to the affected muscles. 
Sulphur baths, iron, arsenic, strychnine, and iodide of potash are recom- 
mended for the more slowly progressive forms, but clinical experience 
does not sustain the claim of beneficial results which have been obtained 
by their use. 

SPINAL APOPLEXY. 



Spinal apoplexy is not of frequent occurrence, except when due to trau- 
matism or to some pre-existing disease of the cord. 

Morbid Anatomy. — A meningeal hemorrhage may extend the entire 
length of the cord ; primary 
hemorrhage, however, usually 
occurs into the gray matter, 
and if slight, may only involve 
one side. The white matter 
is never alone involved, but 
about fifty per cent, of spinal 
hemorrhages are circumscribed. 
In a few cases punctate capil- 
lary hemorrhages are found 
studding the gray substance. 
A clot of varying size, one- 
fourth to one inch in diameter, 
is found in the central portion 
of the cord containing debris of 
nerve-tissue, corpora amylacea, 
fat granules, and pigment. This 
blood sac commonly lies with 
its long axis parallel with the 

cord. The centre may have undergone softening, and the wall 
of ragged nerve-tissue. 




Fie. 215. 
Spinal Apoplexy. 

Section of the Cervical Spinal Cord, showing a small clot in 
the region of the anterior cornu of the left side. 

A. CM. . _ 

B. Meninges adjacent to the clot shoivzng hyperazmia. 

is formed 

About a clot in the white substance, the tissue is 



1072 



DISEASES OE THE NEKVOUS SYSTEM. 



always more or less deeply tinged with blood. When the extravasation 
involves the periphery of the cord there will be hyperemia of the adjacent 
membranes. Capillary aneurisms have usually been found in the spinal 
vessels at the seat of the apoplexy ; and Liouville has found ampullary dila- 
tation of the large vessels, thickening of their walls, and proliferation of 
their nuclei. Charcot states that there is swelling of the nerve cells and 
axis cylinders. The clot may undergo retrogressive changes and result in 
softening, abscess, or a cicatrix. Erb describes softening of the gray sub- 
stance as a not infrequent sequela of spinal apoplexy. White softening 
accompanied by gelatinous oedema surrounds the blood tumor and merges 
imperceptibly into healthy cord substance. Ch. Bastian states that inflam- 
matory softening may start from the clot and extend up or down the 
cord. 1 

Etiology. — Spinal hemorrhage is most commonly the result of trauma- 
tism, and especially of severe concussion. 2 It may result from rupture of 
vessels in or near neoplasia, in foci of myelitic or other softening, or in 
any chronic spinal disease. Small hemorrhages may occur with scorbutus, 
purpura, and in the hemorrhagic diathesis. Atheromatous, fibroid, and 
fatty degeneration of the blood-vessels, nuclear proliferation, and minute 
aneurism al dilatations predispose to spinal hemorrhage. Age and sex are 
also predisposing factors, as it is most frequently met with in men between 
the ages of fifteen and forty. Anything that induces or predisposes to ac- 
tive hyperemia acts as a predisposing causa. 3 

Symptoms. — Sometimes the symptoms of myelitis, spinal irritation, or 
active spinal hyperemia precede the extravasation, but usually it comes on 
suddenly and causes complete paralysis of both motion and sensation be- 
low the site of the hemorrhage, without loss of consciousness. It is at- 
tended by severe pain in the back, that may be localized or extend the 
entire length of the spine. This sometimes disappears when the paralysis 
becomes complete. Pressure does not increase it. At the onset spasmodic 
twitchings may occur in the paralyzed parts ; and all reflex motion is 
abolished — the muscles being completely relaxed. Priapism and dyspnoea 
may occur when the clot is high up. When hemorrhage occurs in the 
dorsal or lower cervical region, the temperature of the paralyzed limb 
— which at first is sub-normal — rises 2° to 3° F. higher than the axillary 
as a result of vaso-motor paralysis. The bladder is at first paralyzed, but 
when the sphincters are also involved the urine passes involuntarily. Cys- 
titis is soon developed and pyelitis rapidly follows. The faeces are passed 
involuntarily and bed-sores appear early. The paralyzed parts begin to 
undergo atrophy, and while so doing exhibit the electrical reaction of 
degeneration. If a clot occupies one-half the gray matter at any point, 
hemi-paraplegia is developed in the limb of the same side as the lesion. 
Should it implicate the root of the phrenic nerve, intense dyspnoea and per- 
haps instantaneous death may result. 

1 Charcot and Hayem regard this lesion as always consecutive to myelitis. 

2 Sir William Gull relates a case where small extravasations were found on the anterior and posterior 
cornua as well as in the posterior columns of the cord. The case was the result of a fall. 

8 Erb claims that variola hemorrhagica, typhoid, yellow, and malarial fevers are causes of spinal hemor- 
rhage. 



TUMORS OF THE SPINAL CORD. 



1073 



Differential Diagnosis. — Apoplexy of the cord may be confounded with 
meningeal apoplexy and thrombotic softening. In meningeal apoplexy sen- 
sory paralysis is absent or but slightly marked ; after the initial motor 
paralysis, improvement is marked and speedy ; pain, hyperesthesia, and 
irritation symptoms are prominent ; and bed-sores, cystitis, and pyelitis 
do not occur. All these are in distinct contrast with the symptoms of 
spinal or intramedullary apoplexy, Vaso-motor disturbances are absent 
in meningeal, but present in spinal hemorrhages. 

Thrombotic softening produces incomplete paraplegia, without loss of 
sensation. The absence of sensory and motor excitement is regarded as 
diagnostic. Hemorrhage not infrequently occurs in a spot of myelitic soft- 
ening, but in such cases the paraplegia follows irritation, pain on pressure, 
fever, vesical symptoms, and the girdle sensation. In apoplexy paraplegia 
is the first symptom, the other symptoms coming on at greater or less in- 
tervals. 

Prognosis. — Charcot states that a true spinal apoplexy is always fatal. 
The prognosis is certainly exceedingly unfavorable when the onset is severe 
or when the thoracic and respiratory muscles are implicated. Death 
may occur in six hours. Incomplete recovery is possible, with paralysis 
and atrophy of the muscles of the lower extremities. Septic fever, cystitis, 
and pyelitis are its complications ; and death may occur from exhaustion 
and marasmus. The chief danger, if life is prolonged a few weeks, is from 
myelitis and extensive softening. 

Treatment. — Absolute rest in the prone (not supine) position, is most im- 
portant. Blood-letting, purgatives, or revulsives are not allowable. Ice-bags 
should be applied along the spine. Bromides and opiates may be employed 
to insure rest. Attention to the bladder is an important element of treat- 
ment. The treatment is the same as for cerebral apoplexy with, transfer- 
ence of local measures from the head to the spine. 

TUMORS OF THE SPINAL CORD. 

As tumors in the spinal canal arise from the same causes and present the 
same anatomical appearances as similar growths in the brain, it is only 
necessary to consider their clinical phenomena. 

Symptoms. — These will vary greatly in their nature and in the order of 
their development, with the seat of the tumor, its extension, and the 
amount of intercurrent changes in the adjacent tissues. 

I. Tumors which primarily involve the substance of the cord are more 
common in the gray matter, and are attended by a gradual abolition of 
function. The changes are due more to pressure than inflammation, so 
that pain is a less common and prominent accompaniment. The earlier 
symptoms are those of paresis, either with hemiplegia or paraplegia of the 
parts below the tumor, according as the growth involves a lateral half or 
the entire substance of the cord. When the lesion is lateral, the paralysis 
may be crossed or mixed ; motor paralysis of one side may be attended 
by anaesthesia of the other. The paralysis is rarely complete at first, but 
is progressive, though liable to remarkable remissions, and eventually be- 

08 



1074 



DISEASES OF THE NEKYOUS SYSTEM. 



comes complete. As these tumors extend and involve the meninges and roots 
of the nerves and are attended by inflammation, peripheral pains and mus- 
cular spasms may develop, while the oedematous softening or ascending and 
descending degenerative changes may cause atrophy and wasting of the 
muscles. Tumors of the substance of the cord may thus resemble muscu- 
lar atrophy, tabes dorsalis, or other forms of sclerosis. 

II. Meningeal growths and tumors* developed exterior to the membranes 
pursue a less latent course. They involve the roots of the nerves early, and 
are productive of more marked inflammatory changes. Hence the early 
symptoms are those of both sensory and motor irritation. There are burn- 
ing, lancinating, and crushing pains, which are irregular and liable to 
severe exacerbations, which may be attended by hyperesthesia and Cuta- 
neous eruptions. There are muscular twitchings and spasms which, as the 
nerves are more seriously affected or the cord becomes compressed, pass on 
to paresis or complete paralysis with muscular atrophy and wasting. The 
sensory symptoms at the same time give place to numbness and anaes- 
thesia. 

Spinal tumors of all forms produce more or less myelitis, and with this 
the reflex excitability is greatly increased and may cause contraction and 
rigidity. 1 Trophic changes are late symptoms. In all forms of spinal 
growths the symptoms are liable to sudden and marked changes either 
favorable or unfavorable. A sudden oedema or hemorrhage may cause ex- 
tensive paralysis, which may be permanent or slowly recovered from. Or 
a rapid and marked improvement may be speedily followed by a more com- 
plete and widespread paralysis. When the new growth involves the verte- 
brae and results in destructive changes, as frequently occurs with cancer, 
the early symptoms of pain and hyperesthesia are usually severe and the 
paralysis rapidly becomes complete. 

Differential Diagnosis. — Inflammation, hemorrhage, and softening of the 
cord are excluded by their abrupt onset, and the fact that their symp- 
toms are more general and uniform in their development than those of a 
tumor. 

The nature of a tumor can seldom be determined, and the diagnosis rests 
almost entirely upon the history and the presence of some adventitious 
growth in other organs. 

Prognosis.— Complete or even partial recovery is not to be expected. The 
paralysis and muscular atrophy are progressive. No estimate of their 
duration can be made. 

Treatment. — Every tumor should be treated as syphilitic, as this is the 
only kind amenable to treatment. When the vertebras are involved, sup- 
porting appliances are indicated. Beyond this the treatment is purely 
symptomatic. 



1 Schiippel claims that the spine is always curved towards the side upon which the tumor is situated, 
and that the combination of irritative aud paralytic symptoms of striking inconstancy is diagnostic of 
tumor. 



SPINA-BIFIDA AND HYDRORACHIS. 



1075 



SPINA-BIFIDA AND HYDRORACHIS. 

Bpina-bifida is a congenital malformation due to arrested development 
of some portion of the spinal column. It is usually associated with dropsy 
of the spinal cord, or hydrorachis. Internal hydrorachis is a collection of 
serum in the central canal, causing atrophy or destruction of the spinal 
medulla. External hydrorachis is an effusion into the subarachnoid space. 
If the spinal canal closes, it is called H. incolumis ; if not, H. dehiscens. 

Morbid Anatomy. — Usually two or three spinous processes and laminae are 
deficient, the rudimentary portions of the vertebral arches are spread out 
and irregularly expanded, and the membranes protrude through the aper- 
ture as a hernial sac. The tumor, which is oval or spherical and at birth 
about one inch in diameter, occurs almost invariably in the lumbar or 
lumbo-sacral region. It is tense and fluctuant, being filled with cerebro- 
spinal fluid. Pressure on the tumor increases the tension, and may produce 
symptoms of cerebral pressure. The skin over the tumor, although some- 
times normal, is usually thin and transparent. The nerve-trunks forming 
the cauda equina often traverse the interior of the sac. The skin at the 
apex of the tumor is sometimes destroyed and the sac exposed. The point 
is excoriated or covered with pus and granulations, and the ulceration may 
go on to perforation. The dura mater always forms one layer of the sac. 

Etiology. — Nothing is known concerning the etiology of the hydrorachis 
which accompanies spina-bifida. 

Symptoms. — The symptoms of hydrorachis are obscure. It may cause 
pressure on various parts of the cord and cause paresis or absolute paralysis 
and wasting of the muscles. When associated with spina-bifida, the tumor 
is the diagnostic symptom. If the effusion is in the central canal and the 
cord is thus implicated, the lower limbs are usually paralyzed as well as the 
bladder and the lower bowel. Convulsions, spinal inflammation, or rupture 
of the sac with escape of its contents, usually precede death, which usually 
occurs within a few weeks after birth. When the fluid oozes away gradu- 
ally, relief follows ; spontaneous and complete cure may then occur, the 
tumor contracting to a small nodule, and the aperture in the canal closing 
more or less completely. When the dropsy is external to the cord and the 
skin thick, the tumor may increase in size without causing serious disturb- 
ance, and may even reach the size of a child's head, and life.be prolonged 
twenty or thirty years. 

Other forms of arrested development often accompany spina-bifida. 

Prognosis. — It is very rare for patients with spina-bifida to reach puberty. 
The majority of cases terminate fatally a few days or weeks after birth. 
The prognosis is favorable when the base of the tumor is narrow, the skin 
over it thick and normal, and when it is situated in the sacral region. 

Treatment. — The process of spontaneous cure has been successfully imi- 
tated by small tappings, frequently repeated, and followed by light com- 
pression. Only a small portion of the fluid should be withdrawn at any 
operation, and the puncture should always be made at the side of the 



1076 



DISEASES OF THE NERVOUS SYSTEM. 



tumor so as to avoid injury to nerye-trunks. Cases have been successfully 
treated by the injection of small quantities of iodine. 

Other operative measures, such as compression of the neck of the tumor 
by means of a clamp or ligature, and excision, have occasionally been em- 
ployed with success ; but no such attempt should be made except when 
the tumor has a very narrow base, and is situated over the sacrum. 



DISEASES OF THE PERIPHERAL NERVES. 

Aside from those conditions which distinctly affect nerve-trunks, some 
others are so prominently manifested through motor and sensory disturb- 
ances, as properly to come under this head. 

I shall here consider — 

I. Peripheral Neuritis. VI. Facial Paralysis. 

II. Localized Spasms and Paraly- VII. Eclampsia and Infantile Con- 
ses. vulsions. 

III. Chronic Lead Poisoning. VIII. Tetanus. 

IV. Chronic Mercurialism. IX. Neuralgia. 
V. Paralysis Agitans. X. Megrim. 



PERIPHERAL NEURITIS. 

Within a comparatively recent period quite a number of conditions for- 
merly supposed to depend upon disease of the nervous centres have been 
found to be associated with inflammatory and degenerative changes in the 
nerve-trunks. They are grouped under the general term peripheral neuritis. 

Morbid Anatomy. — In the acute forms of the disease distinct inflamma- 
tory processes can usually be recognized. The hyperemia is sufficient to 
give the nerve-trunk a distinct pink color, and even extravasations may be 
present. The exudation produces marked swelling, and when the round 
cell infiltration, which is always present in acute cases, becomes more 
prominent, the nerve-sheaths and interstitial tissue show distinct purulent 
infiltration. Changes in the nerve-fibres vary with the extent and severity 
of the inflammation. Always more or less compressed, the parenchyma- 
tous changes may vary from slight softening and cloudy swelling to fatty 
degeneration or complete disintegration of the medullary sheaths and axis- 
cylinders. When vascular and exudative changes have not been followed 
by destruction of the nerves, the process may terminate in simple resolu- 
tion. Often, however, even in these cases, and always when there has been 
loss of tissue, repair takes place by formation of new connective-tissue, 
which may develop quite evenly or in irregular patches {neuritis nodosa), 
and cause, by its subsequent contraction, varying degrees of interference 
with nervous function. When nerve-fibres have been actually destroyed, 
partial restoration may take place, but it is complete only when there has 
been little loss of tissue. 



PEEIPHEEAL NEURITIS. 



1077 



Chronic neuritis is less frequent. In it the vascular and exudative 
changes are subsidiary and even unappreciable. A development of new 
connective-tissue may be the only evidence of pathological changes, but, 
more frequently, the inflammation is so purely parenchymatous as rather 
to deserve the name of degeneration. The changes are those of fatty 
metamorphosis and atrophy rather than simple cloudy swelling. Perma- 
nent injury of the nerve-trunks, rather than regeneration, is the termina- 
tion of these changes. 

Etiology. — Direct traumatism, pressure from dislocated bones, fractures, 
or tumors, and extension of inflammation from adjacent tissues, may each 
induce a local neuritis. It is only when such conditions are complicated 
by sepsis that this neuritis becomes wandering or metastatic {neuritis 
ascendens, aut aberrans, aid migrans). 

Most cases of primary neuritis appear without apparent cause. Many 
forms of neuralgia and paralysis occurring as complications of rheuma- 
tism, gout, lead, arsenic, or mercurial poisoning, and allied conditions, are 
believed to depend often upon neuritis, and these poisons are thus included 
among its causes. Alcohol must be recognized as an unquestioned cause, 
especially of chronic neuritis. Aside from this, little is known. Expos- 
ure to cold, sexual excess, and other "scapegoats" of that class, are made 
responsible for many cases when no evident cause offers. 

The determination of a specific cause of tetanus has led to the belief that 
many cases of peripheral neuritis have a similar specific nature. 

Symptoms. — Acute neuritis may be either primary or secondary. 

Primary neuritis is usually multiple and degenerative in character, its 
etiology coming under the head of constitutional causes. It rarely affects 
the cranial nerves. Its invasion is sudden and attended by the usual symp- 
toms of fever, with a temperature of 101°-105° F. A marked increase in 
the pulse-rate out of proportion to the febrile movement, is a peculiar 
symptom sometimes observed. It probably depends upon some implication 
of the vagus. 

In the early stages of irritation the sensory nerves suffer most, so that 
hyperesthesia and rapidly developing sharp, lancinating, tearing pains, 
which follow rather closely the nerve distribution, are the prominent early 
symptoms, while muscular spasms are often, indeed usually, absent, and 
seldom, if ever, are more than fibrillary twitchings. As the disease pro- 
gresses, however, to the stage of abolition of nervous irritability, the motor 
nerves are the ones to suffer. The sensory disturbances decrease, but do 
not disappear, and gradually or rapidly developing paralysis, w T ith loss of 
all the reflexes, give evidence of the implication of the motor trunks. As 
in other acute disease, the course and extent of the disease are very vari- 
able. In one case paresis or paralysis will be present almost from the first ; 
in another it will be delayed some days, or even weeks. The disease is 
rarely arrested before the development of distinct paralysis, while some 
cases run an exceedingly acute course, and end in death from paralysis of 
the respiratory muscles. Others start in acutely, and then become chronic. 
In all severe cases electrical irritability of the affected muscles is largely or 



1078 



DISEASES OF THE NERVOUS SYSTEM. 



completely lost, and, many times, the reaction of degeneration and atrophy 
of the muscles will be developed. Occasionally multiple neuritis is chronic 
from the start. Recovery is always slow, and proportioned to the extent of 
parenchymatous change in the nerve-fibres. Paralysis in multiple neuritis 
usually begins in the lower extremities, and does not, as a rule, affect the 
bladder and rectum. The symptoms of traumatic neuritis are largely 
local, and include similar sensory and motor disturbances. The constitu- 
tional manifestations are usually those of a simple inflammation. 

Differential Diagnosis. — Multiple neuritis is most liable to be mistaken 
for poliomyelitis. The diagnosis rests upon the acute invasion, the evi- 
dences of sensory disturbances rapidly changing to those of decrease and 
loss of motor function, with muscular atrophy, loss of reflexes, and the 
reaction of degeneration. 

Prognosis. — This is exceedingly uncertain and rather unfavorable. Many 
severe cases, however, go on to a partial recovery, and, when the disease is 
arrested early, this may be complete. 

Treatment. — In the early stage, during the intensity of the sensory mani- 
festations, morphia must be employed for their relief. Hot packs and 
other local sedatives are often of assistance. During the stage of advanc- 
ing paralysis, the treatment is purely tonic and symptomatic. When regen- 
eration of the affected nerves begins, galvanism is of value in connection 
with other tonics, both to hasten the reparative processes and to improve 
the muscular condition. Salol and the salicylates have seemed of service 
in some cases. 

LOCALIZED SPASMS AND PAEALYSES. 

(Scrivener's Palsy, etc.) 

Writer's cramp is one of the more common varieties of anomalous mus- 
cular movements, or of those diseases which Duchenne calls "functional 
impotences." Of essentially the same nature are piano-players' cramp and 
the inability of tailors, dairymen, bricklayers, or telegraphers to execute 
movements to which they have long been accustomed. 

Morbid Anatomy. — It has been thought that degenerative changes occur 
in the spinal cord, but according to Dr. Reynolds these diseases are due to 
a perverted nutrition of these parts. 

Duchenne believes that the primary change is in the nerve centres, and 
gives as a strong argument in favor of this view the fact that the malady very 
quickly affects the left hand when this is used to supply the right in one 
who has writers cramp. Dr. Poore, however, suggests that the lesion in 
typical cases is at the periphery, either in the muscles themselves, or in their 
terminal motor nerves. He attributes the disease to over-use and over- 
fatigue, not to central changes ; and states that muscles which are trained 
to ivork in order together no longer do so when even one of them fails. 

Etiology. — Writer's cramp, like other similar conditions, as from violin 
or piano-playing, telegraphing, milking, etc., is for the most part induced 
by long-continued use of the affected muscles. 

Symptoms. — It will be sufficient to describe writer's cramp as a type of 



LOCALIZED SPASMS AND PARALYSES. 



1079 



all this class of spasms, since they differ only in the muscles involved. It 
generally commences with a sense of weight or stiffness in the affected 
muscles, together with discomfort and indefinite pain, which is perhaps 
relieved by strong contractions or stretching the muscles. This uneasi- 
ness slowly increases, and there is added a tendency to spasmodic movements 
which renders the handwriting irregular and covered with unnecessary lines. 

The pain and spasm at first follow only prolonged use of the pen, but 
soon are induced very readily, until at length all attempts at writing are 
abandoned. In the earlier stages the patient is able to control the spasms 
somewhat and to relieve them by holding his pen in an unusual way or 
by some other device. For a time also after more delicate manipulations 
are impossible, he can still perform coarser operations, but the disease al- 
most invariably extends so long as the muscles are kept in use, and may 
result in severe spasm whenever any attempt is made to use the hand in 
writing. Occasionally it assumes a paralytic form and the patient is un- 
able to hold a pen at all, or pain may be a prominent symptom, radiating 
up the arm as a severe neuralgia. 

The disease may affect any or all the muscles of the hand or arm, and it 
rarely extends to the shoulder and trunk. More commonly the extensors 
and flexors of the thumb or index finger are affected, but though there is 
generally a distinct loss of power the muscles act perfectly in any motions 
save those which induced the disease. 

In the other forms of local spasm the general history will be the same, 
and the deformities and disturbances will depend entirely upon the action 
of the muscles implicated. It is more likely to occur in those who merely 
copy than those who write an equal amount, but think at the same time — 
as authors and journalists. 

Differential Diagnosis. — The history of the case is all-important, and will 
generally be sufficient for a diagnosis. 

Lead palsy, with which scrivener's palsy maybe confounded, is generally 
preceded by several attacks of lead colic ; there is the peculiar blue line at 
the margin of the teeth, the skin assumes an earthy hue, and the " drop- 
wrist" exists, conditions which do not occur in writer's cramp. 

Paralysis agitans, disseminated sclerosis, and the trembling due to old 
age or to chronic alcoholismus will be readily differentiated by the history. 

Prognosis. — The prognosis is favorable. The shorter the duration of the 
condition, and the greater the opportunity the patient has to give the part 
rest, the better the outlook. Writer's cramp is much more easily relieved 
in the weak and nervous than in the strong and robust. 

Treatment. — Absolute rest is essential, and will sometimes alone be suffi- 
cient for a cure. The mild galvanic current, blistering along the nerve- 
trunks, should they be tender, and rhythmical exercise of the affected mus- 
cles short of fatigue, is often of marked service. Morphine hypodermically 
may relieve, but does not effect a cure. The mind and body must have rest 
as well as the muscles. Hypodermic injections of atropia, strychnia, and 
Fowler's solution have been used with success. Massage to the part is rec- 
ommended by Beard. In my experience the only course which has been 



1080 



DISEASES OF THE NERVOUS SYSTEM. 



followed by markedly beneficial results has been absolute rest of the affected 
muscles, with sea bathing and the internal use of iron. 

CHRONIC LEAD POISONING. 
(Lead Palsy.) 

This is a morbid condition produced by the introduction of the salts of 
lead into the system, either through the mucous surfaces or the skin. 

Morbid Anatomy. — After the salts of lead have been received into the 
system, they become deposited in various tissues or are discharged by the 
emunctories. They have been found in all the tissues of the body. They 
are eliminated mainly by the kidneys. In the paralysis caused by lead 
poisoning the muscles and nerves are early affected ; later the nerve- 
centres become implicated. It is probable that the lead deposited in the 
affected tissues impairs their function and leads to their degeneration when 
the paralysis has existed for a long time. 

Etiology. — The sources of lead poisoning are numerous : painters and 
workers in lead are those most frequently affected. Drinking-water, wines, 
and ales frequently become impregnated with it, and then become a source 
of infection. The application of lead powder as a cosmetic to the face and 
neck has caused lead-poisoning. Some persons are much more susceptible 
to its poisonous influences than others ; I have known a few doses of lead 
taken as a medicine to give rise to pronounced symptoms of lead poisoning. 

Symptoms. — The general health of those who are the subjects of chronic 
lead poisoning is always more or less impaired. Their skin becomes sallow, 
dry and harsh, they suffer from dyspeptic symptoms, loss of appetite, and 
constipation. A blue line forms along the edge of the gums immediately 
adjoining the teeth, which is regarded by some as diagnostic of lead poison- 
ing — it is often present in those working in lead who are free from other 
symptoms. 

The most important and characteristic symptoms are intestinal colic, 
and affections of the nervous system. Lead colic has been considered in 
the list of Intestinal Diseases. The most frequent of the nervous affections 
is drop- wrist from paralysis of the extensors of the fore-arm. It generally 
comes on gradually after one or two attacks of colic. Sometimes its ad- 
vent is sudden. In painters the right hand is first affected, but after a 
time both hands are involved. The signs of lead palsy are loss of power 
over the extensor muscles of the fore-arm ; first the patient is unable to ab- 
duct the thumb, then to extend the finger, then to extend the hand on the 
fore-arm, and the hand drops when the arm is held in a prone position. 
The paralysis is generally limited to the muscles supplied by the radial nerve. 

/The paralyzed muscles waste rapidly and lose to a greater or less degree 
their electro-contractility ; there is no loss of sensation in the paralyzed 
limb, and not infrequently it is the seat of severe pains and tenderness. 
In some instances other muscles besides those of the fore-arm are affected, 
as the deltoid and triceps, and the palsy may involve the muscles of the 
lower extremity, especially the extensors of the foot and leg. In rare in- 
stances all the voluntary muscles are involved. Gouty subjects are pecu- 



CHROMIC MERCURIALISM. 



1081 



liarly susceptible to lead poisoning, and in such cases the cirrhotic kidney 
almost always exists, giving rise to albuminuria and the other phenomena 
of the cirrhotic form of Bright's disease. 

This condition is often accompanied by amaurosis and other grave ner- 
vous symptoms. 

Differential Diagnosis. — The diagnosis of lead colic has been considered 
under the head of Intestinal Colic. Lead palsy may be distinguished from 
other forms of palsy, by the history of the case, by the absence of cerebro- 
spinal disturbance, and by the blue line on the gums. When the muscles 
of a paralyzed limb respond to the influence of the electric current lead 
poisoning may be excluded. 

Prognosis. — Chronic lead poisoning is rarely a direct cause of death, 
although it may exist for years, the longer its duration the less prospect 
there is of complete recovery. Extreme wasting of the paralyzed muscles 
with loss of electric contractility renders the prognosis unfavorable. In 
some instances the muscular power may be regained when the excitability 
does not return. 

In most cases the general health is not seriously impaired, and the re- 
covery from the paralysis, if not complete, is partial. The fatal cases are 
those which have been a long time exposed to the poisonous influence of 
lead, and who have been intemperate. 

Treatment. — The first thing to be accomplished is to remove the patient 
from all sources of lead poisoning. Extreme personal cleanliness is im- 
portant for those who cannot avoid such exposure. The habitual use of 
lemonade made with sulphuric acid is regarded, to some extent, as prcs 
tective ; it acts by converting the carbonate and other salts of lead in the 
stomach into the insoluble sulphate. Various methods have been proposed 
for removing the lead from the system, the most effective of which is baths 
containing some soluble sulphide. 1 

Iodide of potassium is recommended on the ground that the iodide 
makes, with the insoluble salts of lead deposited in the tissue, a new soluble 
salt, which can be eliminated by the kidneys. Its administration should 
begin with fifteen grains a day, and be gradually increased to thirty grains 
a day ; it may, in anaemic subjects, be combined with chloride of iron. The 
bowels should always be kept freely open. 

The only effectual remedy for restoring the paralyzed muscle is electric- 
ity in the form of Faradization. Its application should not be continued 
more than ten or fifteen minutes three times a day for two or three months. 
Severe shocks should be carefully avoided, although a current of high 
tension causes no movement in the paralyzed muscles. It is important that 
each paralyzed muscle should be treated separately. 

CHFwO^IC MERCUEIALISM. 

{Mercurial Tremor.) 

Chronic mercurial poisoning may result from the long-continued intro- 

1 Dr. Pereira recommends baths medicated by dissolving sulphide of potassium iu the proportion of 
two ounces in fifteen gallons of water. 



1082 



DISEASES OE THE NERVOUS SYSTEM. 



duction of mercury into the system, either through the stomach, respiratory 
organs, or skin. 

Morbid Anatomy. — No characteristic lesions have been discovered in those 
who have died of chronic mercurialism, except the deposit of mercury in 
the tissues, especially the brain, liver and kidneys. 

Etiology. — Workers in mercury, as gilders, looking-glass manufacturers, 
and those engaged in quicksilver mining, are those who chiefly suffer from 
chronic mercurialism, although it may result from its long-continued 
medicinal use. Those who are exposed to its fumes are especially liable 
to its poisonous effects. 

Symptoms. — The manifestations of chronic mercurialization are mainly 
confined to the nervous and muscular system, and may be designated as 
mercurial tremors. Its first indication is a tremulousness of the hands 
and arms, accompanied by numbness and tingling, with pain in the 
joints. These symptoms may continue for years without interfering 
materially with the general health of the individual ; but sooner or later 
the entire muscular system becomes invaded, and speech, deglutition, and 
respiration are more or less interfered with. Choreic movements occur, 
the patient is unable to walk or stand without assistance, and the face is 
contorted by muscular spasms ; while the patient is in the recumbent pos- 
ture and makes no muscular efforts, the muscular spasms cease, but as 
soon as he attempts to stand or move, the choreic movements commence. 

In an advanced stage of the disease the convulsive movements do not 
entirely cease when the patient is in the recumbent posture. After the 
tremors have continued for a long time and have been severe, the patient 
loses appetite, becomes sallow and emaciated, and cerebral symptoms de- 
velop, the most constant of which are headache, vertigo, delirium, and 
epileptic convulsions. 

Differential Diagnosis. — Mercurial tremor may be confounded with mul- 
tiple sclerosis, paralysis agitans, and chorea. But a history of exposure 
to mercurial poisoning, and the fact that the nervous symptoms were pre- 
ceded by ptyalism, ulcerated, gums, mercurial fetor of the breath, nausea, 
colicky pains and diarrhoea, are generally sufficient to establish a diagnosis. 
It is also to be remembered that in paralysis agitans the muscles of the 
head and neck are not involved in the convulsive movements, and that the 
position of the patient does not influence the spasms. 

Prognosis. — Mercurial tremor does not often directly cause death, but if 
exposures to the causes of mercurial poisoning are continued, death may 
result from exhaustion, intestinal or cerebral complications, or from in- 
tercurrent disease. 

Treatment. — As soon as any of the symptoms of mercurial poisoning are 
present, the individuals must immediately be removed from all chance of 
exposure to the poison. If this cannot be effected, and they are compelled 
to continue occupations where they are exposed to the fumes of mercury, 
they must wear a protection over their face, and exercise the greatest per- 
sonal cleanliness. 

Drugs are of little service, the treatment is altogether prophylactic. 



PARALYSIS AGITAKS. 



1083 



PAEALTSIS AGITANS. 

Shaking palsy, or the trembles, is a disease of advanced life characterized 
by motor weakness and tremors of the voluntary muscles, especially of the 
limbs, occurring independently of muscular exertion, which are finally fol- 
lowed by paralytic symptoms. 

Morbid Anatomy. — As yet no constant changes have been discovered. 
Some authorities consider it of spinal, others of cerebral origin. Among 
the former are Charcot, Lebert, Marshall Hall, and Rosenthal. Among 
the latter are Oppolzer and Skoda. Senile changes in the brain and cord 
are found in a certain number of cases. There may be sclerotic patches in 
the pons, the medulla oblongata, the optic thalamus, and hippocampus 
major, and Charcot has found increase of the epithelium of the central 
canal in the cord with pigmentation of the cells in the posterior columns 
of Clark. Diseased arteries and slight sanguineous exudations have also 
been noticed. 

Etiology. — Rarely occurring before forty, the liability to it is increased 
every year thereafter. It is more common in men than women, and occurs 
chiefly in the lower classes. Violent emotions, as grief, fear, anger or dis- 
tress of mind, degeneration of the heart and vessels, and great bodily 
fatigue and exposure, are among its exciting causes. There are no indica- 
tions that the disease is hereditary. 

Symptoms. — In nearly ail cases paralysis agitans is insidious in its ap- 
proach, and begins in one foot, hand, or possibly a single ringer or the 
thumb, as a slight oscillating motion, which is quite rhythmical and charac- 
teristic. For a time this trembling may be intermittent, but appears with- 
out any apparent cause and unexpectedly. In this early stage it can possi- 
bly be arrested by an effort of the will, a condition in marked contrast 
with the very decided increase in the tremor which late in the disease 
follows every effort to control the muscles. As the disease advances simi- 
lar oscillating movements affect the muscles of the forearm, arms and 
shoulder, and the entire limb is in a continuous tremble. The remaining 
limb of the affected side usually becomes involved before the disease crosses 
the median line. Pain, weariness and stiffness in the affected muscles pre- 
cede, in some cases, the development of the characteristic tremors ; or the 
disease may attain its full development through a series of increasingly fre- 
quent sudden attacks of tremor lasting only a few days each. 

At the height of the disease nearly all the limbs are involved in an inces- 
sant motion which is liable to severe exacerbation upon muscular exertion 
or during mental disturbance, and which ceases only during sleep or anaes- 
thesia. 

Later on, rigidity, painful cramps, and contractions affect not only the 
muscles of the limbs but also those of the trunk, neck and face, giving the 
patient quite a characteristic appearance. The countenance assumes a 
fixed, staring look of distress, the head is drawn forward and the trunk 
flexed ; the lower limbs and arms, which are drawn away from the side. 



1084 



DISEASES OF THE NERVOUS SYSTEM. 



are rigid, and all the joints are flexed, often causing marked deformity of 
the hands, Although the rigidity of the limbs does not prevent walking, 
the patient's gait is characteristic. As he rises, or when he stands, there 
is great unsteadiness and difficulty in maintaining equilibrium, which, as 
he starts to walk, causes him to run forward to avoid falling. This dis- 
turbance of equilibrium is not associated with vertigo. 

The muscles of respiration and deglutition are not involved, but the voice 
is often tremulous and speech is slow, hesitating and laborious, so that 
words are distinctly broken up into syllables. Although muscular move- 
ments are attended with extreme fatigue, the force of the contractions is 
but slightly diminished until late in the disease, when, from increase in the 
rigidity, the patient takes to his bed, and the muscles suffer in their nutri- 
tion or become distinctly fatty. 

As the end approaches, the memory and intelligence fail in connection 
with the generally defective nutrition. Although the disease may last for 
twenty or thirty years, death most commonly results from some intercur- 
rent disease. 

Differential Diagnosis. — In disseminated sclerosis tremors occur only 
when the muscles are in use ; the disease begins in the lower limbs, affects 
younger persons, and paralysis occurs early. The patient has no tendency 
to run forward, and does not present the peculiar physiognomy of shaking 
palsy. Senile, alcoholic, lead and mercurial trembling are readily diagnos- 
ticated by the previous history and concomitant symptoms. 

Prognosis. — Paralysis agitans is a very chronic disease, and the outlook is 
never favorable. It may last twenty-five years. After a few years the 
muscles waste, the patient is confined to his bed, there is physical and 
mental exhaustion, bed-sores form, and death results from asthenia or 
complications. The more common complications are acute lobar pneu- 
monia and pleurisy. Paralysis agitans has been recovered from in the 
early stages, but Eulenberg says that there is reason to doubt the diagno- 
sis in such cases. 1 

Treatment. — No definite results have been attained by the use of any 
remedy. All the nerve stimulants, tonics, and sedatives have been em- 
ployed, of which Charcot considers hyoscyamus the only useful one, and 
the effects of this are temporary. The constant current has seemed to 
have some value as a distinctly curative agent. Beyond this, general tonic 
treatment is the most that can be attempted, and this should never be 
omitted. 

FACIAL PAEALYSIS. 

(Bell's Paralysis.) 

Bell's paralysis is a paralysis of the muscles of the face due to any lesion 
implicating the nucleus or fibres of the seventh pair of nerves. 

Etiology.— It may be caused within the skull by blood extravasations, 

1 Handfield Jones thinks that there are two forms : one entirely incurable, occurring in old persons and 
depending upon organic changes in the central nervous system ; the other, in younger persons, curable, 
and probably not dependent upon organic changes. 



FACIAL PARALYSIS. 



1085 



tumors, and inflammatory products, which give rise to pressure. Fracture 
and morbid growths may cause pressure on the nerve, in its passage 
through the cranial bones, sufficient to produce the paralysis. It may 
occur in connection with disease of the internal or middle ear and from 
local neuritis. Outside the skull, blows, wounds, swellings of the parotid 
gland or other tumors may cause it. It is most frequently the result of a 
draught of cold air on the side of the face, especially while sleeping. 

Symptoms. — Its onset is usually gradual ; but when fully developed its 
symptoms are striking and characteristic. All the muscles supplied by the 
seventh nerve on one side of the face are paralyzed. The forehead is smooth 
and motionless on the paralyzed side, the corner of the mouth is drawn to 
the opposite side, and the paralyzed side closes less perfectly than the other. 
The patient cannot close the eye on the affected side. As soon as the face 
is moved the paralysis is unmistakable. Whistling and drinking are im- 
possible. Certain letters, as P and B, cannot be pronounced; food collects 
between the cheek and teeth on the palsied side. The tears run down over 
the cheek, and, if the chorda tympani is involved, the sense of taste is per- 
verted or destroyed on one-half of the anterior portion of the tongue. At 
the same time the salivary secretion is diminished. The uvula is usually 
deflected; the ala of the nose becomes flaccid, and the nostril on the affect- 
ed side is narrowed and loses its rotundity. Imperfect closure of the eye 
exposes the organ to all sorts of injuries, hence disease of the cornea and 
conjunctiva is very common. During the first two or three days the mus- 
cles show increased irritability to the electrical current ; but they gradually 
lose their Faradic, while they retain their galvanic irritability. 

Differential Diagnosis. — When otorrhoea, disturbances of hearing, obliquity 
of the uvula, diminished salivary secretion, and loss of taste occur, the origin 
of the paralysis is within the aquseductus Fallopii. When the taste is nor- 
mal and the uvula straight the cause is usually peripheral, e. g., cold. In 
these cases also electro-muscular contractility is rapidly lost. The origin 
may be supposed to be central when other nerves are involved. Bell's palsy 
is usually associated with paralysis of the sixth nerve. 

Prognosis. — In organic disease of the brain or with lesions of bone the 
prognosis is unfavorable. When arising from cold, slight injuries, or syph- 
ilis the prognosis is favorable. Complete recovery is usually reached in two 
or three months. There is no rule by which one can estimate its duration. 
The more the electro-muscular contractility is diminished the less the 
chances of complete recovery. 

Treatment. — When due to cold, rpply a few leeches to the mastoid proc- 
ess, followed by hot fomentations ; subsequently blisters behind the ear and 
other counter-irritants may be resorted to, and the alternate Faradic and 
voltaic currents are to be relied upon. Massage and shampooing may be 
tried. Gowers recommends inunctions of oleate of morphia. When due 
to syphilis, anti-syphilitics are indicated. Niemeyer recommends mercu- 
rial ointment. 



1086 



DISEASES OF THE NERVOUS SYSTEM. 



ECLAMPSIA AND INFANTILE CONVULSIONS. 

Epileptiform convulsions are of frequent occurrence in connection with 
distinct lesions of the nervous centres as well as with various reflex disturb- 
ances. Indeed, they may be symptomatic of any cerebral disease, as com- 
pression from fracture, hemorrhage and tumors, or thrombosis, embolism 
and inflammatory processes. In those conditions where they can be 
ascribed to distinct pathological changes they are termed eclampsia. Clini- 
cally such convulsions, as well as those from uraemia and other poisons, are 
often identical in appearance with epileptic fits, and are to be diagnosticated 
by the concomitant symptoms. 

When such convulsions occur in children, as they often do from reflex 
irritation during teething, in gastro-intestinal disorders, in the early stages 
of blood poisoning, and, indeed, in any condition which in the adult pro- 
duces a chill, they are then called infantile convulsions. Although fre- 
quently indistinguishable from epilepsy, the convulsions of eclampsia, and 
more particularly infantile convulsions, may present only a portion of the 
true epileptic fit or even be very slight. They are, moreover, less regular 
in their occurrence, and, until the cause is removed, tend to increase in fre- 
quency and intensity. They are less sudden in their development also, 
and, although much more fatal, owing to their frequent dependence upon 
an irremediable cause, generally cease permanently when the cause is re- 
moved. Infantile convulsions present the widest range of intensity, but are 
always a cause of anxiety, especially when the respiratory muscles are in- 
volved, as is frequently the case. 

The indications for treatment are, of course, found in the cause. In 
syphilis, uraemia, anaemia, gastro-enteritis, etc., the treatment will in most 
cases be under way before the occurrence of convulsions. When, however, 
they are the initiatory symptoms, all possible causes must be carefully 
sought. The discovery of a cause will indicate the treatment. Infantile 
convulsions often arise from slight causes that frequently escape detection. 
In such cases the general health must be improved, the alimentary canal 
freed from a possible hidden cause, and the clothing carefully inspected 
and made loose and unirritating. The usual anti-spasmodics, belladonna, 
the bromides, etc., may then properly be used. Hot baths, counter-irri- 
tants to the back and neck, or cold to the head, are often of service. 
Chloroform is the most appropriate agent for controlling the spasms 
temporarily. 

TETANUS. 

Tetanus, or lock-jaw, is a tonic spasm with paroxysmal exacerbations of 
the voluntary muscles; those of the lower jaw, neck, and pharynx are 
usually first affected. Acute and chronic varieties are recognized ; the 
latter is called tetanus mitis. 



TETANUS. 



1087 



Morbid Anatomy. — There are no constant lesions in tetanus, and those 
which are commonly present are quite as possibly secondary as primary. 

In traumatic tetanus the nerves supplying the affected parts are some- 
times inflamed, but even this condition is not invariably present. In the 
cord there is often more or less hyperemia, with slight effusion, and per- 
haps extravasation. This is frequently attended by some cedematous soften- 
ing and interstitial exudation of finely granular or structureless matter, 
especially in the gray substance, in the fissures, and on the surface of the 
cord. Tetanus is usually traumatic and may follow the most trivial 
injury, as a splinter in the finger, but is more apt to develop after com- 
pound or complex fractures, lacerated, crushed, and punctured wounds, 
and wounds complicated by the presence of foreign bodies. It may occur 
after abortion or normal delivery, and trismus nascentium is ascribed to 
the wound at the navel. 

Climatic conditions have a distinctly exciting influence in the production 
of tetanus. It is much more common in hot than in temperate climates, 
and rapid changes of temperature, cold and wet, are especially favorable to 
its development. It is said that fright, anxiety, or depression markedly 
predisposes to its occurrence, as in armies it prevails most extensively 
among the defeated. 

Clinically, tetanus can be excited by strychnine, ergotin, brucine, picro- 
toxin, and caffein. Occasionally tetanus arises from unknown influences, 
when no wound or abrasion is present, and when the only apparent assign- 
able cause is exposure to wet and cold. More recent investigations have 
seemed to show that tetanus may be a specific disease of bacterial origin. 

Tetanus may occur at any age and in either sex, but is most frequent in 
adult males. 

Symptoms. — Tetanus generally comes on in from six to twelve days after 
the injury, but may be delayed three or four weeks or appear within a few 
hours. In the largest number of cases it begins with stiffness of the mus- 
cles of the neck and jaw. This quickly extends to the muscles of mastica- 
tion and facial expression ; the patient's jaw becomes locked and the head 
fixed, and the face wears a peculiar frown. The tonic stiffness is aggra- 
vated by every attempt to use the muscles. Deglutition is difficult, and 
later becomes almost impossible. By degrees the other muscles are in- 
volved, the trunk is stiff and more or less curved, the abdomen tense and 
hard, and the limbs extended and rigid. When the diaphragm is moved, 
a sharp, sudden pain shoots through the body from the ensiform cartilage, 
which is considered diagnostic. It is accompanied by intense dyspnoea. 
This general rigidity of the muscles is continuous and progressive, but is 
marked by paroxysmal attacks in which all the symptoms are immensely 
exaggerated. They are excited by any muscular action, by jars and other 
slight causes, or may occur spontaneously. During a spasm all the muscles 
become powerfully contracted. The limbs are extended, the back arched, 
and the face assumes the risus sardonicus. The head is retracted, and 
the patient may rest only on his head and heels. The respiratory muscles 
suffer also, and respiration may be entirely arrested, and the face become 



1088 



DISEASES OF THE is T EKVOL T S SYSTEM. 



cyanotic. As the paroxysm passes away it is only a remission ; the muscles 
are still hard and stiff, the jaw closed, and the respiration rapid and shal- 
low. The intense cramping pain of the paroxysm gives place to a heavy 
ache and soreness. 

Notwithstanding the severity of the disease, consciousness and intelli- 
gence are rarely impaired, and the temperature and pulse-rate are only 
elevated on account of the muscular action. Just before death, however, 
in many instances, there is a rapid and enormous rise in the temperature, 
which may reach 112° or 114° E. The urine is scanty, the bowels are con- 
stipated, and the body is bathed in a profuse sweat. Keflex irritability is 
increased to a high degree throughout. 

Differential Diagnosis. — The absence of headache, delirium, and coma, 
and a normal temperature in the intervals between the attacks, will suffice 
to distinguish tetanus from any cerebral or cerebrospinal inflammation. 

Hysteria, hystero-epilepsy, and sometimes epilepsy may simulate it, but 
the development of the disease quickly affords a diagnosis. 

Strychnia poisoning is to be differentiated by the history of the case and 
the examination of voided matter. In strychnia poisoning, consciousness 
is lost, and the muscles of the jaw, head, and neck are last and least 
affected. 

Prognosis. — Tetanus usually terminates fatally before the tenth day ; but 
if the twelfth day be passed and the temperature does not pass 102° F., 
and the respiratory muscles are not involved ; or if the disease has occurred 
at a remote period from the reception of the wound, the outlook is quite 
hopeful. When the patient is young, when strabismus occurs, or the 
wound is very recent, and when rigidity appears early the case is nearly 
always fatal. 

Treatment. — So far as is known, no treatment has any controlling effect 
upon tetanus. Innumerable remedies have been tried, with equally bad 
results. A highly nutritious diet, with alcoholic stimulants, is, perhaps, 
the best treatment. Alimentation must be carried on by a stomach-tube 
or by the rectum. Eecently, curare, nitrite of amyl, and hydrate of chloral 
(in forty-grain doses) seem to be the favorite drugs. Locally, ice and cold 
effusions to the spine prove beneficial, although hot applications are more 
grateful to the patient. 

The utmost care should be taken to avoid all irritation and to keep the 
patient in the most absolute quiet. 

NEURALGIA. 

The term neuralgia is applied in a very general way to pain, which is 
either of idiopathic origin or constitutes the principal and at times the 
only symptom of some obscure lesion. Neuralgia is a symptom indica- 
tive of direct injury to, or altered nutrition of, a sensory nerve, which 
in the former case is more or less persistent, but in the latter is usually 
paroxysmal. 

Morbid Anatomy. — It may be functional or organic ; but in the majority 



NEURALGIA. 



10S9 



of instances no changes can be found after death. 1 When neuralgia is a 
symptom of acute neuritis or peri-neuritis, the nerve trunk is hyperaemic 
and swollen or degenerated and atrophied ; when a symptom of chronic neu- 
ritis, the nerve has undergone sclerotic processes, and compression with 
degeneration of the nerve-substance follows. 

Neuritis may be descending or ascending. When it attacks nerves at 
various points it is called disseminated or migrating neuritis. When 
neuralgia is a symptom of pressure from tumors, either in brain, cord or 
at any point along the nerve trunks, the pain will be confined to the single 
nerve. Gummata, aneurisms, and osteomata are the tumors which usually 
induce such compression. 

Etiology. — Neuralgia is often an hereditary disease in those of a neuro- 
pathic tendency. Any disease causing general, or local, permanent or 
transient anaemia, is a marked predisposing cause. 

Among exciting causes are cold (especially damp cold), lead, mercurial 
and other states of chronic blood poisoning, and traumatism. Disease of 
the genito-urinary tract, especially in women, often excites reflex or sym- 
pathetic neuralgia in remote nerve-trunks. Keflex neuralgia is also induced 
by decayed teeth, dyspepsia, worms, constipation, etc. Neuralgia may 
follow or accompany herpes zoster, and occurs very frequently in convales- 
cence from relapsing fever. 

It is rare before puberty, but just at this epoch there is a marked predis- 
position to it. Those between twenty and fifty years of age suffer most 
frequently. Women are more liable than men ; but males suffer from 
sciatic neuralgia much more frequently than females. 2 

The theory that neuralgia often depends on dilatation of the venous 
plexuses which surround a nerve at its exit from a bony canal, is supported 
by the fact that the first branch of the trigeminus suffers far oftener than 
either the second or third, or both combined. 3 

Symptoms. — Before the actual pain begins in a nerve, there may be 
numbness, slight cutaneous hyperesthesia, or some peculiar skin sensation 
which is well-known by the neuralgic individual. The pain is at first in- 
termitting, later it is continuous with slight remissions. The character 
of the pain varies : it may be dull, boring, stabbing, tearing or darting, 
and is confined very distinctly to the course and distribution of the af- 
fected nerve. Indeed, many patients trace exactly the course of some 
nerve when pointing out the locality of the pain. Sudden movements, as 
turning and coughing, often increase the pain. 

Increase of pain on pressure is an important point ; the exacerbation is 
greatest during a paroxysm, and greater in proportion to the intensity of 
the original pain. Certain points are markedly sensitive : these are at the 
exit of nerves from bony canals, or foramina, the spot where they pass 

1 It is claimed that the acid products of metamorphosis of nerve-tissue acting upon the nervous system 
must be neutralized by the blood, before pain ceases. Also, that nutritive lesions of the central sensory 
tract within the confines of the gray matter are the essential lesions. Peripheral pain is supposed to 
originate in the cord. 

2 Henle states that the left side is predisposed to intercostal neuralgia on account of the arrangement 
of the venous circulation. 

3 Allg. Wien. Med. Zeit, 1876, pp. 24, 26. 

69 



1090 



DISEASES OF THE NERVOUS SYSTEM. 



through, a muscular aponeurosis, at their bifurcation, and where terminal 
branches become superficial. These pain-points are better marked the 
longer the patient has suffered from neuralgic attacks. In connection 
with the pain, there is generally associated with it some vaso-motor dis- 
turbance, as extreme pallor or vivid redness and reflex movements and 
twitchings of the muscles. Should the nerves of a glind be attacked, se- 
cretion will probably be increased. After cessation of the pain the part 
often feels sore and bruised, and there is a general sensation of exhaustion 
and weariness. 

Actual temporary paralysis, muscular spasm, herpetic eruptions, and 
anaesthesia of the skin may complicate or follow an attack of neuralgia, 
and later the muscles supplied by the affected nerves may be atrophied 
and become abnormally weak. During a prolonged paroxysm the pain 
may extend from one nerve to another of a different origin. 1 In a few rare 
cases mental effort or excitement will exacerbate, or even excite, a parox- 
ysm of neuralgia. 

If neuralgia be caused by neuritis the pain is more continuous, and the 
nerve may be felt as a hard cord beneath the skin, which latter is red and 
cedematous. With neuritis of a mixed nerve, twitching and contractions 
occur with the pain. In neuralgia of functional origin, the pain is more 
likely to shift and to involve corresponding tracts on the other side of the 
body or head. 

One of the most common forms of neuralgia is that of the tri-facial 
nerve, usually attended with painful spasm, called tic douloureux. One 
or two, rarely all the divisions, may be involved. The first branch is its 
usual seat, when it is termed brow-ague ; the third is rarely attacked. 
When the ophthalmic division is affected the neuralgia is called hemi-crania 
or migraine. 

Clavis hystericus is a variety of tic in which there is a sensation as of a 
nail being driven into the skull. It is usually met with in anaemic females. 
The hair on one side of the head or one eyebrow may turn white, or pig- 
mentation may occur along the course of the pain, and the tongue on the 
side of the pain may exhibit epithelial overgrowth in long standing tic 
douloureux. 

Acute glaucoma and recurrent iritis are said to result from trophic 
changes due to neuralgia. 2 

Pain on pressure is usually best marked (1) at the exit of the frontal 
branch, (2) the exit of the inferior maxillary branch, (3) over the tempo- 
ral and parietal bones, or (4) along the supra-orbital ridges (supra-orbital 
neuralgia). 

Sciatica is a neuralgic affection of the sensory nerves of the sciatic plexus. 

It may be caused by the pressure of tumors and inflammatory exudation 
within the pelvis, or by caries or carcinomatous vertebras at the point where 
the nerves pass through the intervertebral foramena. Irritation of the pe- 

» Epileptiform neuralgia is that variety of tic douloureux where the seizures are very abrupt and ac 
companied. by spasm of the facial muscles. 

2 Anstie states that near the painful parts the periosteum and the fibrous tissue are thickened. 



NEURALGIA. 



1091 



ripheral branches of the sciatic, due to pressure along the line of the nerve, 
from tumors, etc., may cause sciatica, but in the majority of instances the 
origin is rheumatic and the direct result of taking cold. Chronic malarial 
infection may be the cause of sciatica. It is most frequently met with in 
males between the ages of twenty and sixty. 

It is usually preceded by tingling or stiffness in the buttock, back of the 
thigh, knee and leg. The pain may be continuous or intermittent, 
and its most frequent seats are the posterior and outer part of the thigh 
(particularly near the tuberosity of the ischium), the outer side of the 
ankle, and the dorsum of the foot. It usually comes on gradually, the 
pain becoming more intense at night. The patient usually lies with his 
legs flexed. In walking he moves the affected leg slowly, as any sudden 
motion greatly aggravates the pain. The pain is most markedly increased 
by pressure over the posterior iliac spine, at the fold of the buttock and the 
head of the fibula. Cramps in the muscles of the leg are common. The 
limb may be atrophied and the patient pass into a semi-paralytic condition, 
which is very apt to be chronic. It is a very obstinate affection, lasting 
usually from six weeks to two months, though, it may last for years. Re- 
lapses are not uncommon. 

Intercostal neuralgia is an affection of any of the dorsal nerves ; the an- 
terior branches of two or three of the nerves upon the left side are those 
usually affected. It occurs in women as a rule. Intermittent pain is felt 
in the region of the sixth, seventh, eighth and ninth intercostal nerves, 
tearing or stabbing in character, increased by coughing or sneezing, and 
perhaps accompanied by a dry cough. 

There are three diagnostic points of tenderness : (1) at the exit of the 
nerves from the spine, (2) at the side of the chest, where they become 
subcutaneous, and (3) near the sternum or median line at the terminal 
branches. Cardiac palpitation, dyspnoea, nausea and vomiting are fre- 
quent symptoms of this so-called false pleurisy. Herpes zoster, intolerable 
itching, and attacks of angina pectoris often complicate it. 

Cervico-occipital neuralgia is usually attended by pain along the course 
of the occipitalis major, 1 and often resembles that form of muscular rheu- 
matism called torticollis, or wry-neck. (See art. Rheumatism.) A branch 
of the brachial plexus may be involved ; the ulnar, however, is more fre- 
quently affected than any other. 

Coccyodynia is common in women, and is due to neuralgia of the coc- 
cygeal plexus. 

Headache. — Headache, or cephalalgia, is properly a form of neuralgia, as 
it can only be referred to the sensory nerves supplying the meninges and 
scalp, and like other neuralgias is of both organic and functional origin. 
It is a frequent symptom of cerebral disease, either inflammatory or such 
as produces compression of the cranial contents, and is especially severe in 
the acute forms of meningitis and some cerebral tumors. It results from 
disturbance of the cerebral circulation, which causes either compression of 
the cranial nerves or anaemia, and consequent disturbance of nutrition. Its 



i Gray's Anatomy, pp. 636-637. 



1092 



DISEASES OF THE NERVOUS S 7 STEM. 



primary cause, however, is more frequently in other organs, as the stomach 
or genito-urinary tract, in which cases the headache i»the result of reflex 
disturbances, frequently of the circulation, from vaso-motor irritation. Of 
a similar nature is the headache resulting from the strain of the ciliary 
muscle, consequent upon defects of refraction. Again, headache is fre- 
quently a symptom of blood poisons, as in rheumatism, gout and septic 
diseases. 

In these diseases, as probably also in headache with high temperature, the 
condition is presumably one of direct irritation of nerve centres, or of de- 
fective nutrition. Headache assumes a great variety of forms. It may be 
limited to one half the head, to the forehead, vertex, occiput, temporal re- 
gion, or any point on the cranium, or it may be diffuse and extend to the 
eye, face and neck. • In character and severity it may assume any of the 
characteristics of neuralgia. Headache is a symptom of exceedingly diffi- 
cult interpretation. In a general way, however, it maybe stated that head- 
ache of gastric or hepatic origin is commonly frontal and throbbing in 
character and associated with cerebral congestion. It may be bilateral or 
unilateral. Headache at the vertex is quite constantly symptomatic of cere- 
bral disturbances of local origin, or due to reflex irritation starting in the 
pelvic organs, especially the genital tract of the female. Pain in the occip- 
ital region is mostly an accompaniment of disorders of circulation, and vaso- 
motor spasm and anemia in particular. The pain of cerebral compression 
or tumor, although often diffuse, is generally localized, persistent, and very 
intense. 

All forms of cephalalgia may be attended by hyperesthesia, especially of 
the optic and auditory nerves, with subjective sensations of light and 
sound, by vertigo, nausea, drowsiness or wakefulness, and possibly deliri- 
um. Visceral neuralgias have been considered in the list of Visceral Dis- 
eases. 

Differential Diagnosis. — Neuralgia may be mistaken for myalgia, syphi- 
litic periostitis, and for cerebral abscess. 

Myalgia is distinguished by its non-paroxysmal character, by the pain 
being increased by motion, and by the fact that the attachments of the 
muscles are the points chiefly involved. . 

Syphilitic periostitis is to be distinguished from neuralgia by the pres- 
ence or absence of other symptoms of constitutional syphilis. 

Cerebral abscess often occurs secondarily to caries of the internal ear and 
after otitis in childhood ; neuralgia rarely appears before puberty. Cere- 
bral abscess frequently follows a blow or injury ; neuralgia comparatively 
seldom. In the former there are no true points douloureux ; these are 
present early in severe neuralgia. In cerebral abscess the pain does not 
completely intermit ; intermissions of pain, complete, and of considerable 
length, occur in neuralgia. The pain is at first severe in cerebral abscess ; 
in neuralgia it is slight at first and gradually exacerbates. Pain in cere- 
bral abscess is often limited in situation, seems deep-seated, though often 
it has no relation to the site of the abscess ; in neuralgia pain is superficial, 
and follows the distribution of recognizable nerve branches belonging to 



NEURALGIA.. 



1093 



the trigeminus or great occipital. In cerebral abscess there are no well 
localized vaso-motor or secretory complications, while lachrymation or 
congestion of the conjunctiva usually occurs m neuralgia. Cerebral ab- 
scess is rare in old age, and then generally traumatic ; neuralgia is most 
common at that period. 

Prognosis. — Life is rarely compromised by neuralgia, but when it is per- 
sistent the general health may be seriously affected. When occurring in 
early life and with no hereditary predisposition the prognosis is the most 
favorable. 

Treatment. — Neuralgia has been well said to be the cry of a nerve for let- 
ter Wood. Should anaemia be evidenced, a generous diet, cod-liver oil, the 
hypophosphites, or small doses of phosphorus and the appetizers, along with 
quinine, iron and strychnine should be ordered. Neuralgia due to syphilis 
demands iodide of potash ; to rheumatism, the anti-rheumatics ; to gout, 
colchicum ; and to malaria, quinine, but in many non-malarial cases also, 
especially in tic, quinine is the most effectual remedy. A patient with 
neuralgia should be removed from all exposure to cold and irritations of 
all kinds. 

Locally, blisters, the continuous current, chloroform, opium, belladonna 
and veratria liniments, and cold, or very hot water may be applied, and 
these sometimes afford permanent, nearly always temporary relief. Aco- 
nite enjoys the highest reputation at the present day among local remedies. 
Firing, sinapisms and actual cautery are frequently beneficial. Sometimes 
prolonged residence in a warm, dry climate is the only means of effecting 
a permanent cure. 

For immediate relief of pain, morphine is the most effectual. Neuralgic 
attacks and headache that are accompanied by flushing of the face are often 
relieved by ergot. But when the face is very pale, nitrite of amyl is to be 
preferred. Gelsemium is sometimes especially effectual in the treatment 
of trigeminal neuralgia. This and croton chloral are largely employed. 
In severe chronic neuralgias a portion of the nerve may be excised (neu- 
rectomy), or the nerve may be simply cut (neurotomy). More recently 
antipyrin has been employed in all forms of neuralgia. The results are 
extremely satisfactory in many cases. It is not always successful, however ; 
and, in any case, it requires increasing doses after a short time. It can 
be regarded only as a temporary expedient, and its favorable effects should 
never lead to neglect of radical measures for the removal of the cause. 

Nerve-stretching may be practised upon any trunk which can be sur- 
gically reached. The sciatic is the nerve which has been stretched with 
most success. In headache, cold to the head and heat to the feet, or at 
times the persistent application of heat to the head for several hours, will 
afford relief. Guarana, caffeine, and similar remedies are often very useful 
in sick headache. In these cases a purge or an emetic will also frequently 
bring relief. 

In all severe cases of sciatica, in addition to the treatment of neuralgia 
in general, absolute rest is essential to its successful management. If it is 
caused by gout, rheumatism, or syphilis, treatment appropriate to these 



1094 



DISEASES OF THE NERVOUS SYSTEM. 



conditions must be employed. If there be a chronic malarial taint, quinine 
and arsenic must be given in full doses. The hypodermic injection of 
morphine gives the most speedy relief. The point of the needle should be 
introduced deep into the tissues over the exit of the nerve. In many in- 
stances its daily use for some time will cure sciatica, even of long standing. 
The continuous voltaic current is often palliative and sometimes curative. 
The systematic treatment with baths at the Hot Springs of Arkansas and 
Virginia, I have found especially efficacious in sciatica that has resisted all 
other remedial ^ measures. The application of the hot iron and blisters 
along the course of the nerve have, in some instances, acted remedially. 

MEGRIM. 

{Sick Headache.) 

Sick headache, or hemi-crania, is a form of neuralgia attended by marked 
gastric and nervous disturbances. 

Morbid Anatomy. — Megrim is probably due to disordered cerebral circu- 
lation, the exciting cause of which is vasomotor disturbance. Changes 
similar to those of epilepsy are generally considered to be the pathological 
condition ; that is, vasomotor irritation with arterial spasm and consequent 
anaemia of the cerebral ganglia, followed by relaxation and congestion. 
The neuralgic element is possibly due to compression of nerve trunks. It 
is hardly supposable that irritating elements in the blood could have such 
a selective action upon a single nerve. This condition, however, still de- 
mands an ultimate cause, which is probably nervous (cerebro-spinal) ex- 
haustion, following prolonged irritation, as indicated in its etiology. 

Etiology. — Megrim is often hereditary, or, more exactly, the nervous 
weakness and instability which predispose to the affection are hereditary. 
Whether inherited or acquired, it commonly develops before thirty, and 
subsides in later life. Digestive disturbances are frequent exciting causes, 
but a much larger proportion of cases are due to nervous irritation and 
-exhaustion. It is an almost unfailing symptom of chronic uterine irrita- 
tion or sexual excesses, and is frequently due directly to mental labor, 
worry, or excitement. In neurasthenic patients, it is often excited by 
•over-exertion, or the lack of it, by too much or too little sleep, and by 
irritation of the nerves of special sense — flickering light or loud noises — 
and in some cases the slight disturbance of co-ordination attendant upon 
the use of the stereoscope or opera-glass is sufficient to excite an attack. 

Symptoms. — As the term indicates, hemi-crania is almost invariably 
confined to one side of the head, and is generally distinctly localized in the 
frontal, temporal, or occipital region, and even when it attacks all three 
places, or becomes diffuse, the pain is still most intense and persistent at a 
email circumscribed point in each region. In such cases there is often a 
sensation of an intra-cranial cord joining the painful points. 

Frequently, and especially in cases due to ocular strain, the eye becomes 
the seat of pain and is tender and hyperaesthetie. Early in the attack the 
face may be pale and the cardiac action slow and weak. Very soon, how- 



MEGEIM. 



1095 



ever, the head becomes hot and the pulse slow, and with each heavy heart- 
beat the carotids pulsate strongly and the pain is greatly increased. Gen- 
erally within a few hours nausea supervenes, and may be attended by dis- 
tinct recurring chills and paleness of the surface. The patient is greatly 
depressed and is wretchedly sick. If the pain is not too severe he may fall 
asleep, to wake in the morning with only a soreness about the scalp and 
stiffness of the muscles of the neck remaining. More frequently the nausea 
increases until relieved by an attack of vomiting. A few hours of sleep 
then restores the patient to his usual condition. 

Quite characteristic premonitory symptoms are present in many cases. 
The most common are disorders of vision in the form of retinal anaes- 
thesia or irritation. The anaesthetic spot may be located in any part of the 
retina, but generally affects the macula lutea. Eetinai irritation causes the 
patient to see variously colored lights and scintillations. The disturbance 
in vision may commence with a wavy glimmering at the outside of the 
field of vision or by the appearance of a black spot close to its centre. Simi- 
lar disturbances of the other nerves of sense, either irritative or paralytic, 
may be present, but they are less common than the visual disturbances. 

Hemi-crania may last from a few hours to two or three days, but in most 
cases is relieved within twenty- four hours. It is very apt to recur at regu- 
lar intervals, and become more intractable with each attack. 

Treatment. — By way of prophylaxis, the patient should avoid all known 
causes of the attack, and pursue a tonic course of living. At the beginning 
of the attack full doses of alcoholic or other stimulants may prevent its 
development. Later, the bromides, quinine, strychnia, belladonna, canna- 
bis indica, caffeine, guarana, and chloral at times afford relief. When 
nausea is present, however, an emetic, followed by a few hours' sleep, brings 
about the most speedy cure. Morphia hypodermically is the best and 
surest means for the relief of pain. Antipyrin, as in other forms of neu- 
ralgia, will often afford speedy relief. 

During the interval between the attacks the treatment should be such as 
will as far as possible render inoperative its cause. ~No two* cases will re- 
quire the same hygienic or therapeutic measures. The main thing is to 
overcome the acquired or hereditary neurotic tendencies of the patient by 
diet, exercise in the open air, and cheerful surroundings. .Drugs accom- 
plish very little for this class of sufferers except to give temporary relief. 

During the interval between the attacks the treatment should be such as 
will as far as possible render inoperative its cause. K"o two cases will 
require the same hygienic or therapeutic measures. The main thing is to 
overcome the acquired or hereditary neurotic tendencies of the patient by 
diet, exercise in the open air, and cheerful surroundings. Drugs accom- 
plish very little for this class of sufferers except to give temporary relief. 



1096 



DISEASES OE THE NERVOUS SYSTEM. 



FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM. 



I shall consider under this head : 



I. Epilepsy. 
II. Hysteria. 

III. Hystero- Epilepsy \ 

IV. Catalepsy. 

V, Neurasthenia. 



VI. Chorea. 

VII. Sunstrohe. 

VIII. Spinal Irritation, 

IX. Vertigo. 

X. Sea-sickness, 



EPILEPSY. 

Epilepsy is a chronic functional disease of the nervous centres marked by 
sudden signs of temporary loss of consciousness or some other mental dis- 
turbance, accompanied by tonic or clonic convulsions. 

In its typical and fully developed form the disease has received the name 
epilepsia gravior, or le haut mat, and when mild and incomplete is called 
epilepsia mitior, le petit mal, or epileptic vertigo. 

Morbid Anatomy. — Different portions of the nervous system have been re- 
garded as the seat of lesions which may cause epileptic seizures. Some have 
located these lesions in the convolutions of the hemispheres, the ganglia 
at the base, or the pons and medulla oblongata. Others have claimed that 
all the nervous centres are involved. Death has occurred in some cases dur- 
ing an epileptic seizure in which no change was discovered at the autopsy 
except cerebral hyperemia. Many pathologists claim that the vaso-motor 
centre in epileptics is so easily excited that slight impressions result in ar- 
terial spasm producing anaemia of the brain. Brown-Sequard states that 
the true seat of epilepsy is in nerve cells having the power of producing 
muscular contractions, and that these cells are located chiefly at the base 
of the brain. Experiments on animals show that epileptiform convulsions 
may be produced by irritation of the skin after the removal of the brain 
and cerebellum. 

The pathology of epilepsy is still obscure, and no uniform, constantly 
recurring histological changes have as yet been discovered. Eussell Rey- 
nolds sums up its pathology as follows : 

I. The seat of primary derangement is the medulla oblongata, upper 
portion of the spinal cord, and vasomotor system of nerves. 



EPILEPSY. 



1097 



II. This derangement consists in an increased and perverted readi- 
ness of action in these organs ; 1 the result of such action being the induc- 
tion of spasm in the contractile fibres of the vessels supplying the 
brain, and in those of the muscles of the face, pharynx, larynx, respi- 
ratory apparatus, and limbs generally. By contraction of the vessels, 
the brain is deprived of blood, and consciousness is arrested ; the face is, 
or may become, pale by being deprived of blood ; from contraction of the 
muscles mentioned there is arrest of respiration, the chest walls are fixed, 
and the other phenomena of the first stage of the attack are brought 
about. 

III. The arrest of breathing leads to the special convulsions of asphyxia, 
which are in direct proportion to the completeness and continuance of the 
asphyxia. 

IV. The subsequent phenomena are those of poisoned blood, i. e., of 
blood poisoned by the retention of carbonic acid, and altered by the absence 
of a due amount of oxygen. 

V. The primary nutrition change which is the starting-point of epilepsy 
may exist alone, and epilepsy be an idiopathic disease. 

VI. This change may be transmitted hereditarily. 

VII. It may be induced by conditions acting upon the nervous centres 
directly, such as mechanical injuries, overwork, isolation, emotional dis- 
turbances, excessive venery, etc. 

VIII. The nutrition change of epilepsy may be a part of some gen- 
eral metamorphosis, such as that present in the several cachexias, rheu- 
matism, gout, syphilis, scrofula, and the like ; and further, it may often 
be associated with change in the cortical substance of the cerebral hemi- 
spheres. 

IX. It may be induced by unknown circumstances determining a rela- 
tive excess of change in the medulla during the general excess and per- 
version of organic change occurring at the periods of puberty, pregnancy, 
and dentition. 

X. It may be due to diseased action extending from contiguous portions 
of the nervous centres or their appendages. 

XI. The so-called epileptic aura is a condition of sensation or of motion 
dependent upon some change in the central nervous system, and, like the 
paroxysm, is a peripheral expression of the disease ; not its cause. Paraly- 
sis of the cerebral blood-vessels, and resultant hyperemia of the medulla, is 
a constant change in a severe epileptic seizure. 

Etiology. — Thirty per cent, of epileptics give a history of an inherited 
tendency, either to epilepsy or some neurosis ; and children of consanguin- 
eous marriages are often epileptics. It most frequently develops between 
the ages of ten and twenty. The next most frequent period is between the 
second and the tenth year. In a small number of cases it exists at, or de- 

1 Gowers thinks that loss of inhibitory function of the nerve cell is far more likely than increased irri- 
tability. For a complete and exhaustive. summary concerning pathology and pathogenesis, fide Hugh- 
lings- Jackson, Medical Times and Gazette, 1879, vol. i., p. 223. 



1098 



DISEASES . OF THE NERVOUS SYSTEM. 



velops immediately after, birth. 1 Sex appears to have no influence, except 
in hereditary epilepsy, which develops earlier among girls than boys. 2 That 
puberty is an exciting cause of epilepsy is a fact accepted by the majority 
of authorities. Irritation of some portion of the nervous system is its fre- 
quent exciting cause, such as injury to peripheral nerves, the skull or 
meninges, and diseases of the brain substance. 3 Sunstroke has induced it. 
Epileptiform seizures are not infrequent symptoms of disease of different 
portions of the nervous system. Among its nervous causes, excesses in 
venery and onanism have undoubtedly been over-estimated. 

Among its psychical causes are great anxiety, grief, mental overwork, 
and long-continued depressing emotions. Sympathetic epilepsy is claimed 
to arise in children from dentition and intestinal irritation. It may arise 
from irritation of the genitals, anomalies of menstruation, and phimosis. 
Blood changes are also enumerated as among its causes. 4 

Symptoms, — The phenomena of epileptic seizures differ so widely that it 
is impossible to give a description which will answer for all cases. Epilep- 
sia gravior may or may not be preceded by premonitory symptoms. If 
present, these warnings may precede the seizure for a day or only for two 
or three minutes. The epileptic aura of Galen, the sense of a mist or va- 
por rising from the feet, occurs only in rare instances. Under the head of 
prodromata are included changes indisposition, moroseness and irritability, 
cold feet, spasm of certain muscles, epistaxis, headache, vertigo, a marked 
increase or decrease in the sexual appetite, optical illusions, hallucinations, 
involuntary discharge of urine and fasces, great somnolence or insomnia, 
darkening of the skin, changes in the appetite, cardiac palpitation, cardi- 
algia, vomiting, abundant flow of tears, and excessive secretion of saliva. 
Sometimes the attack is preceded by a definite sensation referred to the 
head, stomach, or limbs. Drawing the head toward one shoulder is some- 
times a warning of an epileptic seizure. In the majority of cases prodro- 
mata are absent, and the onset of the fit in a typical attack is sudden and 
attended by complete loss of consciousness. Uttering a loud, sharp cry, 
the epileptic falls heavily, or sinks to the ground. The face is extremely 
pale immediately before and at the time of the seizure, and there may be 
tonic spasm of the muscles of the eye and face. The pupil is invariably 
dilated at the onset. Tonic spasm of all the muscles immediately occurs ; 
the eyes are fixed and staring, and the muscles of the face, trunk, and ex- 
tremities are rigid. Opisthotonos or emprosthotonos may occur, or the 
body may be bent sidewise. The face soon becomes dark, the veins tur- 
gid, and though the carotid pulsates strongly the radial pulse is weak. 
Bespiration is impeded and asphyxia rapidly develops, until after a few 
seconds — rarely over a minute — clonic convulsions succeed the tonic spasms, 

1 Reynolds and Echeverria state that hereditary epilepsy does not develop later than the twentieth 
year. 

2 Brown-Sequard states that after the twenty-fifth year women are attacked of tener than men. 

3 Westphal {Berlin. Klin. Wochen.) has shown that in guinea-pigs blows on the head may immediately 
give rise to epileptiform attacks ; and that on pinching the skin of the epileptogenic zone several weeks 
after, convulsions will occur. 

4 Gowers states that rickets causes it, through defective nutrition of the nervous system. 



EPILEPSY. 



1099 



which, though general, are usually best marked upon one side. Sensation 
is usually wholly lost, and only in rare cases can reflex action be excited. 
The unconsciousness still continues. The muscles contracting and relaxing 
in quick succession induce the most violent contortions. The tongue is 
thrust between the teeth, which, closing upon it, cause deep indentations 
or lacerations of its edges. The teeth are sometimes broken ; bones may be 
fractured or dislocated, and muscles torn from their attachments. The 
patient froths at the mouth, and, from the injuries to the tongue, the sal- 
iva is often bloody. The body is bathed in a profuse (sometimes very 
fetid) sweat, and frequently the contents of the bladder, bowels and vesic- 
ula3 seminales are forcibly ejected. All secretions are abnormally increased. 
The breathing is forcible, irregular, and rapid, and the auxiliary muscles 
are called into play ; the face is turgid and distorted, the eyes protrude, 
the pupils are alternately dilated and contracted, inspiration is accompanied 
by loud gurgling noises, the pulse becomes full and labored, and when the 
cyanosis reaches its maximum the paroxysm, which seldom lasts longer 
than one or two minutes, begins to abate. 

The fit may terminate suddenly or gradually. If it subsides gradually 
thes}3asms become less violent and frequent, the respiration quieter and more 
regular, and the patient passes into a comatose state. Consciousness grad- 
ually returns, and the patient appears as if waked out of a deep sleep. He 
recovers rapidly or remains confused, delirious, or maniacal for hours. A 
day may elapse before complete recovery is reached. The patient has no 
recollection of the attack. The degree and duration of stupor after an at- 
tack have no relation to the duration of the convulsive period. A slight 
seizure may be followed by great mental disturbance, and vice versa. 
Marked dicrotism of the pulse often occurs as the patient is recovering con- 
sciousness ; and for twenty-four hours the ophthalmoscope shows hypere- 
mia of the fundus oculi. The urine after the attack is increased in quan- 
tity and contains an excess of urea and phosphates. 

Brown-Sequard gives the accompanying table of the causes and effects of 
an epileptic attack: 



Cause. 

I. Excitation of certain parts of 
the excito-motor organs of the nerv- 
ous centre. 

II. Contraction of the facial blood- 
vessels. 

III. Contraction of the blood-ves- 
sels of the cerebral lobes. 

IV. Extension of the excitation 
in the excito-motory organs of the 
nervous centre. 



Effect. 

I. Contraction of blood-vessels of 
the brain and face ; tonic spasm of 
the muscles of the eye and face. 

II. Facial paleness. » 

III. Loss of consciousness, con- 
gestion of the base of the brain and 
the spinal cord. 

IV. Tonic contraction of the 
laryngeal, cervical and some respira- 
tory muscles (laryngismus and trach- 
elismus). 



1100 



DISEASES OF THE NERVOUS SYSTEM. 



Cause. 

V. Tonic contraction of some re- 
spiratory and yocal muscles. 

VI. Further extension of the ex- 
citation in the excito-motory organs. 

VII. Loss of consciousness alone, 
or with tonic spasm in trunk and 
limbs. 

VIII. Laryngismus, trachelismus 
and rigid spasm of some respiratory 
muscles. 

IX. Insufficient breathing, rapid 
consumption of oxygen, and deten- 
tion of venous blood in the encepha- 
lon. 

X. Asphyxia and perhaps pressure 
by accumulated venous blood in the 
base of the brain. 

XL Exhaustion of the nervous 
power generally, and of the reflex 
excitability, especially return of reg- 
ular respiratory movements. 



Effect. 

V. Epileptic cry. 

VI. Tonic contraction reaching 
most muscles of trunk and limbs. 

VII. Fall or precipitation, forward 
or backward, to the ground. 

VIII. Insufficient breathing ; ob- 
stacle to entrance of blood into the 
chest and to its issue from the cra- 
nio-spinal cavity. 

IX. Increasing asphyxia. 



X. Clonic convulsions everywhere: 
contractions of the bowels, the blad- 
der, the womb, increase of secretions, 
efforts to inspire. 

XL Cessation of the fit, coma, or 
fatigue, headache and sleep. 



Le petit mal, or epilepsia mitior, is a momentary loss of consciousness; the 
patient while about his usual avocations suddenly stops, or drops whatever 
he may hold, has a fixed gaze for a second or two, and upon coming out of 
such a faint or blank proceeds as if nothing had happened. Sometimes 
these blanks may be accompanied by vertigo, and then the patient will 
stagger slightly. In rare cases he proceeds mechanically with what- 
ever is occupying him during the paroxysm. He often pales for a 
few minutes and then grows red in the face. The pupils are somewhat 
dilated. The mind may be distinctly confused for a long period after such 
an attack. Sometimes momentary spasmodic contractions occur in the 
muscles of the face, tongue, throat, eyes and neck. The head is turned 
slightly to one side and the face is pale. Clonic spasms never occur. 
There may be slight cyanosis when the diaphragm and respiratory muscles 
are involved. Sometimes certain fingers, or part of one extremity, suffer 
transient spasm. 

The variations from the typical phenomena of an epileptic seizure are so 
numerous that it is impossible to give them in detail ; I shall only refer to 
those which are of common occurrence. 

Sudden tonic spasm of the facial and thoracic muscles may be followed 
by a clonic convulsion without any loss of consciousness. An attack may 
be marked by such motor activity that the patient runs or walks rapidly 



EPILEPSY. 



1101 



during a period of complete unconsciousness. Sometimes maniacal excite- 
ment takes the place of the fit. 1 In this delirium an epileptic maybe 
harmless and wanders around in a dazed condition ; or be exceedingly 
dangerous to those about him. Kleptomania and dipsomania are said to 
be exhibitions of epileptic delirium. Brown-Sequard describes nocturnal 
attacks of epilepsy that not infrequently occur without the knowledge of 
the person so affected. In such cases the individual on waking is tired 
and exhausted; he has pains in the limbs, back and head, his mind is con- 
fused and his memory enfeebled ; he is disinclined to exert himself, and 
remains during the day in a confused state. His tongue shows the indents 
of the teeth, and the pillow may be blood-stained. More rarely it is found 
that an involuntary discharge of urine has occurred. Such attacks, al- 
though frequent and violent, may remain altogether unknown and unsus- 
pected by the patient or his friends. 

Between the paroxysms the condition of epileptics varies greatly. In 
the majority there is no impairment of mental or physical condition ; not 
infrequently, however, there is depression of nervous vitality and mental 
activity. Of all the abnormalities met with, sub-normal temperature is the 
most common. 2 Of the mental faculties, memory is most often impaired. 
Women show mental disturbances more frequently than men. The earlier 
epilepsy commences the less liable are mental changes to occur ; and the 
mental deterioration is in inverse ratio to that of muscular disturbance. 
The most remarkable mental phenomena are those which constitute the 
so-called epileptic mania. Epileptics are frequently gloomy, capricious 
and irritable, all the finer psychical functions are dull, acquisition of new 
ideas is difficult, and hypochondria, melancholia and imbecility may occur 
as late exhibitions of the disease. Motor disturbances, such as tremors 
and clonic or tonic spasms, are not infrequent between the paroxysms. 
Epilepsia major is more common than epilepsia mitior, and hereditary ten- 
dencies seem to predispose more to the former than to the latter. 

As regards frequency of attack there is the widest range : the first fit may 
also be the last ; they may occur once a year, or two or three times in the 
twenty-four hours. In women it sometimes seems to be connected with the 
menstrual epoch. Eighty per cent, of all epileptics are attacked oftener 
than once a month ; sometimes paroxysms occur on days that are multi- 
ples of seven. Often three or four fits occur in a day, and then ensues a 
period of immunity. When the seizures follow one another so closely as 
to leave no rest, 3 we have the status epilepticus, in which the temperature 
may rise to 108° F., or higher as death approaches. If the patient re- 
covers, bed-sores are liable to be formed. Pneumonia and pulmonary 
oedema are apt to occur in this condition. Seizures of petit mal are usually 
very frequent. All the different forms may occur in the same individual. 

Differential Diagnosis. — An epileptic seizure may be confounded with 

1 Delirium epilepticum. 

8 Brown-Sequard, in Quain's Dictionaiy, states that the health is very poor, an.opiaion antagonistic to 
all other anthorities. 

3 In Delasiaure's case there were twenty-five hundred attacks in one month in a boy of fifteen. — Traiie 
de V Epilepsie, Paris, 1854. 



1102 



DISEASES OF THE NERVOUS SYSTEM. 



cerebral apoplexy and hysteria. It is often difficult to distinguish le petit 
mat from an attack of syncope. 

Convulsions from urmmia, opium poisoning, or alcoholismus are at- 
tended by coma as the chief event, and are, each of them, accompanied 
by such peculiar signs, or urinary conditions, and give such a definite 
previous history, that they will not long be mistaken for an epileptic 
seizure. 

In the convulsions of children caused by dentition, falls, and gastric 
disturbances there is not complete loss of consciousness ; the fit is of 
shorter duration than an epileptic paroxysm, is longer in coming on, and 
is not followed by stupor. The discovery of a cause of the seizure is an 
argument against epilepsy. 

Convulsions from organic brain-disease, tumors, chronic softening, men- 
ingitis, and sclerotic processes are distinguished by the attendant inter- 
paroxysmal symptoms, viz. : pain, mental aberration of various kinds, 
paresis or paralysis, and disorders of special senses. In other words, a con- 
vulsion is a part only, and not the chief part, of the symptoms ; whereas a 
paroxysm is the prime event in epilepsy. Moreover, the previous history, 
the slowness of invasion, and the absence of subsequent stupor in organic 
brain disease will confirm the diagnosis. 

Hysterical convulsions are always preceded by hysterical symptoms ; voli- 
tional power is diminished, the fits come on gradually, the pupils are not 
dilated, there is no frothing at the mouth, loss of consciousness is not com- 
plete, tonic and clonic spasms alternate, stupor does not follow,, and the 
subsequent hysterical mania has its own peculiarities. The attack is always 
followed by a profuse flow of pale, limpid urine. 

Syncope differs from le petit mal in that the loss of consciousness is not 
sudden, is always preceded by a weak, faint, sickening sensation, recovery 
is slow, and the patient recollects the details of the syncope. Loss of con- 
sciousness is usually longer in syncope than in epilepsia mitior. 

Malingerers overact their part, the conjunctivae retain their sensibility, 
and the size of the pupils and the color of the face are both normal. 

Prognosis. — Epilepsy rarely directly causes death. But its long duration 
and the suddenness of its onset make it a dreaded disease. About two to 
five per cent, undergo spontaneous cure. 1 The curability of the disease 
diminishes with its duration. Inherited epilepsy is rarely recovered from. 
Epilepsy beginning before the twentieth and after the fiftieth year fur- 
nishes the best prognosis. Eeynolds states that the more obscure the 
origin the worse the outlook. Alcoholismus always renders the prognosis 
worse. 

Treatment. — The two things to be accomplished in the treatment of 
epilepsy are, if possible, to remove the cause or render it inoperative ; and 
to diminish the number, length and severity of the paroxysms. 

When aurm exist it may be possible to abort the fit by tying a hand- 
kerchief around a limb, pinching or rubbing the surface, irritating it by 
means of cold or galvanism, and pricking it with needles. When muscular 



1 Nothnagel. 



EPILEPSY. 



1103 



contraction precedes a fit, forcibly exciting the contracting muscles or a 
blow on them will sometimes prevent the convulsions. When disturbances 
of respiration precede a paroxysm, inhalation of ether, chloroform, or amyl 
nitrite may abort it. An emetic, purge, a hypodermic of morphia and 
atropia, ice to the nape of the neck, hot water to the extremities, valerian, 
belladonna, a large dose of chloral hydrate, breathing very fast, running, 
reading very rapidly and loudly have all been found in some instances to 
abort epileptic paroxysms. Reynolds advocates the administration of dif- 
fusible stimulants. When an epileptic fit is once established there is little 
to be done but to prevent the patient from injuring himself. The chest 
and neck should be freed from close-fitting garments, and if possible a 
piece of rubber or cloth should be inserted between the teeth. 

The measures employed for the cure of epilepsy are innumerable. Tre- 
phining over cranial depressions, operations for phimosis, excisions of 
cicatrices, removal of neuromata, opening of abscesses, ligating the caro- 
tids, application of caustics to the throat, and tracheotomy have all been 
undertaken for its cure. Since epilepsy is a neurosis, different drugs must 
not only be employed with different individuals, but the doses must be 
varied in different cases. The bromides have the most extensive reputa- 
tion, and at the present time are more used than any other remedy. They 
should be given in large doses and continuously for a long period, and only 
discontinued temporarily when the symptoms of bromism appear. Sixty 
grains of bromide of potassium a day in divided doses is the usual amount 
to commence with; it may be gradually increased until one hundred grains 
a day is administered. It is best to commence with the bromide of potash, 
the bromide of ammonium, iodide and bicarbonate of potash in a strong, 
bitter infusion — I prefer hops. With the bromides the oxide of zinc, 
strychnine, arsenic or atropia may be given. 1 Oxide of zinc (one and 
one-half grains a day at first, increasing to five grains per diem), especially 
with valerian root, or belladonna, or hyoscyamus, is regarded as next in 
efficacy to the bromides. Atropine and ammoniated sulphate of copper 
are regarded by Brown-Sequard as forming a most powerful compound in 
idiopathic epilepsy. The same authority ranks next in order the cotyledon 
umbilicus, silver nitrate and bromide of zinc. Whenever there is a weak 
pulse, the sesquicarbonate of ammonia must be substituted for the bromide 
of the same salt in the combination treatment. 2 

In mild epilepsy, or le petit mat, large doses of bronride of ammonium 
should be administered until a condition of bromism is reached. Cod-liver 
oil is especially useful in this form of epilepsy. Iron is only to be used — and 
then as the citrate — in the anaemic or cholorotic. Manganese is often ser- 
viceable here. External applications such as setons, issues, inunctions, 
croton oil, blisters, or the actual cautery to the nuchal region; have been 
extensively used without satisfactory results. Galvanization of the sympa- 



• Echeverria recommends conium, and Clonston the Indian hemp. 
2 Belladonna is recommended by Trousseau is one-fifth grain of the 
to be gradually increased until from one to two grains are taken daily. 



extract daily for the first month 



1104 



DISEASES OF THE NERVOUS SYSTEM. 



fchetic is strongly recommended by some. 1 Epileptics should lead a life 
free from mental excitement or physical excess. 2 

HYSTERIA. 

Hysteria -is a functional disorder of the nervous centres, affecting pri- 
marily the psychical faculties, especially the will, reason, imagination and 
the emotions ; and secondarily both the motor and sensory tracts, in which 
the protean manifestations at different times indicate abolition, exaltation, 
and perversion of functional activity of the nervous centres. 

Morbid Anatomy. — Hysteria has no pathological changes or morbid 
anatomy. The special functional disturbance is generally considered to be 
an exalted irritability of sensory centres and peripheral expansion, which 
results in an acquired, or is associated with a congenital, neurasthenia, 
most marked in the higher centres, but extending to those controlling auto- 
matic movements, and characterized by partial or complete suspension of 
inhibitory influence. 3 It is quite possible that in many cases the centric 
neurasthenia may be the primary condition and the cause of the exalted 
irritability. 4 

Etiology. — Hysteria affects females principally ; usually making its ap- 
pearance between the ages of puberty and thirty years. Over one-fourth 
of the cases occur between the ages of twenty and thirty ; a little less than 
one-fourth between the ages of fifteen and twenty ; and about one-sixth be- 
tween the ages of ten and fifteen. It is rarely developed after the meno- 
pause, although it frequently occurs just at the climacteric. It is most 
liable to occur in women of a neuropathic tendency and in members of 
families in which epilepsy, chorea, catalepsy, and insanity have occurred. 
Anything which affects the emotions powerfully, such as fright, anger, 
jealousy, grief, and disappointment, predisposes to its development, and 
secret nursing of imagined wrong or anxiety is especially liable to induce it. 
Sexual abuse, masturbation, onanism and premature cessation of ovulation 
are at times exciting causes of hysteria. Its relation to uterine and ovarian 
disease is direct and well established, 5 but is by no means constant, as many 
patients with severe ovarian disturbances remain entirely exempt from hys- 
terical phenomena. Hysteria is undoubtedly oftener met with in the single 
than in the married, and is intensified by the menstrual epoch. Occupa- 
tion and position in life have much to do with its production. Women 
who lead a life of continual excitement are more prone to hysteria than any 

1 Nothnagel recommends methodical hydrotherapeia for three or four months, especially in cases that 
are not inveterate. 

2 Reynolds advocates quinine, but Brown-Sequard considers it highly injurious, stating that malarial 
disease in epileptics is better treated by arsenic. Recently Lepine has had success from bleeding and 
depletion. Kunze reports radical cures from subcutaneous injection of curare ; Vallender from apomor- 
phia. Gowers, in Gulstonian Lectures, says borax deserves a trial when bromide fails. Very recently 
picrotoxine and cocculus indicus have been tried and found to produce— especially the former— most bene- 
ficial effects. 

3 Jolly and Buzzard. 

4 Rosenthal states that the vaso-motor system is also involved, and that spasm of the cerebral arteries 
and consequent anaemia are often present in hysterical paroxysms. 

6 Charcot claims that hysterical fits can be produced by firm pressure over the ovaries. 



HYSTERIA. 



1105 



other class. Among savage nations and hard-working women it is unknown 
or rare. It is said that since the blacks have been freed and their education 
and condition bettered, hysteria, previously unknown, has appeared among 
them. 

It not infrequently becomes epidemic, and is apparently contagious. 

Symptoms. — The symptoms of hysteria are manifest through all the 
nervous phenomena, and may be grouped as psychical, motor, sensory and 
sympathetic. 

I. In many cases mental and moral disturbances appear only during the 
attack, and the patient has full control of the mental powers in the inter- 
vals. More frequently, and when the condition has become chronic, the 
patients are constantly irritable and excessively emotional. As a rule their 
judgment, energy, and concentration are enfeebled, and although their 
memory is not ail ected the will-power is greatly impaired. During their hys- 
terical paroxysms they always want an audience ; they crave attention and 
sympathy, and will at all times deceive and practise most dishonest meas- 
ures to obtain them. Their emotions pass beyond their control, tears and 
laughter being apparently always at their command. Hallucinations and 
various kinds of fancies and delusions are common. 

After a violent fit of hysteria, patients often become dangerously un- 
manageable, mischievous, and highly abusive or blasphemous. The coma 
that follows an attack is like a deep sleep, and may last for hours or days. 
More or less analgesia is present, but complete unconsciousness never oc- 
curs. Probably a so-called "trance" is but prolonged hysterical coma. 
Ecstasy and somnambulism, temporary catalepsy and trance, are all 
reckoned by some among chronic hysterical psychoses. 1 

II. The motor symptoms of hysteria are very varied. Globus hysteri- 
cus is the most common ; the patient imagines that a lump rises from the 
epigastric region into the throat and remains there causing a sensation of 
choking. Spasm of the respiratory muscles produces peculiar, harsh, 
rasping, expiratory sounds, and the inspirations are prolonged, rapid, and 
whooping in character, accompanied by yawning, hiccough, laughing, 
crying, and sneezing. There is a loud, barking, brassy cough (the hyster- 
ical cough), but no expectoration. The patients claim that all voluntary 
movements are impossible ; they cannot rise or move from their beds — yet 
they gesticulate wildly and perform irrational movements in excess. The 
facial muscles are in constant action. Keflex action is so exaggerated that 
the slightest irritation produces spasms. Clonic spasms of muscles of the 
face and cervical region and of the muscles of the thigh are common. 2 
Tonic muscular spasms in the limbs are frequent, often lasting for months; 
they may suddenly disappear, but these contractions resist the influence 
of chloroform and persist during sleep. Abdominal phantom tumors are 
thus produced, but long-continued Faradization will reduce them. When 
the tonic spasms affect, as they may, portions of the alimentary canal, 

1 Griesinger and Briquet. 

2 Rhythmical contraction of the thigh muscles induces an apparent pulsation which may be mistaken for 
that of aneurism. 

70 



1106 



DISEASES OF THE NEEYOUS SYSTEM. 



vomiting, griping pains, borborygmi, eructations, diarrhoea or constipa« 
tion, and dysphagia occur. Eetention of urine and great distention of the 
bladder may happen. In rare instances the secretion of urine is almost 
entirely suppressed. 1 In hysterical hemiplegia the face and tongue are not 
involved. While walking, hysterical patients look about, whereas a true 
paralytic keeps his eye on his feet. The paraplegia may be complete and 
the patients unable to walk, but their limbs are perfectly well nourished 
and they can regain the upright position without assistance. Hysterical 
is distinguished from organic aphasia by the fact that the patient is able 
to write his wishes with the greatest readiness. Hysterical aphonia comes 
on abruptly, and as abruptly disappears. When an hysterical patient has 
a convulsive seizure the globus hystericus precedes the fall, which always 
takes place where there is no chance of injury. The patients often talk 
continuously and incoherently during their convulsive seizure, and throw 
themselves into the most grotesque attitudes. Complete loss of conscious- 
ness rarely if ever occurs. The pupils are not dilated, and no respiratory 
symptoms are present sufficient to cause asphyxia. 2 

III. Derangements of sensibility form one of the most common exhibi- 
tions of this disease. Local or general hyperaesthesia is never entirely 
absent ; it is sometimes evinced by increased acuteness of the senses. 
Photophobia is common. The sense of touch is so exaggerated that hys- 
terical women will recognize individuals by the touch ; the olfactory sense 
is also exceedingly acute, and patients are disturbed by the slightest noise 
and can recognize friends by their step at a long distance. Muscae voli- 
tantes, tinnitus aurium, pains and neuralgias in various parts are all com- 
mon. The pains complained of are greatly in excess of any discoverable 
cause, and cease when the attention of the patient is diverted. The pain 
often simulates left intercostal neuralgia or is situated over the vertebral 
spines or stomach, in the joints, mammae, skull or the iliac regions. Pain in 
the skull, as if a nail were being driven into the head, or a kettle were 
simmering on top of it, called by the ancient physicians clavus hystericus, 
is by many regarded as pathognomonic. The whole cutaneous surface 
may be hyperaesthetic, or only parts of it. Sometimes there are ob- 
served hysterical angina pectoris and hysterical peritonitis. All the 
senses in an hysterical patient are abnormally acute. The genital organs 
are often so sensitive that sexual intercourse is impossible. On the other 
hand, anaesthesia is of frequent occurrence in hysterical persons ; it may ap- 
pear in any part of the body and be limited to a distinct portion of a single 
nerve. The anaesthetic parts are usually pale and their temperature sub- 
normal. Anaesthesia may be superficial or so deep that pins can be thrust 
into the deep tissues without any expression of pain. The conjunctiva 
loses its sensitiveness and may be rubbed or touched without causing con- 
tractures of the lids. There may be coexistent loss of sensibility in the mus- 
cles, bones, and joints. 3 

1 T. Buzzard in Quain's Diction of Med. 

2 Hughhngs-Jackson advances the hypothesis that inhibitory control of the spinal cord over reflex action 
is temporarily suspended, the cerebellar influence having full play. 

3 Jolly. 



HTSTEEIA. 



1107 



In some instances the pharynx and epiglottis may be tickled or pinched, 
or irritating vapors inhaled without producing the customary results. 
Large faecal accumulation in the rectum is presumably due to similar 
anaesthesia of its mucous membranes. There may be hemiopia in one or 
both eyes, accompanied by loss of smell, taste and hearing. Sensations as 
if a limb or part were greatly enlarged or attenuated, as if the feet were 
being buoyed up or loaded with lead, or as if pins and needles were being 
thrust into the waist are of common occurrence. 1 

IV. Of the circulatory changes, cardiac palpitation is perhaps the most 
common. Feeble heart action, with a small and hard, or a full and soft 
pulse, is frequently noticed during hysterical fits. The abdominal aorta, 
and sometimes other arteries, pulsate so strongly as to suggest aneurism. Ac- 
cording as there is stimulation or paralysis of the vaso-motor nerves there 
will be a cold, pale surface or hyperemia, redness, and consequent profuse 
sweating. Coldness of the extremities is one of the most common evidences 
of vaso-motor change. The dilatation of the vessels may become so great 
that hemorrhages will occur in the skin, internal organs, genitals, and 
stomach. It is often difficult to diagnosticate hysterical hsematemesis from 
that due to ulcer. A single observation is rarely sufficient for a diagnosis. 3 
The following hysterical phenomena are all undoubtedly due to vaso-motor 
disturbances, viz. : fever and chill, flashes of heat alternating with rigors, 
hyperesthesia, enlargement and oedema of the joints, 3 an abundant flow of 
pale, clear urine deficient in salts, excessive salivation, abnormal dryness 
of the mouth, increased flow of gastric juice, an abundant secretion of 
milk, lasting for years, 4 and profuse uterine and vaginal secretions. 5 

Differential Diagnosis. — Hysteria may be mistaken for epilepsy, multiple 
sclerosis of the train and spinal cord, hypochondria, neuralgia, and uremic 
coma. It is distinguished from epilepsy by its slow onset, by incomplete 
coma, a normal pupil, sobbing and crying, and absence of subsequent 
stupor. The tongue is not bitten in hysteria. An epileptic seizure is short 
and the convulsions are not symmetrical. 

Multiple sclerosis of the train and cord is often accompanied by parox- 
ysms like those of hysteria ; but between the attacks the psychical symptoms 
and emotional disturbances are absent. 

In hypochondria the patient is always morose; there are not those varia- 
tions in temper that are so characteristic of hysteria. Hypochondria is rare 
before the thirtieth year, is more common in men than in women, and is 
seldom marked by convulsions. The two diseases may be conjoined. 



1 Charcot notices that with hemi-ansesthesia there is usually ovarian hyperesthesia of the opposite 
side. 

2 Astley Cooper and Parrot record cases where hemorrhages have occurred from the breast and con- 
junctivae. 

3 Brodie. 

4 Briquet. . 

6 Lasegue has described, under the name of hysteria peripherique, a group of cases of considerable in- 
terest, in which, although the patients do not exhibit the general hysterical temperament, the slightest 
peripheral irritation causes obstinate muscular spasms. Such are certain cases of rheumatic torticollis 
and of blepharospasm from slight and passing irritation of the conjunctiva. Lasegue says : "The tran- 
sition from the typical hysteria to the other (functional) diseases of the nervous system is not abrupt, but 
by imperceptible gradations. " 



1108 



DISEASES OF THE NERVOUS SYSTEM. 



The comatose state following an hysterical seizure is distinguished from 
urcemia by an examination of the urine, by the fact that dropsy is ab- 
sent ; and the coma is preceded by sobbing, crying, and other hysterical 
phenomena. 

Neuralgia, if of hysterical origin, ceases when the patient's attention is 
diverted. In genuine neuralgia the pain follows the distribution of a nerve, 
and there are certain recognizable painful spots ; in so-called hysterical 
neuralgias the reverse is the case. 

Organic paralysis is to be distinguished from hysterical paralysis by the 
plumpness of the limb or part in the latter, and the electrical reaction, 
which is normal. 

Prognosis. — The prognosis in hysteria is always favorable, although re- 
covery is rarely permanent, but exacerbations and remissions occur at ir- 
regular intervals. Some develop every phase of the disease at different 
epochs. Its tendency is to cease after the menopause, but it may continue 
to old age. Briquet states that when it commences in youth it is more 
persistent than when it occurs later in life. If associated with uterine 
diseases and displacements, the prognosis is better than when it is purely 
psychical. 1 When it is constitutional, hereditary, or an evidence of the 
neuropathic tendency, even temporary recovery is rare. 

The hysterical contractures, when prolonged, often cause permanent de- 
formities. 

Treatment. — Moral treatment is far more efficacious than medicines. 
Discipline, exercise in the open air, healthy occupations, early hours, and, 
if possible, a change of residence, all exercise a marked influence on 
hysterical subjects. Bromide of sodium or potassium, valerian, asafoetida, 
belladonna, hyoscyamus, and hydrate of chloral are all at times of service 
in controlling the more active manifestations of hysteria. When a cause 
can be reached it should, if possible, be immediately removed ; and uterine 
diseases and displacements must receive their appropriate treatment. Iron 
should be given when ansemia exists. Many authorities state that half 
their cases have been cured by the use of opium, and all agree that hys- 
terical patients tolerate it in large doses. The attacks may generally be 
shortened by dashing cold water over the patient, and sometimes by pres- 
sure over the ovaries. Subcutaneous injections of morphine, or inhalation 
of ether or chlorofo'rm until complete insensibility is reached, are sometimes 
advisable when the seizure is very violent. 2 In tympanitis and colic, 
enemata of asafoetida are useful. Hysterical vomiting, often very ob- 
stinate, is best treated by the blandest possible diet. In paralyses of 
hysterical origin electricity and the internal use of strychnine are some- 
times of service. Hysterical pains are most efficiently relieved by hypo- 
dermic injections of morphine. Aphonia may be treated by the elec- 
tric current. Sea-baths or a course of hydrotherapy are often highly 



1 Wunderlich and Rullier describe cases of acute fatal listeria with high temperature, great dysphagia, 
and frequent epileptiform convulsions. 

2 Reynolds, quoting Dr. Hare, states that forcibly preventing the patient from breathing for a certain 
time, by holding the nose and mouth, is followed by a long breath and a relaxation of the spasm. 



HYSTEKO- EPILEPSY. 



1109 



advantageous to hysterical subjects. Phosphorus and strychnine are re- 
garded by some as specifics, and may be given in small doses. Children 
who are peculiar and have a tendency to hysteria, should be subjected to 
a firm, gentle discipline during their childhood and period of development. 
The manner of the physician, his conversation in the presence of the pa- 
tient, the behavior of the friends and family both during and between the 
paroxysms, all have a great influence upon the case. 

HYSTEEO-EPILEPSY. 

This is a very grave form of hysteria, attended by epileptiform convul- 
sions and marked by the occurrence of peculiar anaesthesia, paralysis, and 
muscular contraction. It has no especial morbid anatomy. 

Etiology. — Epilepsy may be the primary disease, and some strong psy- 
chical disease superinduce hysteria ; or epilepsy may slowly develop after 
long-continued hysteria, The etiology is the same as that of hysteria ; but 
puberty, the menopause, and extreme fright 1 are among its most frequent 
causes. 

Symptoms. — An hysterical aura, usually abdominal, precedes the convul- 
sion, which at first is identical with an epileptic seizure. Following the 
clonic convulsions is a short period of muscular relaxation, during which 
the patient appears comatose, but which is soon followed by contortions of 
the most violent character. The motions may intentionally indicate any 
or all of the vilest passions or fears, or there may be simply irrational twist- 
in gs. Opisthotonos usually occurs after the attack, the patient usually 
suffering from hysterical excitement, laughing or crying immoderately, and 
has hallucinations and delusions resembling those of delirium tremens. 
Contractures, either paraplegic or hemiplegic, subsequently occur in one 
or more limbs, which may be persistent, and yield only to deep chloroform 
narcosis. It is to be remembered that these hysterical contractures may oc- 
cur without any other symptoms of hysteria ever having existed, or may 
follow burns. 2 After a long duration they sometimes relax from a great 
moral shock. During such a fit the temperature may rise to 105° F. 3 Ova- 
rian hyperesthesia almost invariably precedes these attacks. 4 Anaesthesia 
and analgesia are common, but usually affect only one half of the body. 

The special senses may all be affected, and color-blindness is not uncom- 
mon. 

Differential Diagnosis. — The diagnosis of hystero-epilepsy in a well-marked 
case is easily made. The salient points of hysteria and epilepsy are com- 
bined, and the picture of a patient in the fit is one that will not be con- 
founded with any other condition. 

Prognosis.— The prognosis is the same as in hysteria, and far more favor- 
able than in epilepsy. 

1 The tragedies of the Commune in Paris during the Franco-Prussian war are said to have produced man5 
severe attacks in hysterical females. 

2 Progres Medical, Feb. and March, 1883. 

3 Charcot. 

4 Charcot states that ovarialgia is an important part of the seizure. 



1110 



DISEASES OF THE NERVOUS SYSTEM. 



Treatment. — The treatment will require a combination of the remedies 
proposed for hysteria and epilepsy in the proportion that each enters as an 
element of the disease. Metallo-therapentics have been extensively em- 
ployed in the treatment of this affection. A few discs of metal are bound 
at intervals around an anaesthetic limb ; in ten to twenty minutes sensation 
returns to the skin around the discs, and then to the whole limb, but, un- 
fortunately, in the mean time corresponding parts on the other limb grad- 
ually lose their sensibility, and the results are not permanent. The slight- 
est electrical currents produce the same results. Contractures of years' 
duration often can be cured or transferred in like manner. Metals, mag- 
nets, bits of wood — all have produced the same effect. Different metals 
act on different subjects. Gold, silver, iron, tin and copper have all been 
used. Long-continued blistering and Faradization have removed contrac- 
tures of long standing. 

CATALEPSY. 

Catalepsy is a functional disease of the nervous system, closely allied to 
hysteria and epilepsy. It is characterized by loss of consciousness, sensa- 
tion and volition, accompanied by a peculiar muscular rigidity in which 
the limbs remain for some time in whatever position they are placed. 
There are no appreciable pathological changes, but the muscular rigidity 
is generally considered to be of centric origin. 

Etiology. — Catalepsy may occur at any age, but is rarely met with except 
in females about the age of puberty, and is usually associated with hys- 
terical phenomena. It may precede melancholia and epilepsy. Trau- 
matism, strong emotions, fright, shock, and, in many instances, religious 
excitement may induce an attack. Hereditary influence is frequently 
marked, and it occurs in families where insanity, mania, epilepsy, etc., have 
occurred. 1 

Symptoms. — Catalepsy occurs in paroxysms which are either regular or 
irregular. Headache, vertigo, hiccough, etc., may precede the attack. 
Consciousness is suddenly lost, and the limbs — remaining in the position 
occupied at the onset — are as rigid as if petrified, soon relax a little, how- 
ever, and can be moved, but will remain in whatever position they are 
placed. They resist passive movement as if made of wax, hence the name 
flexililitas cerea. The rigidity slowly yields to the force of gravity. Sen- 
sibility and reflex movement may be totally or partially lost ; rarely is 
there paroxysmal hyperesthesia. The respiration and heart movements 
are weak ; the face is expressionless, and often has a death-like appearance. 
The skin is cold, and the temperature is commonly lowered perhaps 2° or 
3° below normal. Substances placed in the back of the mouth are slowly 
swallowed. In a few cases there is only partial loss of consciousness, the 
patient being able to appreciate strong sensorial or emotional impressions. 
When the attack is of short duration it vanishes as quickly as it appeared ; 
and an impression upon the patient remains like that following a confused 
dream. When the attack lasts for many hours or days several paroxysms 



1 Eulenburg inclines to the view that malarial infection may cause it. 



NEURASTHENIA. 



1111 



go to make up the whole attack. Between the attacks there are no symp- 
toms as a rule. 1 The attacks may occur at regular intervals ; the slightest 
mental disturbance or excitement may bring on a paroxysm. 

Differential Diagnosis. — True catalepsy cannot be mistaken ; but it may 
be, and often has been, successfully simulated. 

Prognosis. — The prognosis is favorable, except in those cases where there 
is a marked nervous tendency in the family. The prognosis is best where 
there are no symptoms between the attacks. 

Treatment.— Treatment should be directed more especially to the accom- 
panying hysterical diathesis, but we may endeavor to rouse the patient by 
the use of ammonia, snuff, or the Faradic current. An emetic will gener- 
ally cut short an attack. 2 The wet pack and the cold douche have been 
used. Between the attacks iron, quinine and antispasmodics — valerian 
especially — are indicated. 

NEUKASTHENIA. 

Neurasthenia spinalis is a functional weakness of the spinal cord; or, as 
Rosenthal calls it, a depressed form of spinal irritation. 3 It is commonly 
known as nervous debility. Rolando, Luys and others have advanced views 
concerning the cerebellum that may lead to this organ being regarded as 
the seat of the disorder. Some authors claim that it is an anaemic condition 
of the spinal cord, but its morbid anatomy is not as yet determined. 

Etiology. — Men are far more liable to this condition than women. It 
often develops at puberty, but is common in adult and middle life. It is 
most frequent in those of a neuropathic tendency. Sexual excesses, mas- 
turbation and onanism are said to induce it. Excessive mental labor, late 
hours, long-continued emotional disturbances of any kind, insomnia, insuf- 
ficient or improper food, and excessive use of tobacco or alcohol may excite 
it in those who are predisposed to neuroses. Rosenthal claims that the pro- 
longed action of these causes in the young produces irritability of the med- 
ullary and vaso-motor centres, and thus the vascular equilibrium of the cord 
is lost. 

Symptoms. — These patients are weak, easily fatigued and prostrated by 
slight muscular exertion. They are languid and despondent. There is 
aching in the limbs, the sleep is broken, or there is actual insomnia, and 
they complain that they are always tired and the subjects of nervous debil- 
ity. They suffer constantly from dorsal and lumbar pains and nocturnal 
emissions, and the passage of a urethral sound produces excessive pain and 
sometimes convulsions. The sexual powers are enfeebled. During excite- 
ment or after the use of alcoholic stimulants, neurasthenic patients are able 
to perform a large amount of mental labor, but afterwards they are greatly 
prostrated. The emotions are easily excited, and they often imagine that 
they are the subjects of some grave organic disease. There is a tendency 

J Eulenburg states that cataleptic children are often remarkably bright.— Ziemsseri's Encyc. 
3 Gowers advocates the subcutaneous injection of apomorphia — one-twentieth to one-twelfth grain. 
3 Erb claims that it is not a manifestation of hypochondria, and that, although often combined with It 
it is to be regarded as distinctly of spinal origin. 



1112 



DISEASES OF THE NERVOUS SYSTEM. 



to melancholia and hypochondriasis. Neurasthenia is not at first accom, 
panied by anaemia, but later the insomnia and anorexia induce it. The 
tongue is coated. Flatulence, dyspepsia, and dilatation of the stomach 
are usually present. 

Often the patients haye a healthful appearance, which leads one to suspect 
that they are feigning disease. 

Differential Diagnosis. — Neurasthenia may be mistaken for incipient ataxia, 
incipient myelitis, or commencing vertebral carries. 

In ataxia the lancinating pains, disorders of sensation, the iron band sen- 
sation, the ocular symptoms and the increased galvanic excitability will 
enable one to reach a diagnosis. The paralysis which occurs in myelitis 
distinguishes it from neurasthenia. 

In spinal caries the pain on motion and the angular curvature, in con- 
nection with the traumatic history of the case, will establish the diagnosis. 

Prognosis. — The prognosis in neurasthenia is always good. It may con- 
tinue for months, or relapses occur ; but complete recovery may always 
finally be reached under proper treatment. 

Treatment. — The most important indication in this condition is to secure 
absolute rest. Change of scene, nutritious diet, outdoor life, and especially 
sound sleep at night tend to produce a cure. Sea bathing is highly rec- 
ommended, and a light wine or beer with meals is frequently of service. The 
functions of the skin should be carefully attended to. Iron, strychnine and 
some form of the hypophosphites are indicated. 

CHOEEA. 
{St. Vitus s Dance!) 

Chorea is a disease of the nervous system marked by clonic muscular con- 
tractions without order or rhythm, which tend to subside spontaneously 
after a few weeks' duration. 

Morbid Anatomy. — Chorea has usually been regarded as a purely func- 
tional disease, but recent investigations, although leaving the pathology 
still somewhat obscure, seem to indicate that active hyperemia of the 
brain and cord is always present, if not the exciting morbid condition, and 
is due to vaso-motor disturbance, which may be associated with the rheu- 
matic diathesis or result from various mental and reflex irritations. 

The occasional occurrence in chorea of capillary emboli and thrombi, 
with consequent minute points of softening in the gray matter of the 
brain, corpora striata, optic thalami and cord, together with the fact that 
in nearly all fatal cases endocarditis, with valvular vegetations, is present, 
has given rise to the supposition that these conditions represent the 
pathology. The commonly unilateral nature of the disease, its cessation 
during sleep, the absence of large emboli with consequent paralysis, and 
finally the fact that it is only in a small proportion of cases that the 
capillaries are found obstructed, are serious and fatal objections to this 
theory. 



C'HOKEA. 



1113 



Whatever the morbid condition, it probably affects more especially the 
corpus striatum, thalamus, or a single hemisphere primarily, but in severe 
cases, when the muscles of deglutition and phonation are affected, extends 
to the medulla. An ataxic gait occasionally indicates disturbance of the 
cord. 

Etiology. — Chorea is most frequently met with between the ages of six 
and sixteen, i.e., from second dentition until puberty, in children whose 
parents have suffered from hysteria, epilepsy, and other forms of func- 
tional nervous disease ; from two-thirds to three-fourths of all cases occur 
in girls. Feebleness of constitution, and the injurious system of forcing 
the education of children, as well as the conditions which tend to the 
premature development of the sexual instincts, predispose to chorea. 
Ansemia, chlorosis, onanism, and anomalies of menstruation are also pre- 
disposing causes. 

Acute articular rheumatism and its cardiac complications bear such an 
intimate relationship to chorea that many authorities regard them as one 
and the same affection under different forms. The rheumatic diathesis 
and the resulting cardiac disease must certainly be accepted as among the 
most important causes of chorea. The more directly exciting causes are 
fright, shock, and extreme mental labor or any form of severe nervous 
disturbance. 

Symptoms. — The onset is seldom well marked, although cases are record- 
ed where, after a fall or shock, not more than four hours have elapsed before 
distinct choreiform movements occurred. It may be said that in these 
cases recovery is also rapid. As a rule, the child's disposition becomes 
irritable or moody, and although choreic subjects are very excitable, there 
is decided mental weakening, indicated by loss of memory and interest in 
things that have before interested them. The sleep is disturbed and hal- 
lucinations are common, and actual mania may be a precursor of chorea. 

The first direct indications of the disease are a restlessness of movement 
and clumsy handling of the limbs. There will usually for a while be inter- 
vals when these children act naturally for a short time, but, if observed care- 
fully, and especially when they are conscious of being watched, they are 
seen to drag a foot, fidget with their fingers, twitch the shoulders, or jerk 
the head in a peculiar manner. As they gradually lose control of their 
movements they stumble in walking, spill their food or drink, and fre- 
quently drop articles they may be holding. The choreic movements are 
usually unilateral, at first confined to one hand, leg, or side of the face, 
and in a small per cent, of cases the manifestations remain limited to one 
side, but more commonly extend to the other side within a few days. 1 

In the fully developed disease the symptoms vary in degree rather than 
kind. In the mildest cases a child simply seems awkward, breaking dishes, 
stumbling about the room, hurting himself with knife and fork, or, in the 
case of older children, never being able to correctly perform tasks where 



1 Broadbent considers the parallelism between hemichorea and hemiplegia so perfect as to suggest at 
once that the two affections represent different conditions of the same nerve-centres, and that it is 
made more complete by the very discrepancies as they may at first sight appear. 



1114 



DISEASES OF THE NEKVOUS SYSTEM. 



slight dexterity is required. Irregular action of the muscles of speech 
may occur, and words may be uttered against the will of the patient. 
Spontaneous pain is often complained of in the affected side. 

In the worst form of the disease every feature and limb may be hideously 
contorted, the teeth ground together or snapped off, and bones may be 
broken. A patient will turn somersaults without rest, rush around in a 
circle, colliding with nearly everything in the room ; or, if in bed, may be 
suddenly contorted and thrown therefrom with violence enough to produce 
a fracture or dislocation. Between these two extremes are cases of every 
degree, but in all the convulsions are made up of irregular, sudden, im- 
pulsive movements, which are entirely involuntary and aggravated by every 
attempt at voluntary movements. After the muscles involved have been 
in incessant action and violent contraction for hours, muscular exhaustion 
does not occur. In most instances, however, the muscles enjoy complete 
repose during sleep. When this is not the case rapid and intense anaemia 
occurs. As in these cases movement is almost continuous, and the patient 
can neither eat nor be comfortably fed, death from exhaustion may result. 

Chorea of the laryngeal muscles is marked by a monotonous voice having 
a deep pitch, and deglutition is often greatly interfered with. The pupils 
are commonly dilated and the special senses may be slightly blunted, but 
the cutaneous sensibility is rarely affected. The bowels are constipated as 
a rule, although sometimes the faeces are involuntarily discharged. 1 After 
chorea has lasted for a long time the heart's action is disturbed ; anaemia is 
marked, and the mental condition of the child approaches that of the idiot. 
In girls who are old enough the menstrual functions will usually be de- 
ranged. The skin is harsh and dry, and in this class of patients hysteria 
often develops as a sequel. 

Chorea is almost invariably accompanied by some paresis and often by 
complete paralysis during or preceding the development of the con- 
vulsions. 

Differential Diagnosis. — Disseminated sclerosis of the nerve centres is 
accompanied by tremor and jactitation that may be mistaken for chorea, 
especially as it is a disease occurring in children. But ankle-clonus, paresis 
of both lower extremities, and the occurrence of tremor on voluntary ex- 
citation of the muscles, will decide the case. Hysteria and epilepsy are 
readily distinguished from it, as is also the tremor of old age. 

Prognosis. — Chorea is a chronic disease of varying duration, but in most 
cases lasting for two or three months. Eelapses frequently occur dur- 
ing puberty; but may occur after intervals of twenty or thirty years. 
Complete recovery is the rule ; the patient fully recovers his intelligence 
and muscular strength. Among children the mortality is about five per 
cent., and death is usually preceded by delirium, and is due usually to 
asthenia or some complication. Hemiplegia, aphasia, hemianaesthesia, 
anaemia, heart disease, rheumatism, and erysipelas or abscesses originating 
in wounds which the sufferer inflicts on himself, may be reckoned among 
the complications. Abortion or premature delivery may occur when a 



1 Bence-Jones states that the amount of urea excreted is increased. 



SUNSTROKE. 



1115 



mother is choreic. Very rarely does permanent mental derangement 
follow. 

Treatment. — Should an exciting cause be discovered (constipation or in- 
testinal worms), it must be immediately removed. In all cases mental and 
bodily rest, a generous but bland diet, and pleasant, and, if possible, rural 
surroundings should be ordered. Children with chorea should not go to 
school. Many authorities advocate a generous wine in connection with 
iron. Sleep should be secured by the use of hydrate of chloral if necessary ; 
Harley advocates conium. The most useful drugs are arsenic, zinc, the 
bromides, and hydrate of chloral. Arsenic has given me better results than 
any other drug ; it must be given in proportionately increasing doses until 
its specific physiological effect is produced. Copper, the silver salts, and 
strychnia are much used by the French. 1 AYeir Mitchell has successfully 
used salicylate of soda, probably in rheumatic cases. In extreme cases 
chloroform and other anaesthetics may be needed. The hypodermic injec- 
tion of curare, friction-electricity, and galvanism are recommended. Baths, 
wet packs, or a thorough rubbing often act beneficially, and the ether 
spray along the spine seems to induce sleep and diminish violence of the 
choreic movements 2 

SU^STEOKE. 

(Insolation.) 

Insolation is that complex of symptoms occurring in persons exposed to 
extreme heat under unfavorable circumstances. 

Morbid Anatomy. — The heart is usually firmly contracted, but it may be 
flaccid. Tha left heart is empty, while the right side and the venous tracts 
are filled with dark, often fluid blood. The blood is seldom coagulated ; 
its corpuscles are crenated and do not tend to form rouleaux, and contain 
less oxygen than normal. The lungs are intensely congested, cedematous, 
and sometimes exhibit spots of hemorrhage. The spleen is swollen 
and soft, and, with the kidney and liver, exhibits cloudy swelling or paren- 
chymatous degeneration. The meninges are intensely hypersemic, and there 
may be evidences of incipient meningitis. • The ventricles of the brain con- 
tain more or less serum, and the brain substance itself is congested or hem- 
orrhage has occurred into it. The cord is sometimes abnormally soft. In 
severe cases the body is covered with ecchymoses, and sub-serous hemor- 
rhages are common. In the neck the sympathetic ganglia, the vagi, and 
the connective-tissue are surround 2 J by, or infiltrated with blood. Eigor 
mortis comes on very rapidly. 3 

Insolation generally results from exposure to heat, in persons who are 
exhausted by either mental or physical labor. 

1 Gaz. Medical, Paris, Oct., 1846. Jour, de VAnat. et de Phys., 1874 ; also Trousseau. 

2 In the Children's Hospital at Paris much, reliance is placed on gymnastic exercise, performed with 
pleasant surroundings and music. 

3 Very recently Arndt states that in his autopsies there was anaemia of the brain and its membranes ; 
and that observers must have been misled by the blood escaping from large congested vessels, and running 
over an anaemic brain. By him all the viscera are described as pale and cedematous. Yirchow''s Archiv., 
vol.&4, pp. 15-39. See also Koster in Berlin. Klin. WocTien., No. 34, 1875. Also for July 17th, 1876. 



1116 



DISEASES OF THE NEBVOUS SYSTEM. 



Etiology. — Workmen, soldiers on the march, stokers and cab-drivers, or 
brain-workers and those who are suffering anxiety or mental distress are 
more liable to be overcome by the heat. Hot, wet, muggy days — our Au- 
gust dog-days — are the most favorable for its occurrence. Acclimatization 
has very much to do with its development. Nearly all new arrivals in India 
at first suffer more or less severely from the heat. Nevertheless, when a 
certain temperature of the air is reached all alike succumb. 1 Dry, hot 
winds are not prejudicial. In Dakota men can work all day exposed to the 
sun when the temperature of the air is at least 140 c to 160° R, while in 
New York on a cloudy, wet day in August, with the temperature at only 
93° F., large numbers of men and animals are prostrated. The vigorous, 
thin, healthy individual who leads a temperate and regular life seldom 
suffers from the heat; while those who drink freely of alcoholic beverages 
and dissipate during the summer months are those that most commonly 
suffer. Large numbers are affected just after eating a hearty meal. 2 

Symptoms. — The majority of cases occur in the middle of the day. In 
mild cases the patient suddenly becomes exhausted, and probably faints or 
becomes semi-comatose. He is utterly prostrated ; the skin is pale, cold, and 
moist, the pulse is quick and feeble, various colored spots appear before the 
eyes, and all kinds of symptoms are referred to the head — floating, swim- 
ming, vertigo, fulness, neuralgic pains, etc. These cases may recover, or 
collapse may terminate fatally from heart failure. 

In the fondroyante form a man may be struck down suddenly, or there 
may be prodromata, which are generally depression of spirits, muscular 
weakness, dyspnoea, epigastric oppression, and perhaps nausea and vomit- 
ing. Unconsciousness suddenly follows ; the skin is cold, the pulse is fee- 
ble, respiration and circulation are markedly interfered with, and death 
may result from heart-failure due to injury of the nerve centres from sud- 
den elevation of temperature. Reaction may set in, but it is, at best, te- 
dious and imperfect. This form is a true coup de soleil. 

In another form called tliermic j 'over the temperature rises to 108° ot 
110° F., or even higher. This is due to the influence of heat on the 
nerve centres and subsequent action upon the vaso-motor system. It often 
occurs at night and in those who are dissipated or worn out, or are in the 
midst of anti-hygienic surroundings. There is great restlessness, thirst, 
and dyspnoea. The skin is burning hot, and either dry or moist. The 
upper part of the body is congested and livid ; the pulse may be full and 
labored or quick and jerking, and the carotids pulsate forcibly. The 
pupils are at first contracted but later widely dilated, and the frequent 
micturition of the early stages gives place to urinary suppression. De- 
lirium and epileptiform convulsions are common. Toward the end the 
pulse becomes extremely rapid and feeble, the patient passes into a com- 
plete coma, the breathing is sighing or stertorous, sometimes peculiarly 
moaning, and the urine and faeces are passed involuntarily. Some of these 



1 The East Indian loomarna, or hot wind stroke. 

2 J. Fayrer states that the most freqnent cases are those that come on in houses, ships, tents, laundries, 
cook-rooms, etc., during the night, or in the day, away from the direct solar rays. 



SPINAL IRRITATION. 



1117 



cases are marked by persistent vomiting and purging ; such cases rarely 
recover. 

Differential Diagnosis. — Severe cases attended by hyperpyrexia cannot be 
confounded with any other disease. Moderately severe cases, however, 
may be mistaken for acute meningitis. In the latter the projectile vomit- 
ing, the boat-belly, the pale face, the tdche cerebrate, and the tense, hard, 
wiry puLe are in striking contrast to the symptoms of the former. The 
history of the case is always important. Under the head of acute alco- 
holismus, are given the symptoms of alcoholic coma, which may be con- 
founded with sunstroke. 

Prognosis. — The prognosis, except in mild cases, is very bad ; nearly one- 
half die. Many who recover are invalids for life. Among the sequelae 
are a sub-acute or chronic meningitis, epilepsy, insanity (in every degree), 
partial paraplegia or hemiplegia, loss of memory, blinduess, extreme in- 
tolerance of heat, almost constant headache and, in many cases, great irri- 
tability of temper. 

Treatment. — In all cases the patient must have absolute rest and plenty 
of cool, fresh air. The more these patients are carried about the worse 
their chances. All tight or needless clothing should be at once removed. 
Stimulants are often necessary ; if they excite vomiting they should be 
given hypodermically or as enemata. Ether, musk, carbonate of ammonia, 
turpentine, etc., are recommended. 

In most cases the cold water treatment is the best. The patient should 
be taken to the nearest pump, stream, or water-tank and immersed for a 
considerable time, or a stream of cold water should be poured over the 
head, neck and back. Between the baths dry cups may be applied, and 
during the baths stimulants may be given if the pulse demands them. A 
patient should always be removed from the bath before the temperature 
falls to normal. Purgative enemata and cardiac stimulation, with the 
cold water treatment, are all that is required in those moderately severe 
cases where the temperature does not rise above 105° F. 

In thermic fever, venesection is contra-indicated. Ice water should be' 
applied to the surface, the bowels should be moved by a brisk saline, and 
morphine and quinine given hypodermically. Blisters about the nuchal 
region are often beneficial. The severe cerebral symptoms in this form 
are often relieved by the inhalation of ether or chloroform. These patients 
need careful watching during convalescence, and should remove to a cool 
climate, and engage in no business that demands active brain work. It is 
in this last-named variety that rapid lowering of the temperature by the 
application of cold to the surface is of the greatest importance. 

SPINAL IRRITATION. 

This is always functional. Strictly speaking, it has no morbid anatomy, 
but in most cases is associated with congestion or anaemia. 

Etiology.— It occurs chiefly in women between the ages of fifteen and 
twenty-five. Spinal shock, or concussion from any cause, and all those 



1118 



DISEASES CF THE NEKVOUS SYSTEM. 



practices and habits which cause nervous strain and result in nervous ex- 
haustion, may also produce spinal irritation. Chronic alcoholism and the 
opium habit may also induce it. All severe diseases where there is a pro- 
longed drain 1 on the system will be followed by spinal irritation. A neu- 
ropathic tendency or hysteria often accompanies or causes spinal irrita- 
tion. 

Symptoms. — The one constant and special symptom of spinal irritation is 
tenderness, which may be excited either by pressure or motion. It may 
extend along the entire spine, or be localized over a single vertebra. This 
tenderness, which varies greatly in degree, becomes marked on the ap- 
plication of heat, cold, electricity, and other irritants. The spinous proc- 
ess is the place where pressure causes greatest pain, and . if severe it 
may excite convulsions and paraplegic or cataleptic symptoms. Tactile 
hyperesthesia is very marked, but anaesthesia is rare, and myalgia may co- 
exist with pains in internal organs. In about half the cases it is spon- 
taneous ; its character is very variable, but its seat is generally at the 
point of exit of the nerves from the spinal column. 

Motor disturbances are common. Weariness, heaviness, and pseudo- 
paraplegia of the lower limbs follow the slightest exertion. Contraction 
occurs in some muscles, especially those of the forearm, and twitchings, 
spasms, and choreic movements may be present. Cardiac palpitation is 
very common ; and nausea and vomiting, nervous cough, embarrassed 
phonation, deglutition, and breathing, or attacks of fainting are not un- 
common. 

Patients with spinal irritation are depressed, melancholy, and irritable, 
and subject to insomnia, headache, dizziness, and disturbances of the 
special senses. Vaso-motor changes are marked. The extremities are cold, 
sometimes blue, and the face alternately pales and flushes. 

When the point of tenderness is in the cervical region the pains are re- 
ferred to the head, pharynx, and chest, and are associated with psychical 
disturbances. When it is lower there are respiratory and cardiac symptoms, 
and if in the dorsal region it is accompanied by pain in the stomach, with 
dyspepsia, nausea, and vomiting. This last is the most frequent seat of 
the disease. Lumbar spinal irritation is less common and is indicated by 
neuralgic pains and weakness in the lower limbs, myalgia in the abdomi- 
nal and lumbar regions, spasm of the vesical and anal sphincters, uterine 
and ovarian pains, and disorders of menstruation. 

In many cases there is dysuria and vesical spasm, increased desire to 
urinate, and the discharge of a large amount of pale, limpid urine may 
occur. Sometimes the liver, kidneys, or bowels are the seat of functional 
derangements. The disease may progress slowly or it may be of short du- 
ration, and rapidly become severe or as rapidly improve. 

The symptoms are always variable and inconstant, and the pains often 
shift from one part to another. No true paralysis of limbs or of the sphinc- 
ters ever occurs. Sometimes spinal irritation will suddenly pass into neu- 
rasthenia. 

» Hammond calls spinal irritation anaemia of the posterior columns of the cord. 



VERTIGO. 



1119 



Differential Diagnosis. — Spinal irritation may be mistaken for spinal con- 
gestion, meningitis, myelitis, tumors, and tetany. 

In spinal congestion there is no tenderness. Paralytic symptoms are 
frequently present, and gastric and cardiac derangements are never prom- 
inent. In spinal congestion the symptoms are aggravated by the supine 
position, in spinal irritation the reverse is the case. It is claimed that the 
subcutaneous injection of one-thirtieth grain of strychnine will aggravate 
the symptoms in spinal congestion, while in spinal irritation its adminis- 
tration affords relief. Spinal irritation is of much longer duration than 
congestion. 

Spinal meningitis is accompanied by pyrexia, and the pain in the spine 
is increased by motion, so that the patient assumes, and remains in a fixed 
position. The pain is violent and diffused in meningitis, and muscular 
spasms occur in the back and neck, which are never present in spinal irri- 
tation. 

The presence of the iron-band sensation about the waist, paralyses, vesi- 
cal irritation, and relaxation of the sphincters, and anaesthesia, especially 
in the early part of the disease, are almost diagnostic of myelitis, and are 
never met with in spinal irritation. 

Spinal irritation is differentiated from spinal tumors by the fact that in 
the latter the symptoms are localized, permanent, and unaccompanied by 
visceral derangements, which in irritation assume such a variety of forms. 

The rare disease called tetany by Trousseau is differentiated from spinal 
irritation by the muscular contractions, which are accompanied by trem- 
bling, anaesthesia, and a feeling of intense fatigue. 

Prognosis. — The prognosis is favorable, although after apparent recovery 
the disease is apt to return. Yery frequently it resists treatment, especially 
if gout, rheumatism, scrofula or syphilis exist. 

Treatment. — The remedies which are employed in the treatment of anae- 
mia are always indicated in spinal irritation. Alcoholic stimulants are 
usually of service and in many cases must be given freely, combined with 
a meat diet and exposure to sunlight and fresh air. Injections of morphia 
or atropia combined with strychnine should be given over the site of ten- 
derness, the dose at first being small and gradually increased to the point 
of relieving pain. Aconite and veratria may be applied locally in the form 
of an ointment. The galvanic current and the Faradic current in some 
cases will give immediate relief. The daily application of the ice-poultice 
or the actual cautery is highly recommended. Absolute rest in the coun- 
try with a highly nutritious diet often does more for this class of patients 
than any other treatment. 

YERTIGO. 

Vertigo has bc-n well defined as the consciousness of disordered equili- 
bration. It may vary from an uncomfortable sensation to one in which 
the patient is unable to maintain his equilibrium. It may be momentary 
or of long duration. 



1120 



DISEASES OF THE NERVOUS SYSTEM. 



Morbid Anatomy. — Lesions are only found in labyrinthine or apoplecti- 
form vertigo, called Meniere's disease ; all other varieties are purely func- 
tional. In aural vertigo there may be found hemorrhage, congestion, or 
inflammation of the labyrinth ; or there may be evidences of otitis media, 
obstruction of the Eustachian tube, or the presence of foreign bodies which 
press upon the tympanic membrane. 

Etiology. — Vertigo has been divided into ocular, aural, stomachic, ner- 
vous, epileptic, and gouty. 

I. Paralysis of a single muscle may cause ocular vertigo. 

II. Meniere's disease may be caused by disease of the semicircular 
canals and cochlea, tympanic catarrh, or spasm of the tensor tympani, 
paralysis of the stapedius, or by syringing the ears, especially when the 
tympanic membrane is perforated. Wax and foreign bodies in the meatus 
externus may also induce it. 1 

III. Gastric vertigo is the most common, and is an almost invariable 
attendant on dyspepsia. Hepatic disorders, perhaps cholaemia, or choles- 
terasmia may induce it. 

IV. Nervous vertigo is induced by physical or nervous excesses, and 
Eamskill ranks vertigo from overwork as next to gastric in frequency. 
Those who are ill-fed and overworked are predisposed to it. It is also 
caused by excessive use of tea, coffee, tobacco, and alcohol. Vertigo is 
commonly present in megrim or sick or nervous headache. 

V. Epileptic vertigo precedes an epileptic seizure, and usually does not 
occur without a well-marked paroxysm. Vertigo is also a common symp- 
tom in many diseases of the nervous system, such as cerebral tumors, cere- 
bral apoplexy, sclerosis, tabes, and cerebellar disease. 

VI. Gouty vertigo is due to the blood-changes which characterize the 
gouty diathesis. The vertigo of the aged is a result of disordered cerebral 
circulation, produced by the senile condition of the heart and vessels. 
Chronic malarial infection frequently induces "cachaamic" vertigo. 

Symptoms. — The sensation may be that of objects moving around the pa- 
tient, or of the patient moving around objects which remain stationary. 
There may be a feeling of confusion or instability, or the movements may 
be uncertain and unsteady. More or less suddenly a giddy sensation comes 
on, objects become indistinct, the patient staggers, and perhaps falls, un- 
less he grasps something to steady himself. There is no loss of conscious- 
ness. Nausea and vomiting are not infrequent, and there is ringing in the 
ears, fluttering in the heart, and external sounds are greatly magnified. 

The first symptoms in ocular vertigo will be running together of the 
letters on the page, headache, nausea, and pains in the eyes. In Meniere's 
disease slight or serious tinnitus aurium accompanies the vertigo. Sud- 
denly it becomes greatly exaggerated, and the patient feels as if he were in 
motion, or actually moves in a direction opposite to the side on which the 
ear is affected. The motion may be forwards or backwards, to one side, or 
about a vertical axis. These patients may be thrown to the ground, so in- 



1 Knapp believes that there is always either a hemorrhage or serous or purulent exudation into the 
semi circular canals.— Archir. Ophth. and Otol, vol. ii., No. 1. 



VERTIGO. 



1121 



tense are the movements. The eyes sometimes oscillate. Consciousness is 
rarely lost. 

After the attack of vertigo passes off deafness remains. The vertigo and 
vomiting may continue for some time, and are increased by the upright 
position. One attack follows another, until a persistent vertiginous state 
is reached. When permanent deafness occurs, the vertigo ceases. 

Gastric vertigo is accompanied by dyspeptic symptoms, nausea, pyrosis, 
heartburn, flatulence, diarrhoea, or constipation with pain and fulness in 
the hypogastrium. It is often so severe and sudden in its onset that the 
patient thinks he is soon to have a stroke of paralysis. The mental state 
is often deplorable, and true melancholia may ensue. 

Nervous vertigo is apt to occur after excessive mental effort : the 
patient while standing experiences a dizzy, sick sensation, which, is rarely 
severe ; objects seem to whirl for a moment, and there is a slight tendency 
to fall. This form of vertigo not infrequently precedes softening of the 
brain in those who are overworked and badly nourished. Irritability, 
restlessness and insomnia often accompany it. And though gastric dis- 
turbances may be present, their relief is not followed by a relief of the 
vertigo. Sick headaches are frequently accompanied by nausea, vomiting 
and this form of vertigo. 

In epileptic vertigo the vertiginous sensation either replaces the fit or 
accompanies it. After a paroxysm of gouty arthritis an attack of vertigo 
is not uncommon. 

Differential Diagnosis. — The vertigo of Meniere's disease may be distin- 
guished from that of epilepsy, apoplexy, gastric derangements and the other 
causes of vertigo, by the co-existence of tinnitus aurium, deafness, com- 
bined with syncope, nausea and vomiting. The movements are in a uni- 
form direction and tingling and numbness are absent. 1 

An otoscopic examination should be made in all cases of continued 
vertigo, &nd the tuning-fork and watch test should be employed. 

Prognosis. — Vertigo in the adult, unaccompanied by visceral diseases, is 
not dangerous. In Meniere's disease, when the labyrinthine affection is 
due to some remediable defect, the disease will subside on removal of the 
cause — such as cerumen, tympanic catarrh, etc. When the lesion is pri- 
marily of the labyrinth, a certain degree of deafness and tinnitus always 
remains, and recurrence of the attack is to be anticipated. The longer 
an attack has existed the better the prognosis. 

Treatment. — Gastric vertigo demands the treatment already given under 
the head of dyspepsia. When disorders of vision are the cause of vertigo, 
rest for the eyes and properly adjusted glasses will remove it. In Me- 
niere's disease the patient should be placed in the recumbent posture and 
a full dose of bromide of potassium or ammonium given, followed by qui- 
nine in full doses. Charcot states that this plan is attended by the best 
results. 2 

1 Woakes states that aching of the upper extremities and discoloration of the hands may occur from 
irradiation of the irritation from the inferior cervical ganglion to the brachhil plexus. 

2 Gowers and MacKenzie recommend- gelseminm, salicylate of soda, counter-irritants, or even the 
actual cautery applied to the mastoid region. 

71 



1122 



DISEASES OF THE NERVOUS SYSTEM. 



In nervous vertigo, iron, quinine, strychnine, and the removal of the 
cause are sufficient. In the overworked and under-fed, wine, hypophos- 
phites and a nutritious diet are indicated. 

The vertigo of old age is benefited by the bichloride of mercury and the 
tincture of iron ; a highly nutritious diet and small doses of Burgundy 
wine are also of service in such cases. 

SEASICKNESS. 

The term seasickness is applied to a peculiar form of functional disturb- 
ance of the nervous system characterized by severe depression and persistent 
nausea and vomiting. 

Morbid Anatomy. — The only organic changes which have been found, 
which are probably secondary, are slight hyperemia of the gastric mucous 
membrane, due to the prolonged efforts at vomiting and the presence of 
abnormal quantities of gastric juice, and cerebral ansemia with congestion 
of the spinal centres. The primary irritation may properly be considered 
as a form of shock arising from the unusual combination of nervous im- 
pressions calling for unaccustomed action on the part of the nerve centres. 
In other words, the nerve centres are embarrassed, and the resulting nervous 
irritation manifests itself through vaso-motor disturbances in precisely the 
same manner as is seen when persons blush under embarrassing circum- 
stances or pale when startled. In the present instance this disturbance, 
though general, is most marked in gastro-intestinal and cardiac derange- 
ments. Paleness of the surface from vaso-motor irritation is probably asso- 
ciated with anaemia of the brain and congestion of the spinal centres. 1 As 
a consequence there is irritation of those centres, manifested by severe gas- 
tric irritability, with nausea and vomiting of centric origin. 

Etiology.— As indicated in the name, seasickness is most commonly the 
result of the motion of a ship. It may, however, be the result of any un- 
usual motions to which the person is unaccustomed, and especially such as 
raise the body rapidly or suddenly allow it to fall, as the motion of a swing 
or an elevator. Waltzing, riding backwards, turning a somersault, or the 
sudden jerk of a railroad train as it starts or stops or goes rapidly around 
curves in the track, may each produce a precisely similar condition. They 
are not usually followed by the full development of the disease, solely be- 
cause they are not repeated or continued sufficiently long. 

Moreover, it is not always necessary that the patient himself should be 
moved. Frequently, simply watching oscillating objects is sufficient to 
produce a mild form of sickness. Personal idiosyncrasy is a very impor- 
tant factor in predisposing to seasickness. 1 Some persons never suffer, even 



1 Dr. Clapham reports an autopsy nride four hours after death upon a man accidentally killed while 
vomiting, in which there was intense congestion of the spinal cord and distention of the vessels, closely 
resembling the condition found in an epileptic who had died during an epileptic seizure.— London Lancet, 
1864. 

' 2 In some instances naval officers of many years' experience have been led to leave their profession 
from their inability to accustom themselves to the sea. 



SEASICKNESS. 



1123 



under the most trying circumstances, while others are unable to enaure the 
slightest motion on the water or elsewhere. This peculiar susceptibility 
varies also in the same person, and an individual who has resisted through 
several sea voyages may finally succumb during a sail on some small inland 
lake. 

Habit and experience are generally suffiicent to do away entirely with the 
susceptibility to the disease, but occasionally an individual suffers, it may 
be with increasing severity, whenever he is on rough water. 

Symptoms. — Seasickness usually presents the two stages of (1) depression 
and exhaustion, and (2) reaction. 

It begins with a sense of weight and epigastric oppression, often described 
as a feeling of coldness, which at first may be distinctly intermittent, oc- 
curring only during the rapid rise and fall of the vessel. It may, however, 
be continuous from the start, and even at first be a distinct nausea. In any 
event it speedily becomes so, and is accompanied by vertigo and headache. 

ausea is quickly followed by vomiting, which partakes of the nature of both 
gastric and cerebral vomiting. Nausea is always most intense, and at the 
same tinlo the vomiting is often sudden and projectile, as from a central 
cause. As the vomiting continues the ejected matter is composed of in- 
tensely acid gastro-biliary secretions. Constipation is the rule, and all the 
secretions except the saliva are decreased. The appetite is entirely lost, and 
there is a marked repugnance to food, and especially to all forms of fat. In 
many cases the simple smell or thought of food is sufficient to excite a 
paroxysm of vomiting. In this stage the mental depression is very charac- 
teristic, the patients almost exulting in the thought of shipwreck as afford- 
ing relief from their sufferings. In the majority of cases this condition con- 
tinues from three to five days, provided the voyage is of that length, during 
which time the nausea, vomiting and mental depression continue with vary- 
ing intensity, and is then followed by reaction and a more or less rapid dis- 
appearance of the vomiting, with return to the normal condition. 

In such cases, owing to the enforced abstinence, there is for a time a rav- 
enous appetite and a feeling of special well being. 

In other cases, however, the stage of depression continues until the pa- 
tient is again on terra fir ma, lasting it may be for weeks, or it may in a few 
days pass into a stage of partial collapse. The patient is sleepy and apa- 
thetic, the surface is cold, and he suffers from neuralgic pains or general 
numbness. Finally, a partial coma may supervene and the case assume a 
very grave aspect. 

Convalescence is generally rapid, and the patient passes from a state of 
the greatest depression to one of comfort and entire recovery within a few 
hours ; but when the case has been prolonged, convalescence may be de- 
layed and be attended by rise in temperature and other febrile conditions, 

Other forms of seasickness present differences of degree rather than of 
kind. 

Diagnosis. — Owing to the peculiar circumstances under which it is devel- 
oped, seasickness can rarely be mistaken for any other condition. It may 
simulate an attack of gastro- enteritis in the early stages. In seasickness 



1124 



DISEASES OF THE NERVOUS SYSTEM. 



constipation is the rule, and the intense nausea, the persistent violent vom- 
iting, and the loathing of food are much more marked. Gastro-enteritis is 
most common in children, while they seldom suffer severely from seasickness. 

Prognosis. — It is very rarely fatal, but occasionally a condition of collapse 
develops which, if not assiduously treated, may pass into coma and death. 
A general irritability of the gastro-intestinal mucous membrane often re- 
mains for some time after a prolonged sickness. 

Treatment. — The remedies proposed and tried for seasickness are innu- 
merable, but as most of them are only palliative or worse than useless it is 
unnecessary to enumerate them. Two general plans of treatment have been 
adopted, based upon the accepted pathology of vaso-motor disturbance and 
spinal congestion, (1) the sedative, and (2) the stimulant. Among the 
remedies of the first class counter-irritation to the spine, or ice bags, the 
bromides and nitrite of amyl have proved the most useful. The applica- 
tion of ice to the spine was advocated by Dr. Chapman as being the best 
means for controlling spinal congestion. It is of decided value, but is un- 
comfortable and hardly available for a large number of cases. The bro- 
mides are often used successfully, but their use must be begun some time 
before the voyage and continued in large doses until the patient is fully ac- 
customed to the motion of the sea. Amyl nitrite, both from the rapidity 
with which it acts and the certainty of its results, seems to be the most de- 
sirable and efficacious remedy yet proposed. It should be given in full 
doses upon the first appearance of epigastric distress, and repeated as nec- 
essary. 1 

Under the class of stimulant remedies the various forms of alcohol and 
the diffusible stimulants are most used, but the results, though good in some 
cases, are generally far from satisfactory. 

In some cases of slight disturbance, any device which controls the move- 
ments of the diaphragm may be sufficient to prevent the development of vom- 
iting. Among the most successful of these is a prolonged even inspiration 
as the vessel rises, followed by a similar expiration during descent. It 
must be confessed, however, that in many instances all remedies are un- 
availing, and only time and experience can effect a cure. 

1 Dr. Clapham {Lancet, vol. ii., 1875, p. 276) reports 121 successful cases out of a total of 124 iu which amy! 
nitrite was used. 



INDEX. 



Abdominal aneurism, differential diagnosis, 568. 

etiology, 507. 

morbid* anatomy, 567. 

pbysical signs, 5fc8. 

prognosis, 568. 

symptoms, 567. 

treatment, 568. 
Abdominal dropsy. See Ascites, 365. 
Abortive form of "typhoid fever, 674. 
Abortive typhus, 772. 
Abscess, 4. 

abscess, bronchial, 157. 
Abscess, metastatic, 725. 

Abscess of the brain. See Brain, abscess of, 1017. 
Abscess of the liver. See Hepatitis, suppurative, 383. 
Abscess, pericaecal. % See Perityphlitis, 313. 
Abscess, perinephritic. See Perinephri tis, 637. 
Abscess, retropharyngeal. See Retropharyngeal ab- 
scess, -251. 
Acholia. See Bile-ducts, 431. 
Achorion Schonlinii, 34. 
Actinomyces, 34. 

Active hvperaemia of the liver. See Liver, hypere- 
mia of, 369. 

Acute anterior polio-myelitis. See Infantile spinal 

paralysis, 1048. 
Acute aortitis 547. 

Acute articular rheumatism. See Rheumatism, artic- 
ular, 835. 

Acute ascending paralysis. See Paralysis, acute 

ascending, 1070. 
Acute Bright's disease of the kidney. See Kidney, 

acute Brighfs disease of, 592. 
Acute bulbar paralysis. See Paralysis, acute bulbar, 

1043. 

Acute capillary bronchitis, 72. 
Acute catarrhal bronchitis, 68. 
Acute catarrhal laryngitis, 43. 
Acute coryza, 35. 
Acute croupous laryngitis, 53. 
Acute endarteritis. See Endarteritis, acute, 547. 
Acute endocarditis. See Endocarditis, acute, 465. 
Acute gastric catarrh. See Sub-acute gastritis, 251. 
Acute general diseases, classification of, 648. 
definition of, 647. 

theories regarding the nature of, 64S. 
Acute hydrocephalus. See Meningitis, tubercular, 
985. 

Acute intestinal catarrh. See Enteritis, 287. 
Acute meningitis. See Meningitis, acute. 977. 
Acuta miliary tuberculosis. See Tuberculosis, acute 

miliary, 749. 
Acute myelitis. See Myelitis, acute, 1037. 
Acute panceatitis. See Pancreatitis, acute, 444. 
Acute parenchymatous nephritis. See Nephritis, 51)2. 
Acute pericarditis. See Pericarditis, acute, 454. 
Acute phthisis. See Pulmonary tuberculosis, 202. 
Acute spinal paralysis of adults. See Paralysis, 

acute spinal of adults. 1051. 
Acute ulcerative endocarditis. See Endocarditis, 

infectious. 437. 
Acute uraemia. See Uraemia, 578. 
Acu e yellow atrophv of liver. See Parenchymatous 

hepatitis, 359. 
Addison, 92?. 

Addison's disease, differential diagnosis, 939. 
etioloiry. £38. 
morbid anatomy, 937. 
prognosis, 939. 
symptoms, 939. 
treatment, 940. 



Adhesive pleurisy. See Pleurisy, 192. 
Adhesive pylephlebitis. See Pylephlebitis, adhesive, 
396. 

Adults, acute spinal paralysis of. See Paralysis, 

acute spinal, of adults, 1051. 
Albrecht, 740. 
Albumen in urine, 571. 
Alcoholism, differential diagnosis, 955. 

etiology, 954. 

morbid anatomy, 953. 

prognosis, 956. 

symptoms, 954. 

treatment. 956. 
" Alcoholismus.*' See Alcoholism, 953. 
AUbutt, 235, 479. 
Althaus, 905. 

Amaurosis in renal disease. 615. 
Ammonaenria, differential diagnosis, 941. 

etiology, 940. 

morbid anatomy, 940. 

prognosis, 941. 

symptoms, 940. 

treatment, 941. 
Amyl nitrate, in valvular diseases, 505. 
Amyloid degeneration of arteries, 549. 
Amyloid degeneration of the heart. See Heart, 

amyloid degeneration of, 529. 
Amyloid degeneration of the intestines. See Intes- 
tines, waxy degeneration of, 329. 
Amyloid degeneration of the liver^ 400. See Liver. 
Amyloid de<?enerati< n of the spleen. See Spleen, 

waxy degeneration of, 451. 
Amyloid form of Bright's disease. See Kidney, 617. 
Amyotrophic lateral sclerosis, differential diagnosis, 
1U68. 

etiology, 1067. 

morbid anatomy, 1067. 

prognosis, 1068. 

symptoms, 1068. 

treatment, 1068. 
Anaemia, differential diagnosis, 924. 

etiology, 923. 

morbid anatomy, 923. 

prognosis, 925. 

symptoms, 924. 

treatment, 925. 
Anaemia, cerebral. See Cerebral anaemia, 975. 
Anaemia of the lungs, 157. 

Anaemia, progressive pernicious. See Progressive 

pernicious anaemia, 928. 
Anaemia, pulmonary, 157. 

morbid anatomy of, 157. 

symptoms of. 157. 
Anaesthesia. 969. 
Anchylostomum duodenale, 341. 
Andral, 928. 

Aneurism, abdominal, 567. See Abdominal aneu- 
rism. 

Aneurism of the brain. See Cerebral tumors, 1019. 
Aneurism of the heart. See Heart, aneurism of, 535. 
Aneurism, thoracic, 559. See Thoracic aneurism. 
Aneurism, valvular, 468. 474. 
Angina pectoris, differential diagnosis, 540. 

etiology, 539. 

prognosis, 540. 

s3 T mptoms, 539. 

treatment, 541. 
Angiomata of the brain. See Cerebral tumors. 1019. 
Annuske, 1024. 
Anderson, 209. 
Anotie, 199, 1090. 



1126 



IKDEX. 



Anterior polio-myelitis, acute. See Infantile spinal 

paralysis, 1048. 
Anterior polio-myelitis, chronic. See Polio-myelitis, 

chronic anterior, 1052. 
Anthracosis, 139. 
Antif'ebrin, 654. 
Antipyretics, 652. 
Antipyretics in pneumonia, 125. 
Antipyrin, 654. 

Antiseptic treatment of phthisis, 231. 
Aortic insufficiency. See Aortic regurgitation, 482. 
Aortic obstruction. See Aortic stenosis, 478. 
Aortic regurgitation, differential diagnosis, 486. 

etiology, 483. 

morbid anatomy, 482. 

physical signs, 484. 

pulse of, 484. 

symptoms, 483. 
Aortic stenosis, differential diagnosis, 481. 

etiology, 475. 

morbid anatomy, 478. 

physical signs, 480. 

symptoms, 480. 
Aortitis, 547. 

Aphasia. See Cerebral thrombosis and embolism, 
999. 

Apoplectic coma, 973. 

Apoplexy, cerebral. See Cerebral apoplexy, 1006. 
Apoplexy, circumscribed pulmonary, 148. 
Apoplexy, diffuse pulmonary, etiology of, 153. 

morbid anatomy of, 152. 

physical signs of, 153. 

prognosis of, 153. 

symptoms of, 153. 

treatment of, 153. 
Apoplexy, nodular pulmonary, 148. 
Apoplexy, spinal. See Spinal apoplexy, 1071. 
Aphthous stomatitis. See Follicular stomatitis, 238. 
Appendicitis, differential diagnosis, 312. 

etiology, 311. 

morbid anatomy, 311. 

prognosis, 312. 

symptoms, 311. 

treatment, 312. 
Arndt, 1115. 
Arterial pyaemia, 469. 
Arteries, calcification, 549. 
Arteries, cancer of, 549. 

classification of diseases of, 547. 
Arteries, diseases of, 547. 

fatty degeneration of, 549. 

general dilatation of, 550. 
Arteries in interstitial nephritis, 611. 

syphilis of, 549. 

tuberculous granules in, 549. 

waxy degeneration of, 549. 
Arterio-fibrosis general diagnosis, 550. 

etiology, 552. 

morbid anatomy, 550. 

symptoms, 553. 

treatment, 554. 
Arterioma, 548. 

Arthritis deformans, differential diagnosis, 905. 

etiology, 903. 

morbid anatomy, 903. 

prognosis, 905. 

symptoms, 904. 

treatment, 905. 
Arthritis rheumatoid. See Arthritis deformans, 903. 
Articular rheumatism, acute. See Rheumatism, 
acute articular, 895. 

chronic. See Rheumatism, chronic articular, 
901. 

Ascaris lumbricoides, 340. 

Ascending paralysis, acute. See Paralysis, acute 

ascending, 1070. 
Ascites, differential diagnosis, 367. 

etiology, 365. 

morbid anatomy, 365. 

physical signs, 366. 

prognosis. 368. 

symptoms, 366. 

treatment, 368. 
Aspiration of pericardium, 463. 
Aspiration in pleurisy, 185. 
Asthma, bronchial, 85. 

differential diagnosis, 88. 

etiology, 85. 



Asthma, bronchial, physical signs, 87. 
Asthma, potters', 139. 

prognosis, 88. 

symptoms, 86. 

treatment, 89. 
Asystolism, 519. 

Ataxia, locomotor. See Locomotor ataxia, 1060. 
Atelectasis, 157. 

Atelectasis, pulmonary, differential diagnosis, 159. 

etiology of, 158. 

morbid anatomy of, 157. 

physical signs, 158. 

prognosis of, 159. 

symptoms, 158. 

treatment, 159. 
Atheroma. See Chronic endarteritis, 536. 
Atonic dyspep-ia and chronic gastritis, 266. 
Atrophic nasal catarrh, 39. 

differential diagnosis, 40. 

etiology, 39. 

morbid' anatomy, 39. 

prognosis, 40. 

symptoms, 40. 

treatment, 40. 
Atrophy, 10. 

Atrophy of the brain. See Brain, atrophy of, 
1030. 

Atrophy of the heart, 531. 

Atrophy of the liver. See Liver, chronic atrophy of, 
404. 

Atrophy of the lung, 172. 

Atrophy, progressive muscular. See Progressive 

muscular atrophy, 1053. 
Autumnal fever. See Typhoid fever, 655. 

Bacillus Anthracosis, 33. 

Bacillus cholera, £3, 706. 

Bacillus, definition of, 29. 

Bacillus Lepra?, 28, £3. 

Bacillus Mallei. 33. 

Bacillus (Edematis Matignaa, 33. 

Bacillus Of Eberth (Typhoid), 662. 

Bacillus syphilis, 33. 

Bacillus Pneumoniae, 33, 34. 

Bacillus Rhinoseleroma, 34. 

Bacillus Tuberculosis, 23, 33. 

Bacillus Tuberculosis, method of staining, 28. 

Bacillus Tuberculosis, significance in phthisis, 216. 

Bacillus Typhosus, 33. 

Bacteria, 26. 

attenuation of virus of, 31. 

biology of, 29. 

cultures of, 26. 

classification, 29, 30, 34. 

in endocarditis, 469. 

in fevers, 651. 

pathogenic, 31, 32, 33. 

spores of. 30. 

staining of, 26. 

structure of, 29. 
Bacteriology, 24. 

classification, 25. 

technology, 25. 
Balfour, 489, 491, 497. 
Bamberg, 320. 
Bamberger, 46?, 494. 
Bard, 729. 
Barloive, 505. 
Bartel, 597. 
Barthez, 953, 991. 
Bartholcw, 620. 
Barton, 697. 
Barwell, 901. 9C4. 

Basedow's disease, differential diagnosis, 545. 

etiology, 544. 

morbid anatomy, 544. 

prognosis, 545. 

symptoms, 544 

treatment, 545. 
Bastian, 1004, 1053, 1072. 
Baths in fever, (553. 
Baumgarten, 26. 
Beard, 1079. 
Beck, C03. 
Bedvar, 978. 
Begbie, 500. 
BeVingham, 568. 

Bell's 'paralysis. See Facial paralysis, 1084. 



INDEX. 



1127 



Bence-Jones, 1114, 
Benedict, 843. 
Benecke, 234. 
Benjamin, 1022. 
Bennett, 121, 235, 931. 
Bergmann, 1055. 
Berlin, 496, 500. 
Bernard, 294. 
Biermer, 929. 
Bile in urine, 571. 

Bile-ducts, catarrh of, differential diagnosis, 431. 

etiology, 430. 

morbid anatomy, 429. 

physical signs, 431. 

prognosis, 431, 

symptoms, 430. 

treatment, 431. 
Bilharzia haematobia. 640. 
Biliary calculi. See Gall-stones, 435. 
Biliary colic, 433. 

Biliary passages, exudative inflammation of, differ- 
ential diagnosis, 433. 

etiology, 432. 

morbid anatomy, 432. 

physical signs, 432. 

prognosis, 433. 

symptoms, 432. 

treatment, 433. 
Bilious remittent fever, 862. 

Biliousness. See Functional derangement of liver, 
440. 

Billroth, 724, 727, 729, 780. 
Binz. 842. 

Birch- Hirschf eld, 1050. 
Bird, 842. 

Black measles, 826. See Measles. 
Black vomit, 699. 

4 ' Bleeders. " See Haemophilia, 942. 
Bleeding piles. See Haemorrhoids, 336. 
Blood in urine, 574. 

Blood-vessels, classification of diseases of, 547. 
Bloody flux. See Dysentery, 305. 
Blum. 1063. 

Bothriocephalic latus, 340. 
Bouchard, 1007. 
Bouchut, 988. 
Bouillard, 98. 
Bouillaud, 475. 
Bouillon, preparation of, 25. 
BourneviUe, 1000. 

Brain, abscess of, differential diagnosis, 1019. 

etiology, 1018. 

morbid anatomy, 1017. 

prognosis, 1019. 

symptoms, 1018. 

treatment, 1019. 
Brain, anaemia of. See Cerebral anaemia, 975. 
Brain and meninges, tumors of differential diagno- 
sis, 1024. 

etiology, 1023. 

morbid anatomy, 1020. 

prognosis, 1026. 
Brain and meninges, tumors of, symptoms, 102i. 

treatment, 1026. 

varieties, 1019. 
Brain, aneurisms of. See Cerebral tumors, 1023. 
Brain, angiomata of. See Cerebral tumors, 1023. 
Brain, atrophy of, differential diagnosis, 1032. 

etiology, 1031. 

morbid anatomy, 1039. 

prognosis, 1032. 

symptoms, 1031. 

treatment, 1032. 
Brain, cholesteatoma of. See Cerebral tumors, 1022. 
Brain, cysticerci of. See Cerebral tumors, 1023. 
Brain, cysts of. See Cerebral tumors, 1022. 
Brain, embolism and thrombosis of. See Cerebral 

thrombosis and embolism, 998. 
Brain, fibromata of. See Cerebral tumors, 1023. 

gliomata of. See Cerebral tumors, 1021. 

hydatids of. See Cerebral tumors, 1023. 

hyperemia of. See Cerebral hypeiaemia, 972. 
Brain, gummata of, 1021. 

Brain, hypertrophy of, differential diagnosis, 1030. 
etiology, 1029. 
morbid anatomy, 1029. 
prognosis, 1030. 
symptoms, 1030. 



Brain, lipomata of. See Cerebral tumors, 1022. 
Brain, localization of lesious within, 1012. 
Brain, myxomata of. See Cerebral tumors, 1022. 

osteomata of. See Cerebral tumors, 1022. 

papillomata of. See Cerebral tumors, 1023. 

psammomata of. See Cerebral tumors, 1021. 

sarcomata of. See Cerebral tumors, 1022. 
Brain, sclerosis of. See Sclerosis of the brain, 1027. 
Brain, softening of. See Cerebral softening. 1001. 
Brain, thrombosis and embolism of. See Cerebral 

thrombosis and embolism, 993. 
Brain, tubercle of, 1020. 
Bramivett, 930. 
Breakbone fever, 8S7. 
Bright, 295, 550, 591, 991. 

Bright's disease, amyloid form of. See Kidney, 617. 
Bright's disease, cirrhotic. See Nephritis, chronic 

interstitial, 610. 
Bright's diseases of the kidneys. See Nephritis, 591. 
Brigidi, 929. 
Brimer, 838. 
Brinton, 325. 
Briquet, 1105, 1107. 
Bristowe, 326. 
Broadbent, 1113. 
Brodie, 1107. 
Bronchial abscess, 157. 
Bronchial asthma, 85. 
Bronchial hemorrhage, 91. 

differential diagnosis, 94. 

etiology, 91. 

morbid anatomy, 91. 

prognosis, 95. 

symptoms, 93. 

treatment, 95. 
Bronchiectasis, 81. 

differential diagnosis, 83. 

etiology, 82. 

morbid anatomy, 82. 

physical signs. 

symptoms, 82. 

treatment, 83. 
Bronchitis, acute capillary, 72. 

differential diagnosis, 73. 

etiology, 72. 

morbid anatomy, 72. 

physical signs, 73. 

prognosis, 74. 

symptoms, 73. 

treatment, 74. 
Bronchitis, acute catarrhal, 68. 

differential diagnosis, 71. 

etiology, 69. 

morbid anatomy, 69. 

prognosis, 71. 

symptoms, 70. 

treatment, 71. 
Bronchitis, chronic catarrhal, 75. 

differential diagnosis, 79. 

etiology, 77. 

morbid anatomy, 76. 

physical signs, 79. 
Bronchitis, chronic catarrhal, prognosis, 80. 

symptoms, 78. 

treatment, 80. 
Bronchitis, classification of, 63. 
Bronchitis, croupous (fibrinous), 83. 

differential diagnosis, 84. 

etiology, 84. 

morbid anatomy, 84. 

physical signs, 84. 

prognosis, 85. 

symptoms, 84. 

treatment, 85. 
Bronchitis, fetid. See Chronic bronchitis, 77. 
Bronchitis, vesicular. 157. 

Broncho-pneumonia. See Lobular pneumonia, 127. 
Broncho-pneumonia of phthisis, 202. 
Bronchorroea, 18. 
Bronchorrhagia, 92. 
Bronchorrhagia vicarious, 93. 
Brown, induration of the lungs, 142. 
Brown cedema of lungs, Virchow's. 143. 
Brcwn-Sequard. 711, 937, 1011, 1013,1037, 1039, 1096, 

109S, 1099, 1101, 1103, 1104. 
Bruit de Diable, 475. 
Bruit de Souffle, 475. 
Brundes, 121, 122. 



1128 



Brunei, 685. 
Buck, 791. 

Buhl, 172, 840, 938, 950. 

Bulbar paralysis, acute. See Paralysis, acute bulbar, 
1043. 

chronic. See Paralvsis, chronic bulbar, 1044. 
Bulimia, 927. 
Burns, 475. 
Button-hole slit, 474. 
Buzzard, 1104, 1106. 
Byssinosis, 139. 

Cachexia Africana, 342. 

Caseitis. See Typhlitis, 309. 

Calcification, 16. 

Calcification of arteries, 549. 

Calculi, biliary. See Gall-stones, 435. 

Calculi of the pancreas. See Pancreas, calculi of, 447. 

Calculi renal. See Kenal calculi, 629. 

Calmeil, 984. 

Cancan i, 921. 

Cancer of arteries, 549. 

of brain. See Cerebral tumors, 1019. 

of gall-bladder. See Gall-bladder, cancer of, 
433. 

of heart, 536. 

of intestine. See Intestine, cancer of, 330. 
of kidney. See Real cancer, 633. 
of larynx, 65. 

of liver. See Liver, cancer of, 411. 
of lungs, 168. 

of oesophagus. See (Esophagus, cancer of, 254. 
of mediastinum, 568. 

of pancreas. See Pancreas, cancer of, 445. 

of pericardium, 537. 

of pleura. See Pleura, cancer of, 192. 

of rectum, 331. 

of spleen, 452. 

of stomach. See Stomach, cancer of, 269. 

of tongue. See Tongue, cancer of, 244. 

pulmonary, 168. 
Cancrum oris. See Gangrenous stomatitis, 239. 
Canstatt, 896, C50. 
Capillary bronchitis, acute, 72. 
Caput Medusa?, 377. 
Cardiac dilatation, 515. 

differential diagnosis, 519. 

etiology, 516. 

morbid anatomy, 515. 

physical signs, 518. 

prognosis, 520. 

symptoms, 517. 

treatment, 5*21. 

varieties of, 515. 
Cardiac hypertrophy, 507. 

differential diagnosis, 513. 

etiology, f.08. 

morbid anatomy, 507. 

physical signs, 511. 

prognosis, 513. 

relation to nephritis, 510. 

symptoms, 510. 

treatment, 514. 

varieties of, 507. 
Cardiac murmurs and their relation to valvular dis- 
ease of the heart. 475. 
Cardiac murmurs. See Murmur, cardiac, 475. 
Cardiac murmurs in pleurisy, 191. 
Cardiac neuroses, varieties of, 537. 
Cardiac palpitation, nervous, differential diagnosis, 
538. 

etiology, 537. 

prognosis. 539. 

symptoms, 53S. 

treatment, 539. 
Cardiac thrombosis, differential diagnosis, 534. 

etiology, 533. 

morbid anatomy, 532, 533. 

physical signs, 534. 

prognosis, 534. 

symptoms, 534. 

treatment, 535. 
" Carditis." See Myocarditis, 522. 
Carnification of lung, 142. 
Carre, 1062. 
Gary, 931. 
Caseation, 21. 
Caseous pneumonia, 210. 



Caseous pneumonia of tuberculosis, 200. 

Casts in the urine, 575. 

Catalepsy, differential diagnosis, 1111. 

etiology, 1110. 

prognosis, 1111. 

symptoms, 1110. 

treatment, 1111. 
Catarrh, acute gastric. See Sub-acute gastritis, 
257. 

Catarrh, atrophic nasal. See Atrophic nasal catarrh, 
39. 

Catarrh, chronic nasal. See Chronic coryza, 36. 
Catarrh, chronic naso-pharyngeal. See Hypertrophic 

catarrh, nasal, 37. 
Catarrh, dry nasal. See Atrophic nasal catarrh. 39. 
Catarrh, epidemic. See Influenza, 837. 
Catarrh, fetid nasal. See Ozsena, 41. 
Catarrh, hypertrophic nasal, 37. 

differential diagnosis, 38. 

etiology, 38. 

morbid anatomy, 37. 

prognosis, 38. 

symptoms, 38. 

treatment, 39. 
Catarrh, intestinal. See Enteritis. 287. 
Catarrh of the bile-ducts. See Bile-ducts, catarrh 
of, 429. 

Catarrh of the larynx, chronic phthisical, 49. 
Catarrhal bronchitis, acute. See Bronchitis, acute 
catarrhal, 69. 

Catarrhal bronchitis, chronic. See Bronchitis, chron- 
ic catarrhal, 76. 

Catarrhal laryngitis, acute. See Laryngitis, acute 
catarrhal, 43. 

Catarrhal laryngitis, chronic syphilitic. See Laryn- 
gitis, chronic catarrhal syphilitic, 51. 

Catarrhal laryngitis, simple chronic. See Laryn- 
gitis, chronic catarrhal, 47. . 

Catarrhal pharyngitis. See Pharyngitis, catarrhal, 
221. 

Catarrhal phthisis, 210. 

Catarrhal pneumonia. See Pneumonia, lobular, 1*27. 

Catarrhal stomatitis. See Stomatitis, 236. 

Cavalie, 946. 

Cavities in phthisis, 211. 

Cayley, 1022. 

Celborne, 1017. 

Celli, 846. 

Cephalalgia, 906. 

Cerebral abscess. See Brain, abscess of, 1017. 
Cerebral anaemia, diffeientiai diagnosis, 976. 

etiology, 975. 

morbid anatomy, 975. 

prognosis, 976. 

symptoms. 976. 

treatment, 976. 
Cerebral apoplexv, differential diagnosis, 1014. 

etiology, 1008. 

morbid anatomy, 1006. 

prognosis, 1015. 

symptoms, 1009. 

treatment, 1016. 
Cerebral hypersemia, differential diagnosis, 974. 

etiology, 972. 

morbid anatomy, 972. 

prognosis, 974. 

symptoms, 973. 

treatment, 974. 
Cerebral lesions, localization of, 1012. 
Cerebral softening, differential diagnosis, 1005. 

etiology, 1G03. 

morbid anatomy, 1001. 

prognosis, 1005. 

symptoms, 10d4. 

treatment, 1005. 

varieties of, 1001. 
Cerebral thrombosis and embolism, differential diag 
nosis, 1000. 

morbid anatomy, 998. 

prognosis, 1001. 

symptoms, 999. 

treatment, 1001. 
Cerebral tumors. See Brain and meninges, tumors 
of, 1019. 

Cerebro-spinal fever. See Cerebro-spinal meningitis, 
712. 

Cerebro-spinal meningitis, complications, 72Q. 
I differential diagnosis, 718. 



INDEX. 



1129 



Cerebrospinal meningitis, etiology, 714. 

morbid anatomy, 712. 

prognosis, 719. 

symptoms, 714. 

treatment, 720. 
Cerebro spinal sclerosis, differential diagnosis, 1059. 
• etiology, 1058. 

morbid anatomy, 1057. 

prognosis, 1059. 

symptoms, 1058. 

treatment, 1059. 
Chalicosis, 139. 

Charcot, 168, 494, 903, 904, 914, 1003, 1011, 1029, 1041, 
1045, 1057, 105S, 1061, 1065, 1068, 1072, 10S3, 
1104, 1107, 1109, 1121. 
Charcot and Loomis, 896, 1008, 1014. 
Chauveau, 475. 
Chickahominy fever. 866. 
Chicken-pox. See Varicella, 803. 
Chlorosis, differential diagnosis, 927. 

etiology, 926. 

morbid anatomy, 926. 

prognosis, 927. 

symptoms, 926. 

treatment, 927. 
Cholera, English. See Cholera morbus, 296. 
Cholera epidemic, differential diagnosis, 709. 

eruption, 709. 

etiology, 706. 

morbid anatomy, 704. 

prognosis, 710. 

symptoms, 707. 

synonyms, 704. 

treatment, 711. 
Cholera infantum, differential diagnosis, 299. 

etiology, 298. 

morbid anatomy, 298. 

prognosis, 300. 

symptoms, 299. 

treatment, 300. 
Cholera morbus, differential diagnosis, 297. 

etiology, 296. 

morbid anatomy, 296. 

prognosis, 298. 

symptoms, 296. 

treatment, 298. 
Cholera nostras. See Cholera morbus, 296. 
Cholera, sporadic. See Cholera morbus, 296. 
Cholesteatoma of the brain. See Cerebral tumors, 

1019. 
Chomel, 134. 

Chorea, differential diagnosis, 1114. 
etiology, 1113. 
morbid anatomy, 1112. 
prognosis. 1114. 
symptoms, 1113. 
treatment, 1115. 
Chronic anterior polio-myelitis. See Polio-myelitis, 

chronic anterior, 1052. 
Chronic articular rheumatism. See Rheumatism, 

chronic articular, 901. 
Chronic atrophy of the liver. See Liver, chronic 

atrophy of, 404. 
Chronic Bright's, of the kidney. See Nephritis, 
chronic, 604. 

Chronic bulbar paralysis. See Paralysis, chronic 
bulbar, 1044. 

Chronic catarrhal bronchitis, 75. 

Chronic catarrh of the larynx in phthisis, 43. 

Chronic catarrh of the stomach. See Chronic gas- 
tritis, 259. 

Chronic coryza. 36. 

Chronic endarteritis, 547. 

Chronic endocarditis. See Endocarditis, interstitial, 
473. 

Chronic endophlebitis, 550. 
Chronic general diseases, classification, 895. 
Chronic hydrocephalus. See Hydrocephalus, chronic, 
990. 

Chronic inflammatory dyspepsia. See Chronic gas- 
tritis, 259. 

Chronic laryngitis, 47. 

Chronic laryngitis of syphilis, 51. 

Chronic lead poisoning. <S'eeLead poisoning, chronic, 
1080. 

Chronic malarial infection, differential diagnosis, 
892. 
etiology, 891. 



Chronic malarial infection, morbid anatomy, 891. 

prognosis, 893. 

symptoms, 891. 

treatment, 893. 
Chronic meningitis. See Meningitis, chronic, 983. 
Chronic mercurialism. See Mercurialism, chronic, 
1080. 

Chronic myelitis. See Myelit is, chronic, 1041. 
Chronic myocarditis. See Fibroid disease of the 
heart, 525. 

Chronic nasal catarrh. See Chronic coryza, 36. 
Chronic naso-pharyngeai catarrh. See Hypertrophic 

nasal catarrh, 37. 
Chronic pancreatitis. See Pancreatitis, chronic, 445. 
Chronic pericarditis. See Pericarditis, chronic, 463. 
Chylnria, etiology, 642. 

morbid anatomy, 642. 

prognosis, 643. 

symptoms, 642. 

treatment, 643. 
Cicatrization in inflammation, 4. 
Circumscribed pulmonary apoplexy, 148. 
Circumscribed pulmonary gangrene, 153. 
Circumscribed suppurative hepatitis. See Hepatitis, 

circumscribed suppurative, 383. 
Cirrhosis, 5. 

Cirrhosis of the liver, 374. 

Cirrhosis of the lung, 134. 

Cirrhotic nephritis. See Nephritis, 610. 

Clapham, H22, 1124. 

Clark, 948, 1009, 1033, 1057, 1061, 1065, 1083. 

Clavus hystericus, 1106. 

" Clergyman's sore throat, 47. 

Climate in etiology of phthisis, 205. 

Climatic treatment of phthisis, 233-5. 

Climatic treatment of pleurisy, 182. 

Clonston, 130. 1103. 

Cloudy swelling of the heart. See Heart, parenchy- 
matous degeneration of, £36. 
Coagulation-necrosis in phthisis, 202. 
Coal-miner's lung, 139. 
Cobbold, 536. 
Coccyodynia, 1091. 

Cohnheim, 146, 148, 150, 550, 597, 780, 788, 928, 957, 

959, 988, 1068. 
Cold, rules for use of, in acute pneumonia, 125. 
Colic, biliary, 437. See Gall-stones. 
Colic, copper. See Colic, 351. 
Colic, gall-stone, 438. 

Colic, intestinal, differential diagnosis, 352. 

erioloiry, 349. 

prognosis, 352. 

symptoms, 350. 

treatment, 352. 

varieties of, 349. 
Colic, lead. See Intestinal colic, 349. 
Colic, renal, 631. 

Colica pictonum. See Lead colic, 349, 351. 
Colitis. See Enteritis, 287. 
Collapse of the lungs, 157. 
Collie, 796. 

Colloid caseous pneumonia, 211. 
Colorado, climate of, 234. 
Coma, causes of, 971. 
Coma, definition, 970. 
Coma vigil, 760. 

Compensatory hyperemia of the lungs, 142. 
Confluent variola. See Small-pox, 792. 
Congestion, hypostatic, 142. 

Congestion of the brain. See Cerebral hyperemia, 
972. 

Congestion of the kidneys. See Renal hyperemia, 
583. 

Congestion of the liver. See Liver, passive hypere- 
mia of, 371. 
Congestion of the lungs, 141. 
Congestive fever. 877. 
Constipation, differential diagnosis, 348. 

etiology. 346. 

morbid anatomy, 316. 

prognosis, 348. 

symptoms, 347. 

treatment. 348. 
Consumption of the lungs. See Pulmonary tubercu- 
losis. 199. 
Contagion, definition of, 647. 
Continued malarial fever, 866. 

differential diagnosis, 872. 



1130 



INDEX. 



Continued malarial fever, etiology, 868. 

morbid anatomy, 867. 

prognosis, 874. 

symptoms, 868. 

treatment, 875. 
Contracted kidney. See Nephritis, 610. 
Convulsions, 969. 

Convul>ions, infantile, and eclampsia, 1086. 
Cooper, 1107. 

Coordination, disorders of, 970. 
Copland, 837. 

Copper colic. See Intestinal colic, 349. 
Cor bovinum, 508. 
Corlie*, 545. 
Cor nil, 401. 

Comil and Ranxier, 136, 141, 508, 522, 556, 611, 617, 

694, 933,943, 1021, 1022, 1027, 1058, 1061. 
Corpora amylacea, 19. 
Corrigan, 136, 475. 
Corrigans pulse, 484. 
Corvisart, 475. 
Coryza, acute, 35. 

differential diagnosis, 36. 

etiology, 35. 

morbid anaromy, 35. 

prognosis, 36. 

symptoms, 35. 

treatment, 36. 
Coryza, chronic, 36. 

differential diagnosis, 37. 

etiology, 36. 

morbid anatomy, 36. 

symptoms, 36. 

treatment, 37. 
Cough in phthisis, 217. 
Coup de soleil, 1115. 
Creeping palsy, 1005. 
Croup, 53. 

Croup, false, 63. See Laryngitis. 
Croup, membranous. See Acute croupous laryngitis, 
53. 

relation to diphtheria, 54. 
Croupous bronchitis, 84. 
Croupous inflammation, 7. 
Croupous laryngitis, acute, 53. 
Croupous pharyngitis, 251. 

Croupous stomatitis. See Follicular stomatitis, 238. 
CrudelL 849. 

Cruveilhier, 81, 1006, 1008, 1023. 
Currie, 684. 
Curshmann, 791. 

Cyanotic induration of kidneys, 585. 

Cysticerei of the brain. See Cerebral tumors, 1019. 

Cysticercus cellulosae, 339. 

Cystic kidneys, etiology and morbid anatomy, 628- 

629. 
Cystine, 573. 

Cystitis, differential diagnosis, 645. 

etiology, 644. 

morbid anatomy, 643. 

prognosis, 645. 

symptoms, 644. 

treatment. 645. 

varieties. 606, 644. 
Cysts in the heart, 536. 

Cysts in the pancreas. See Pancreas, cysts of, 416. 
Cysts of the brain. See Cerebral tumors, 1019. 
Cysts of spleen, 452. 

Da Cost a, 121. 
Dandy fever. 887. 
Davos am Plalz, 235. 
Degenerations, 11. 

amyloid, 18. 

calcareous, 16. 

classification, 12. 

colloid, 15. 

fatty, 14. 

lardaceous, 18. 

mucoid, 16. 

parenchymatous, 12. 

waxy, 18. 
Dejerine. 1070. 
Delasiaure, 1101. 

Delirium tremens. See Alcoholism, 954. 
Dengue fever, differential diagnosis, 889. 

etiology, 887. 

morbid anatomy, 887. 



Dengue fever, prognosis, 890. 

symptoms, 888. 

treatment, 890. 
Dermoid cysts in the lung, 170. 

Desgranges, 923. 

Diabetes decipiens, 918. * 
Diabetes insipidus, differential diagnosis, 922. 

etiology, S22. 

morbid anatomy, 922. 

prognosis, 922. 

symptoms, 922. 

treatment, 923. 
Diabetes niellitus, differential diagnosis, 920. 

etiology, 918. 

morbid anatomy, 917. 

prognosis, 920. 

symptoms, 918. 

treatment, 920. 
Diarrhoea, acute, differential diagnosis, 295. 

prognosis, 295. 

symptoms, 294. 

treatment, 295. 

varieties of, 293. 
Diarrhoea, chronic, 295. 

choleraic, 294. 

colliquative, 294. 

fatty, 294. 

irritative, 293. 

lienteric, 294. 

mechanical, 293. 

nervous, 294. 

vicarious, 294. 
Diathesis, the hemorrhagic. See Haemophilia, 942. 

scrofulous, 204. 

tubercular, 204. 
Dickenson, 505, 615, 922, 923. 

Diffuse catarrhal ulcers of the intestine. See Intes- 
tinal ulcers, 317. 
Diffuse parenchymatous hepatitis. See Hepatitis, 

parenchymatous, 389. 
Diffuse pulmonary apoplexy, 152. 
Diffuse pulmonary gangrene, 153. 
Digestive system, diseases of, 236. 
Digitalis in cardiac dilatation, 521. 

in nephritis, 601, 609, 615. 

in uraemia, 581. 

in valvular diseases, E04. 
Dilatation of the heart. See Cardiac dilatation, 515. 
Dilatation of the stomach. See Stomach, dilatation 

of, 283. 
Diphtheria, definition, 729. 

differential diagnosis, 739. 

etiology, 732. 

laryngeal, 735. 

morbid anatomy, 730. 

prognosis. 741. 

sequelae, 740. 

symptoms, constitutional, 736. 

symptoms, local, 734. 

treatment, 742. 
Diphtheritic endocarditis. See Endocarditis, 467. 
Diphtheritic inflammation, 8. 
Diphtheritic paralysis, 738. 
Diphtheritic pharyngitis, 251. 
Discrete variola, See Small-pox, 786. 
Diseases, acute general, 647. 

acute general, c lassification, 648. 

chronic, general, 895. 

of the blood-vessels, classification, 547. 

of the biain. classification. 972. 

of the gall bladder, classification, 429. 

of the gall ducts, classification, 429. . * 

of the heart, classification, 454. 

of the intestines. 287. 

of the kidneys. 583. 

of the larynx, 43. 

of the liver, 369. 

of the lung, 96. 

of the mouth, 236. 

of the nasal passages, 35. 

of the nervous system, functional, 1096. 

of the nervous system, general symptomatol- 
ogy, 965. 

of the pancreas, 444. 

of the peripheral nerves, 1076. 

of the pharynx, 247. 

of the pleura, 96. 

of the stomach, 256. 



IKDEX. 



1131 



Diseases of the spinal cord, 1032. 

of the spleen, 447. 
Disseminated sclerosis. See Cerebro-spinal sclerosis, 
1057. 

Disseminated tuberculosis, 210. See Tuberculosis. 

Dobeirs solution, 37. 

Dochmius duodenalis, 341. 

Dorkin, 921. 

Drachmann, 1005. 

Drake, 886. 

Draper, 919. 

Dropsv. abdominal. See Ascites, 365. 
Drop.-y of the gall-bladder. See Gall-bladder. 433. 
Dropsy of the kidney. See Hydronephrosis, 626. 
Dropsy of the pericardium. See Hydropericardium, 
541. 

Dropsy in nephritis, 598, 614, 620. 

Dry nasal catarrh. See Atrophic nasal catarrh, 39. 

Duchenne. 1045, 1047, 1051. 

Duchenne's disease. See Locomotor ataxia, 1060. 
Dvjardin-Beaumetz, 614. 
Duodenitis. See Enteritis, 290. 
Duodenum, ulcer of. etiology, 316. 

morbid anatomy, 315. 

prognosis, 316. 

symptoms, 316. 
Dupont, 382. 

Durand-Fardel, 1003. 1004, 1015, 1031. 
Dysentery, acute, differential diagnosis, 307. 

etiology. 304. 

morbid anatomy, 302. 

prognosis, 307. 

symptoms, 3C5. 

treatment, 303. 
Dysentery, chronic, 307. 
Dysentery, varieties of, 302. 
Dyspepsia, gastric, 266. 

differential diagnosis, 268. 

etiology, 266. 

morbid anatomy, 266. 

prognosis, 269. 

symptoms, 267. 

treatment, 269. 
Dyspepsia, gouty, 441. 
Dyspepsia, intestinal, etiology, 301. 

symptoms, 301. 

treatment, 301. 
Dysphagia, inflammatory. See Oesophagitis, 252. 

Echeverria. 1098, 1103. 
Echinococci, 419. 

Echinococci in the lungs. See Hydatids, 172. 
Echinococci of the liver. See Liver, hydatids of, 419. 
Eclampsia and infantile convulsions, 1086. 
Ecker, 972. 
Ehrlich, 928. 
Eichborn, 690. 
Mchhorst, 928. 

Electrical irritability of muscle, 966. 

Embolic pneumonia. See Pulmonary infarction, 148. 

Embolism, definition of. 557. 

morbid anatomy, 558. 
Embolism of lung, fat, 150. 

Embolism of the brain. See Cerebral thrombosis 

and embolism, 998. 
Embolism of the kidney. See Renal hemorrhage. 

588. 

pulmonary fat, 150. 
Emphysema, compensatory, 162. 
Emphysema, interlobular, 162. 
Emphysema, pulmonary, 159. 
Emphysema, senile, 161. 
Emphysema, vesicular, 159. 

differential diagnosis, 165. 

etiology, 162. 

morbid anatomy, 159. 

physical signs, 164. 

prognosis, 166. 

symptoms, 163. 

treatment, 166. 
Empyema, 186. 

differential diagnosis, 189. 

etiology, 187. 

morbid anatomy, 186. 

physical sign*. 189. 

prognosis, 1«9. 

symptoms, 188. 

treatment, 189. 



Encephalitis, 1017. 
Enchondromata in the lungs, 170. 
Endarteritis, acute, 547. 

etiology, 547. 

morbid anatomy, 547. 

symptoms, 547. 
Endarteritis, chronic, differential diagnosis, 549. 

etiology, 548. 

morbid anatomy, 547. 

prognosis, 549. " 

symptoms, 548. 
Endarteritis, deformans. See Chronic endarteritis, 
547. 

Endemic haematuria, 640. 
Endocarditis, classification, 465. 
Endocarditis, acute non-infectious, 465. 

differential diagnosis, 471. 

etiology. 468. 

morbid anatomy, 465. 

physical signs, 470. 

prognosis, 472. 

symptoms, 469. 

treatment, 472. 
Endocarditis, chronic. See Endocarditis, interstitial, 
473. 

Endocarditis, infectious, etiology, 468. 

morbid anatomy, 467. 

physical signs, 470. 

prognosis, 471. 

sjTnptoms, 4f:9. 

treatment, 472. 
Endocarditis, interstitial, etiology, 475. 

morbid anatomy, 473. 
. symptoms, 475. 

varieties of, 465. 
Endophlebitis, 554. 

English cholera. See Cholera morbus, 296. 
English sweating sickness. 834. 
Enlarged call-bladder. See Gall-bladder, enlarged, 
433. 

Enlarged spleen. See Spleen, hypertrophy of, 450. 
Enteric fever. See Typhoid fever, 655. 
Enteritis, acute, 287. 

differential diagnosis, 291. 

etiology, 289. 

morbid anatomy, 287. 

prognosis, 292. 

symptoms, 299. 

treatment, 292. 
Enteritis, varieties of, 287. 
Enteritis, chronic, 291. 

Enteritis, follicular. See Intestinal ulcers, 315. 
Enteritis, membranous, 295. 
Enteritis, phlegmonous, 288. 
Enteritis, strumous. See Intestinal ulcers, 315. 
Enteroliths. See Intestinal obstruction, 324. 
Ependymitis, chronic, 991. 
Epidemic catarrh. See Influenza, 837. 
Epidemic cerebro-spinal meningitis. See Cerebro- 
spinal meningitis, epidemic, 712. 
Epidemic cholera. See Cholera, epidemic, 704. 
Epidemic roseola. See German measles, 83i. 
Epilepsy, differential diagnosis, 1101. 

etiology, 1097. 

morbid anatomy, 1096. 

prognosis, 1102. 

symptoms, 1098. 

treatment, 1102. 
Epistaxis in typhoid fever, 669. 
Epithelioma myxomatodes psammomum, 1020. 
Epithelioma of tongue. See Cancer of tongue, 244. 
Epithelium in urine, 574. 

Erb, 1038, 1042, 1043. 1046, 1048, 1052, 1058, 1063, 1065, 

1068. 1072, 1111. 
Erlanger, 946. 

Erysipelas, differential diagnosis, 748. 

etiology, 746. 

morbid anatomy, 745. 

prognosis, 748. 

symptoms, 746. 

treatment, 749. 
Erythism of the stomach. See Stomach. 231. 
Eulenbera. 544, 1063, 1068, 1083, 1110. 1111. 
Ewart, 308. 

Exophthalmic goitre. See Basedow's disease. 544. 
External pachymeningitis. See Pachymeningitis 

externa, 993. 
Exudation, inflammatory, 3. 



1132 



INDEX. 



Exudative inflammation of the biliary passages. See 
Biliary passages, etc., 432. 

Fabra, 944, 1033. 

Facial paralysis. See Paralysis, facial, 1084. 

Faage, 505. 

Fainting fit, 976. 

Fal^e pleurisy, 1091. 

Fat embolism of the lungs, 150. 

Fat in urine, 571. 

Fate of pus, 9. 

Fatty degeneration, 14. 

Fatty degeneration of arteries, 549. 

Fatty degeneration of the heart. See Heart, fatty de- 
generation of, 526. 

Fatty degeneration of the pancreas. See Pancreas, 
fatty degeneration of, 445. 

Fatty hypertrophic cirrhosis of the liver, 381. 

Fatty infiltration, 13. 

Fatty infiltration of liver. See Fatty liver, 406. 
Fatty liver, differential diagnosis, 408. 

etiology, 407. 

morbid anatomy, 406. 

physical signs, 408. 

prognosis, 408. 

symptoms, 407. 

treatment, 408. 
Faulkner, 91. 
Fayrer, 1116. 
Fede, 928. 
Feinberg, 1034. 
Festination, 1028. 

Fetid bronchitis. See Chronic bronchitis, 75. 
Fetid nasal catarrh. See Ozsena, 41. 
Fever, continued malarial. See Continued malarial 
fever, 866. 

dengue. See Dengue fever, 887. 

enteric. See Typhoid fever, 655. 

infantile remittent, 290, 863. 

intermittent. See Intermittent fever, 846. 

malarial. See Malarial fever, 846. 

miliary. See Miliary fever, 834. 

pernicious malarial. See Pernicious malarial 
fever, 877. 

relapsing. See Relapsing fever, 778. 

remittent. See Remittent fever. 858. 

rheumatic. See Rheumatism, acute articular, 
895. 

scarlet. See Scarlet frver, 805. 
spotted. See Cerebro-spinal meningitis, 112. 
typhoid. See Typhoid fever, 655. 
typho-malarial. dee Continued malarial fever, 
866. 

typhus. See Typhus fever, 752. 
Fibroid induration of the lung and cancer of the 

lung, 170. 
Fibromata m lungs, 170. 

Fibromata of the brain. See Cerebral tumors, 1019. 

Fibromata of the heart, 536. 

Fibromata of the kidney, 635. 

Fibrous phthisis. See Tuberculosis, 214. 

FUz, 843. 

Fletcher, 1026. 

Flexibilitas ceiea, 1110. 

Flichsig, 1067. 

Flint, 126, 939. 

Floating or movable kidney. See Kidney, floating 

or movable, 639. 
Fluid veins, 475. 

Flux, the bloody. See Dysentery, 302. 

Follicular enteritis. See Intestinal ulcers. 317. 

Forster, 983, 994, 1008. 

Foster, 992, 983, 984, 1017, 1047. 

Fotherqill, 925. 

Fox, 121, 122, 134, 135, 1020. 

Frank, 918. 

Fremissement cataire, 930. 
Fremissement, systolic, 480. 
Friedreich, 545, 1061. 
Friedrich, 927. 
Friedrichs, 475. 
Frommann. 1C58. 

Functional derangements of the liver, 440. 
Functional diseases of the intestines, 448. 
Functional diseases of the nervous system, 1096. 
Fungus hsematodes, 633. 
Furbvrger, 597. 



Gaffky, 662. 

Galen, 1098. 

Galezoicski, 988. 

Gall-bladder, cancer of, 433. 

Gall-bladder, diseases of, 429. 

Gall-bladder, dropsy'of, 433. 

Gall-bladder, enlarged, differential diagnosis, 434. 

etiology, 434. 

morbid anatomy, 434. 

physical signs, 434. 

prognosis, 435. 

symptoms, 434. 

treatment, 435. 
Gall-ducts, diseases of, 429. 
Gall-stone colic, 438. 
Gall-stones, differential diagnosis, 439. 

etiology, 437. 

morbid anatomy, 435. 

prognosis, 439. 

symptoms, 437. 

treatment, 441. 
Gangrene, 20. 

Gangrene, circumscribed pulmonary, 153. 
Gangrene, dry, 20. 
Gangrene, hospital, 21. 
Gangrene, moist, 21. 

Gangrene, pulmonary, differential diagnosis of, 155 
etiology of, 154. 
morbid anatomy of, 153. 
physical signs, 155. 
prognosis of, 156. 
symptoms of, 154. 
treatment of, 156. 
varieties, 153. 
senile, 21. 

Gangrenous stomatitis. See Stomatitis, gangrenous, 

239. 
Gardner, 928. 
Garrod, 896, 898, 900. 

Gastric catarrh, acute. See Gastritis, 257. 
Gastric dyspepsia, 266. 
Gastric influenza, 838. 
Gastritis, acute, 256. 

differential diagnosis, 257. 

etiology, 256. 

morbid anatomy, 256. 

prognosis, 257. 

symptoms, 256. 

treatment, 257. 
Gastritis, chronic, 259. 

differential diagnosis, 263. 

etiology, 261. 

morbid anatomy, 259. 

prognosis, 263. 

symptoms, 261. 

treatment, 263. 
Gastritis, phlegmonous, differential diagnosis, 266. 

etiology, 265. 

morbid anatomy, 265. 

symptoms, 265. 

prognosis, 266. 

treatment, 266. 
Gastritis, sub-acute, differential diagnosis, 259. 

etiology, 258. 

morbid anatomy, 257. 

prognosis, 259. 

symptoms, 258. 

treatment, 259. 
Gastritis, toxic. See Acute gastritis, 256. 
Gastro-enteritis, 290. 
Geigel, 491. 
Gendrin, 476. 

General arterio-fibrosis, 550. 
General dilatation of arteries, 549. 
General paralysis, 966. 
Gerborett, 994. 
Gerhardt, 152. 
Germain See, 468. 

German measles, differential diagnosis, 833. 

etiology, 832. 

morbid anatomy, 831. 

prognosis, 833. 

symptoms, 832. 

treatment, 833. 
Giant cells, 22. 
Gibb, 869. 
Gibney, 638. 
GUI, 126. 



INDEX. 



1133 



Glandulae pacchionii, 983. 

Gliomata of the brain. See Cerebral tumors, 1021. 

Globus hystericus, 1105. 

Glossitis,"242. 

differential diagnosis, 243. 

etiology, 243. 

morbid anatomy, 242. 

prognosis, 244. 

symptoms, 243. 

treatment, 244. 

varieties of, 243. 
Glosso-labio-laryngeal paralysis. See Chronic bulbar 

paralysis, 1044. 
Glottis, cedenta of, 51. 
Glucosuria. See Diabetes mellitus, 917. 
Glycohaemia. See Diabetes mellitus, !)17. 
Glycosuria. See Diabetes mellitus, 917. 
Goitre, cystic, 545. 

Goitre, exophthalmic. See Basedow's disease, 544. 

Goldinq Bird, 842. 

Golgi, 975. 

Golis, 991. 

Gonococcus, 33. 

Goodhart, 925. 

Gougovenheim, 1012. 

Gout, differential diagnosis, 912. 

etiology, 910. 

morbid" anatomy, 908. 

prognosis, 913. 

symptoms, 911. 

treatment, 913. 
Gout, chronic, 912. 

irregular. 911. 

latent, 441. 

metastatic, 912. 

misplaced, 911. 

retrocedent, 911. 

suppressed, 441. 
Gouty kidney. See Nephritis, 610. 
Gouty liver. See Interstitial hepatitis, 375. 
Gowers, 1068, 1085, 1097, 1098, 1104, 1111, 1121. 
Graefe, 730. 

Gram's method of staining, 27. 

Granular liver. See Interstitial hepatitis, 374. 

Granulation, 4. 

Grapecure, in enteritis, 309. 

Gravel, renal, 630. 

Graves' disease. See Basedow's disease, 544. 
Greenho.c, 940. 

Griesinger, 769, 973, 994, 1105. 
GHsolle, 121, 134. 
Gutter, 578, 1010, 1013. 
Gull, 948, lu72. 

Gull and Sutton, 525, 550, 578, 900, 1017. 
Gummata of spleen, 452. 

Gummau of the brain. See Cerebral tumors, 1019. 
Gummata of the heart, 543. 

Gummy tumor of the liver. See Liver, gummata of, 

417. 
Gusserow, 929. 
Guttman, 491, 499. 

Ilaematemesis, differential diagnosis, 282. 

etiology, 282. 

prognosis, 283. 

symptoms, 282. 

treatment, 283. 
Htematinuria, 641. 
Haeinatoma, definition, 977. 

of the dura. 995. 
Haematomata in the lungs, 170. 
Haematuria, differential diagnosis, 641. 

etiology, 640. 

prognosis, 642. 

symptoms, 640. 

treatment, 642. 
Hematuria, endemic, 640. 
Hemoglobinuria, 641. 
Haamopericardium, 542. 
Haemophilia, differential diagnosis, 943. 

etiology, 942. 

morbid anatomy, 942. 

prognosis, 943. 

symptoms, 942. 

treatment, 943. 
Haemophthisis, 923. 
Haemoptysis, 91. 

in phthisis, 217. 



Haemoptysis, differential diagnosis, 94. 

etiology, 91. 

morbid anatomy, 91. 

prognosis, 95. 

symptoms, 93. 

treatment, 95. 
Haemothorax, 199. 

etiology, 199. 

symptoms, 199. 

treatment, 199. 
" Hairy heart," 455. 
Hall, 1083. 
Hamilton, 213. 

Hammond, 1012, 1017, 1029, 111S. 

Hare, 1108. 

Harkin, 943. 

Harley, 1115. 

Harvard, 150. 

Hayden, 488, 494, 496, 568. 

Hay em, 1002, 1072. 

Hay fever, 89. 

Headache, 1091. 

Headache, sick. See Megrim, 1094. 

Heart, amyloid degeneration of, etiology, 530. 

morbid anatomy, 529. 

symptoms, 530. 

treatment, 530. 
Heart, aneurism of, 475. 

etiology, 535. 

morbid anatomy, 535. 

physical signs, 536. 

prognosis, 536. 

symptoms, 535. 

treatment, 536. 
Heart, atrophy of. etiology, 531. 

morbid anatomy, 531. 

prognosis, 532. 

symptoms, 531. 

treatment, 532. 
Heart, cancer of, 536. 

connective tissue hypertrophy, 525. 
Heart, cysts of, 537. 

Heart, dilatation of. See Cardiac dilatation, 515. 
Heart, diseases of, 454. 

Heart, fatty degeneration of, differential diagnosis, 
529. 

etiology, 527. 

morbid anatomy, 526. 

physical signs, 528. 

prognosis, 529. 

symptoms, 528. 

treatment. 529. 

varieties, 526. 
Heart, fatty infiltration. 526. 

Heart, fibroid disease of, differential diagnosis, 526. 

etiology, 525. 

morbid anatomy, 525. 

prognosis, £26. 

symptoms, 525. 

treatment, 526. 
Heart, fibroma of, 536. 
Heart, gummata of, 543. 

Heart, hvpertrophy of. See Cardiac hypertrophy, 
507. 

in nephritis, 614. 
Heart, lipoma of, 536. 
Heart, lymphoma of, 536. 
Heart, myoma of, 536. 
Heart, new formations in, varieties, 536. 
Heart, parasites of, 536. 

Heart, parenchymatous degeneration of, differential 
diagnosis, 530. 

etiology, 530. 

morbid anatomy, 530. 

prognosis, 530. 

symptoms, 530. 

treatment, 530. 
Heart, pigmentary degeneration, 530. 
Heart, rupture of, etiology, 532. 

morbid anatomy, 532. 

prognosis of, 532. 

symptoms, 532. 

treatment, 532. 
Heart, sarcoma of, 536. 
Heart, syphilitic disea>e of, etiology, 543. 

morbid anatomy, 543. 

symptoms, 543." 
Heart, tubercle in, 536. 



1134 



INDEX. 



Heart, valvular disease of, prognosis of, 501. 

valvular diseases of, treatment, 504. 
Heartburn, 261. 
Hebra, 804. 
IleidenJiain, 104. 

Heller, 905. * 
Helmholtz, 81. 

Hematogenous jaundice. See Jaundice, 427. 
Hemiplegia, causes of, 967. 

definition of, 967. 
Hemorrhage, intestinal, differential, diagnosis, 321. 

etiology, 320. 

morbid anatomy, 319. 

prognosis, 321. 

symptoms, 320. 

treatment, 321. 
Hemorrhagic diathesis. See Haemophilia, 942. 
Hemorrhagic nodular infarction, 148. 
Hemorrhagic variola. See Small-pox, 787, 793. 
Hemorrhoidal flux, 334. 
Hemorrhoids, differential diagnosis, 338. 

etiology, 337. 

morbid anatomy, 336. 

prognosis, 338. 

symptoms, 337. 

treatment, 338. 

varieties of, 336. 
Henle, 10S9. 

Hepatitis, circumscribed suppurative, differential 
diagnosis, 387. 

etiology, 384. 

morbid anatomy, 383. 

physical signs, 386. 

prognosis, 388. 

symptoms, 385. 

treatment, 388. 
Hepatitis, diffuse parenchymatous, differential diag- 
nosis, 392. 

etiology, 391. 

morbid anatomy, 389. 

physical signs, 392. 

prognosis, 392. 

symptoms, 391. 

treatment, 393. 
Hepatitis, interstitial diagnosis, 379. 

etiology, 376. 

morbid anatomy, 374. 

physical signs, 378. 

prognosis, 380. 

symptoms, 376. 

treatment, 380. 
Hepatization of pneumonia, 96. 

morbid anatomy, 98, 99. 
Hepatogenous jaundice. See Jaundice, 427. 
Heredity in phthisis, 204. 

Hernia, internal. See Intestinal obstruction, 326. 
Hertz, 162. 
Sine, 1039. 
Hirsch, 104, 686. 
Hirscliberg, 1025. 

Hob-nailed liver. See Hepatitis, 374. 
Hodgkin's disease, differential diagnosis, 936. 

etiology, 936. 

morbid anatomy, 935. 

prognosis, 937. 

symptoms, 936. 

treatment, 937. 
Holmes, 726. 
Hoppe, 991. 
Hoppe-Seyler, 643. 
Hubner, 806. 
Huguenin, 978, 994, 996. 
Hunter, 475. 
Huss, 122. 
Hutchinson, 1009. 
Hitter, 840. 

Hydatids of the brain. See Cerebral tumors, 1019. 
Hydatids of the kidney. See Kidney, hydatids of, 
636. 

Hydatids of the liver. See Liver, hydatids of, 419. 
Hydatids of the b"ig, 172. 
Hydatids of the spieen, 452. 
Hydraemia. See Anaemia, 923. 
Hydrocephalic cry, 987. 

Hydrocephalus, acute. See Meningitis, tubercular, 
985. 

Hydrocephalus, chronic, differential diagnosis, 992. 
etiology, 991. 



Hydrocephalus, chronic, morbid anatomy, 990. 

prognosis, 992. 

symptoms, 991. 

treatment, 992. 
Hydrocephalus senilis, 991. 
Hydrocephalus, spurious, 299. 
Hydronephrosis, differential diagnosis, 627. 

etiology, 627. 

morbid anatomy, 626. 

prognosis, 628. 

symptoms, 627. 

treatment, 628. 
Hydropericardium, etiology, 541. 

morbid anatomy, 541. 

prognosis, 542. 

symptoms, 542. 

treatment, 542. 
Hydrophobia and (Esophasitis, 254. 
Hydrophobia, differential diagnosis, 845. 

etiology, 843. 

morbid anatomy, 843. 

prognosis, 845. 

symptoms, 844. 

treatment, 845. 
Hydrops cystidis iellse. See Gall-bladder, 434. 
Hydrorachis, 1075. 
Hydrothorax, 197, 198- 
Hygroma of the dura mater, 995. 
Hyperaemia, cerebral. See Cerebral hyperaemia, 972. 
Hyperaemia, inflammatory, 1. 

Hyperaemia of the liver, acute. See Liver, hyperae- 
mia of, 369. 

Hyperaemia of the lungs, 141. See Lungs. 

Hyperaemia of the spinal cord and meninges. See 
Spinal cord and meninges, hyperaemia of, 
1033. 

Hyperaemia of the spleen. See Spleen, hyperaemia 

of, 447. 
Hyperesthesia, 970. 
Hyperplasia of fixed cells, 4. 

Hypertrophic cirrhosis of the liver, 381. See Liver. 
Hypertrophic nasal catarrh, 37. 
Hypertrophy, 9. 
etiology, 9. 

Hypertrophy of the brain. See Brain, hypertrophy 
of, 1029. 

Hypertrophy of the heart. See Cardiac hypertrophy, 
507. 

Hypertrophy of the spleen. See Spleen, hypertro- 
phy of, 450. 
Hypostatic congestion, 142. 
Hypostatic pneumonia, 143. 
Hysteria, differential diagnosis, 1107. 

etiology, 1104. 

morbid anatomy, 1104. 

prognosis, 1108. 

s\ mptoins, 1105. 

treatment, 1108. 
Hystero epilepsy, differential diagnosis, 1109. 

etiology, 1109. 

prognosis, 1109. 

symptoms, 1109. 

treatment, 1110. 

Icterus. See Jaundice, 427. 

Ileitis. See Enteritis, 287. 

Immerman, 926, 928. ' 

"India liver, 1 ' 373. 

Induration, brown, 141. 

Induration, inflammatory, 5. 

Induration of lung, brown, 142. 

Induration, pigment, 142. 

Int i utile convulsions and eclampsia, 1086. 

Infantile remittent fever, 863. 

Infantile spinal paralysis. See Paralysis, infantile 

spinal, 1048. 
Infarction, 558. 

Infarction, hemorrhagic, nodular, 148. 
Infarction of the kidney. See Eenal hemorrhage, 
588. 

Infarction of the lungs, 148. 

Infarction of the spleen, 448. 

Infarction, pulmonary, differential diagnosis, 151. 

etiology, 150. 

morbid anatomy, 148. 

physical signs, 151. 

prognosis, 151. 

symptoms, 151. 



INDEX. 



1135 



Infarction, pulmonary, treatment, 152. 
Infectious endocarditis, 467. See Endocarditis. 
Inflammation, adhesions in, 6. 

catarrhal. 6. 

cellular elements in, 3. 

cicatrization in, 4. 

croupous, 7. 

definition of, 1. 

diphtheritic, 7. 

exudative changes in, 2. 

fate of pus in, 9. 

interstitial, 9. 

mucous, 6. 

necrosis in, 4. 

of free surfaces, 5. 

of mucous surfaces, 6. 

of serous membranes, 5. 

parenchymatous, 8. 

parenchymatous changes in, 3. 

resolution in, 3. 
Inflammation, serous, 5. 

suppuration in, 3. 

terminations of, 3. 

ulceration in, 7. 

vascular changes in, 1. 
Influenza, differential diagnosis, 839. 

etiology, 838. 

morbid anatomy, 837. 

prognosis, 839. 

symptoms, 838. 

treatment, 839. 
Inherited syphilis. See Syphilis, 962. 
Inoculation, 799. 
Insolation. See Sunstroke, 1115. 
Insufficiency at the aortic orifice. See Aortic regur- 
gitation, 482. 

Insufficiency at the mitral oiifice. See Mitral regur- 
gitation, 491. 

Insufficiency at the pulmonary orifice. See Pulmonic 

regurgitation, 501. 
Insufficiency at the tricuspid orifice. See Tricuspid 

regurgitation, 496. 
Intercostal neuralgia, 1091. 
Intermittent fever, differential diagnosis, 855. 

etiology, 851. 

morbid anatomy, 850. 

prognosis, 855. 

symptoms, 851. 

treatment, 855. 

varieties, 851. 
Intermittent fever, masked, 857. 
Internal hernia. See Intestinal obstruction, 326. 
Interstitial endocarditis, 473. See Endocarditis. 
Interstitial hepatitis. See Hepatitis, interstitial, 374. 
Interstitial nephritis, acute. See Nephritis, 602. 
Interstitial nephritis, chronic. See Nephritis, 610. 
Interstitial pneumonia, 134. 
Intestinal catarrh. See Enteritis, 287. 
Intestinal colic. See Colic, intestinal, 349. 
Intestinal dyspepsia. See Dyspepsia, intestinal, 301. 
Intestinal hemorrhage. See Hemorrhage, intestinal, 
319. 

Intestinal obstruction, definition of, 321. 

differential diagnosis, 326. 

etiology, 321, 322. 

morbid anatomy, 322. 

prognosis, 327. 

symptoms, 324. 

treatment, 328. 

varieties of, 321. 
Intestinal parasites, description of, 338. 

differential diagnosis, 344. 

etiology, 342. 

morbid anatomy, 338-342. 

prognosis, 344. 

symptoms, 342. 

treatment, 344. 

varieties of, 306-342. 
Intestinal ulcers, diffuse catarrhal, etiology, 317. 

morbid anatomy, 317. 
Intestinal ulcers, follicular, symptoms, 288, 317. 
Intestinal ulcers, tuberculous, differential diagnosis, 
319. 

etiology, 318. 

morbid anatomy, 317. 

physical signs, 319. 

prognosis, 319. 

symptoms, 318. 



Intestinal ulcers, tuberculous, treatment, 319. 

Intestinal ulcers, varieties of, 315. 

Intestine, cancer of, differential diagnosis of, 332. 

etiology, 331. 

morbid anatomy, 330. 

prognosis, 333. 

symptoms, 331. 

treatment, 333. 
Intestines, classification of diseases of, 287. 
Intestines, waxy degeneration of, differential diag- 
nosis, 330. 

etiology, 329. 

morbid anatomy, 329. 

prognosis, 330. 

symptoms, 329. 

treatment, 330. 
Intra-thoracic tumors and sub-acute pleurisy, 183. 
Intubation of larynx, 46, 5S. 
Intussusception. See Intestinal obstruction, 322. 
Invagination. 322. 
Irritability, electrical, 966. 
Irritation, spinal. See Spinal irritation, 1117. 
Ischsemia, 923. 

Jaccoud, 467. 

Jackson, 1018, 1009, 1097, 1106. 
Jaundice, differential diagnosis, 428. 

etiology, 428. 

morbid anatomy, 427. 

varieties of, 427. 
Jaundice, malignant. See Parenchymatous hepatitis, 
389. 

Jejunitis. See Enteritis, 287. 
Jenner, 219, 525, 799, 1020. 
Johnson, 550, 611. 
Jolly, 1004-1006. 
Jones. 1084. 

Jiirgensen, 123, 127, ISO, 133, 148. 

KaMer, 1062. 
Kelley, 1070. 

Kidney, acute Bright's disease of, differential diag- 
nosis, 599. 

etiology, 594. 

morbid anatomy, 592. 

prognosis, 599. 

symptoms, 595-598. 

treatment, 600. 
Kidney, amyloid form of Bright's disease of, 617. 
Kidney, amyloid, 617. 

differential diagnosis, 620. 

etiology, 618. 

morbid anatomy, 617. 

prognosis, 620. 

symptoms, 619. 

treatment, 621. 
Kidney, Bright's diseases of, varieties of, 591. 
Kidney, calculi in. See Renal calculi, 629. 
Kidney, cancer of. See Renal cancer, 633. 
Kidney, chronic Bright's diseases of, 604. 
Kidney, chronic parenchymatous inflammation of. 

See Nephritis, chronic parenchymatous', 604. 
Kidney, cirrhotic, Bright's diseases of, differential 
diagnosis, 615. 

etiology, 612. 

morbid anatomy, 610. 

prognosis, 615. 

symptoms, 613. 

treatment, 615. 
Kidney, congestion of. See Renal hyperemia, 583. 
Kidney, cystic. See Cystic kidney, 628. 
Kidney, diseases of, 583. 
Kidney, dropsy of. See Hydronephrosis, 626. 
Kidney, embolism of. See Renal hemorrhage, 588. 

fibromata of, 635. 
Kidney, floating or movable, 639. 
Kidney, gummata of, 635. 

Kidney, hemorrhage of. See Renal hemorrhage, 588. 
Kidney, hydatids of, morbid anatomy, C36, 637. 
Kidney, hyperemia of. See Renal hyperemia, 583. 
Kidney, infarction of. See Renal hemorrhage, 588. 
Kidney, large granulo-fatty, G04. 
Kidney, large while, 605. 
Kidney, leukemic tumors in, 635. 
Kidney, lipomata of, 635. 
Kidney, lymphadenomata of, 635. 
Kidney of heart disease, 5S5. 



1136 



INDEX. 



Kidney, parasites in, 636. 
Kidney, sarcomata of, 635. 
Kidney, small granular, fatty, 605. 
Kidney, surgical. See Nephritis, acute interstitial, 
602. 

Kidney, tuberculosis of, differential diagnosis, 636. 

etiology, 636. 

morbid anatomy, 635. 

prognosis, 636. 

symptoms, 636. 

treatment, 636. 
Kidney, waxy degeneration of, differential diagno- 
sis, 620. 

etiology. 618. 

morbid anatomy, 617. 

prognosis, 620. 

symptoms, 619. 

treatment, 621. 
ffirchoff, 1046. 
Klebs, 467, 603, 849. 
Klein, 807. 
Klob, 978. 
Knapp, 1120. 
Knec/it, 791. 
Koehler, 1035. 
Kolliker, 937. 
Roster. 1115. 
Kreizmg, 473. 
Kvnze, 1104. 
Kiittner, 149. 
Kussmaul, 549. 

Lady Montague, 799. 
Laennec, 117, 211. 232, 475. 
Lae'nnec's rale, 165. 
Lafayette mixture, 646. 
Lancereavx, 1003. 

Laporotomy in intestinal obstruction, 329. 

Lardaceous degeneration of the intestines. See In- 
testines, waxy degeneration of, 329. 

Lardaceous degeneration of the liver. See Amyloid 
liver, degeneration of, 400. 

Large white kidney. See Nephritis, chronic paren- 
chymatous, 605. 

La Roche, 693. 

Laryngeal paralysis. 60. See Larynx, neuroses of. 

differential diagnosis, 62. 

etiology, 61. 

prognosis, 62. 

symptoms. 61. 

treatment, 63. 
Laryngeal spasm, hysterical and acute catarrhal 

laryngitis. 45. 
Laryngismus stridulus, 63. 
Laryngitis, acute catarrhal, 43. 

differential diagnosis, 45. 

etiology, 44. 

morbid anatomy, 44. 

prognosis, 45. 

symptoms, 44. 

treatment, 46. 
Laryngitis, acute croupous, 53. 

differential diagnosis of, 56. 

etiology of, 54. 

morbid anatomy of, 54. 

prognosis of, 56. 

symptoms of, 54. 

treatment of, 57. 
Laryngitis, chronic catarrhal, differential diagnosis 
of, 48. 

etiology of. 47. 

morbid anatomy, 47. 

prognosis, 48. 

symptoms, 47. 

treatment, 48. 
Laryngitis, chronic catarrhal in phthisis, 49. 

differential diagnosis, 50. 

etiology, 50. 

morbid anatomj', 50. 

prognosis, 50. 

symptoms, 50. 

treatment. 50. 
Laryngitis, chronic catarrhal in syphilis, 51. 
Larynx, cancer of, 65. 

catarrhal ulcer of, 58. 

classification of diseases of, 43. 

cystic tumors of, 65. 

diseases of, 43. 



Larynx, fibro-cellular growths of, 65. 

fibromata of, 65. 

follicular ulcer of, 58. 

glandular growths of, 65. 
Larynx, neuroses of, differential diagnosis, 62. 

etiology, 61. 

morbid anatomy, 60. 

prognosis, 62. 

symptoms, 61. 

treatment, 63. 
Larynx, oedema of, 51. 

papilloma of, 65. 

phthisical ulcers of, 58. 
Larynx, spasmodic affections of, 63. 

differential diagnosis, 64. 

etiology, 63. 

morbid anatomy, 63. 

prognosis, 64. 

symptoms, 64. 

treatment, 64. 
Larynx, syphilitic ulcers of, 59. 
Larynx, tumors of. 65. 

differential diagnosis, 67. 

etiology, 65. 

morbid anatomy, 65. 

prognosis, 67. 

symptoms, 65. 

treatment, 67. 
Larynx, typhus ulcers of, 58. 
Larynx, ulcers of, differential diagnosis, 60. 

etiology, 59. 

morbid anatomy, 58. 

prognosis, 60. 

symptoms, 59. 

treatment, 60. 

varieties of, 58. 
Larynx, variolus ulcer of, 58. 
Lasegve, 1107. 

Lateral sclerosis, amyotrophic. See Amyotrophic 

lateral sclerosis, 1067. 
Lavaran, 846. 
Lay cock, 923. 

Lead colic. See Colic, intestinal, 349. 

Lead palsy. See Chronic lead poisoning, 1080. 

Lead poisoning, 350. 

Lead poisoning, chronic, differential diagnosis, 1082. 

etiology. 1080. 

morbid anatomy, 1080. 

prognosis, 1082. 

symptoms, 1080. 

treatment, 1082. 
Lebert, 121, 122, 472, 754,755, 900, 928, 929, 1019, 1026, 

1083. 
Leqq, 942. 

Lenitis. See Phlegmonous gastritis, 765. 
Leo, 791. 
Lepine, 1104. 

Leptothrix buccalis. See Thrush, 241. 

Letulle, 938. 

Letzreich, 840. 

Lenbe, 597. 

Leucin, 571. 

Leucocvtes, 3. 

Leucocythgemia, differential diagnosis, 934. 

etiology, 933. 

morbid anatomy, 931. 

prognosis, 934. 

symptoms, 933. 

treatment, 935. 
Leucocytosis. 931. 
Leucoma'ines in fever. 
" Leukaemia." See Leucocythsemia, 931. 
Leukaemia, pseudo. See Hodgkin's disease, 935. 
Leukemic tumors of the kidney, 635. 
Leuko-mvelitis, 1060. 
Leyden, 494, 1039, 1041, 1045, 1050. 
Lichen lividus, 946. 
Lichtheim, 158. 
Liebermeister. 126. 
Lipomata in the lungs, 170. 

Lipomata in the brain. See Cerebral tumors, 1019. 
Lipomata in the heart, 536. 
Lipomata of the kidney, 635. 
Liouville, 1072. 
Lithaemia, 915. 

etiology, 915. 

symptoms, 915. 

treatment, 916. 



1137 



Litten, 928. 

Liver, abscess of. See Hepatitis, 383. 
Liver, active bvperaemia of, differential diagnosis, 
370. 

etiology, 370. 

morbid anatomy, 369. 

physical signs, 370. 

prognosis, 371. 

symptoms, 370. 

treatment, 371. 
Liver, acute yellow atrophy of. See Hepatitis, 3S9. 
Liver, amyloid degeneration of, differential diagno- 
sis, 403. 

etiology, 402. 

morbid' anatomy, 400. 

physical signs, 403. 

prognosis, 403. 

symptoms, 402. 

treatment, 403. 
Liver, cancer of, differential diagnosis, 415. 

etiology, 414. 

morbid anatomy, 412. 

physical signs, 415. 

prognosis, 416. 

symptoms, 414. 

treatment, 416. 

varieties, 411. 
Liver, cbronic atrophy of, differential diagnosis, 405. 

etiology, 405. 

morbid anatomy, 404. 

physical signs, 405. 

prognosis, 405. 

symptoms, 405. 

treatment, 406. 
Liver, cirrhosis of. See Hepatitis, interstitial, 374. 
Liver, congestion of. See Passive hypersemia of the 

liver, 371. 
Liver, diseases of, 369. 

Liver, fatty degeneration of. See Fatty liver, 406. 
Liver, hypertrophic cirrhosis of, 381. 

differential diagnosis, 382. 

etiology, 332. 

morbid anatomy, 38*1. 

prognosis, 383. 

symptoms, 382. 

treatment, 3S3. 
Liver, fatty infiltration of. See Fatty liver, 406. 
Liver, fatty metamorphosis of. See. Fatty liver, 406. 
Liver, functional derangements of, differential diag- 
nosis, 443. 

etiology, 440. 

prognosis, 443. 

symptoms, 441. 

treatment, 443. 
Liver, gouty. See Hepatitis, interstitial, 374. 
Liver, granular. See Hepatitis, interstitial, 374. 
Liver, gummata of, differential diagnosis, 418. 

etiology, 418. 

morbid anatomy, 417. 

physical signs, 418. 

prognosis, 418. 

symptoms, 418. 

treatment, 418. 
Liver, hvdatids of. differential diagnosis, 422. 

etiology. 421. 

morbid anatomy, 419. 

physical signs, 422. 

prognosis, 423. 

symptoms, 421. 

treatment, 423. 
Liver, hypertrophic cirrhosis of, 381. 

differential diagnosis, 882. 

etiology, 332. 

morbid anatomy, 381. 

prognosis, 383. 

symptoms, 382. 

treatment, 333. 
Liver, melanotic sarcoma of, 412. 
Liver, multilocular hydatids of, differential diagno- 
sis, 425. 

etiology, 425. 

morbid anatomy, 424. 

physical signs, 425. 

prognosis, 426. 

s} r mptoms, 425. 

treatment, 426. 
Liver, passive hypereemia of, differential diagnosis, 
373. 

72 



| Liver, passive hyperemia of, etiology, 372. 

morbid anatomy, 371. 

physical signs, 373. 

prognosis, 373. 

symptoms, 373. 

treatment, 373. 
Liver, pigment degeneration of, differential diagno- 
sis, 411. 

etiology, 410. 

morbid anatomy, 409. 

physical signs, 411. 

prognosis, 411. 

symptoms, 410. 

treatment, 411. 
Liver, pulsating, 499. 

Liver, torpid. See Functional derangements of 

liver, 440. 
Liver, tuberculosis of, etiology, 427. 

morbid anatomy, 426. 

symptoms, 427. 
Liver, waxy. See Amyloid degeneration of, 400. 
Livingstone, 865. 

Lobular pneumonia. See Pneumonia, lobular, 128. 
Localization of cerebral lesions, 1012-1014. 
Localized spasm and paralysis, differential diagno- 
sis, 1079. 

etiology, 1078. 

morbid anatomy, 1078. 

prognosis, 1079. 

symptoms, 1078. 

treatment, 1079. 
Lock-jaw. See Tetanus, 1086. 
Locomotor ataxia, differential diagnosis, 1064. 

etiology, 1061. 

morbid anatomy, 1060. 

prognosis, 1065. 

symptoms, 1062. 

treatment, 1065. 
Louis, 105. 
Lumbago, 906. 
Lung, atrophy of, 172. 

etiology, 172. 

morbid anatomy, 172. 

physical signs, 172. 

symptoms, 172. 
Lungs, active hyperaemia of, 141. 
Lungs, ansemia of, 155. 
Lungs and pleura, diseases of, 96. 
Lungs, brown induration of, 142. 
Lungs, cancer of, 168. 

differential diagnosis, 169. 

etiology, 169. 

physical signs, 169. 

prognosis, 170. 

symptoms, 169. 

treatment, 170. 

varieties of, 168. 
Lungs, carnification of, 142. 

cirrhosis of, 134. 

coal-miner's, 139. 

compensatory hyperemia of, 141. 

compression of. See Atelectasis, 157. 

congestion of, 141. 

dermoid cysts in, 170. 

echinococci. See Hydatids, 172. 

enchondromata in, 170. 

epithelioma of, 171. 

fat embolism of, 150. 

fibromata in, 170. 

gangrene of, 153. 

haematomata in, 170. 
Lungs, hydatids of, 172. 

differential diagnosis, 173. 

etiology, 173. 

morbid anatomy, 173. 

prognosis, 173. 

symptoms, 173. 
Lungs, hydatids of, treatment, 174. 
Lungs, hypersemia of, 141. 

differential diagnosis, 143. 

etiology, 143. 

morbid anatomy, 141. 

physical signs, 143. 

prognosis, 143. 

symptoms, 143. 

treatment, 143. 

varieties, 141. 
Lungs, infarction of, 148. 



1138 



INDEX. 



Lungs, lipomata in, 170. 

melanotic tumors in, 170. 

"Millers'," 139. 

myxomata in, 170. 
Lungs, non-malignant growths in, 170. 

differential' diagnosis, 171. 

symptoms, 171. 
Lungs, oedema of. See. (Edema, pulmonary, 145. 

osteomata in, 170. 

passive hyperaemia of, 141. 

sarcomata in, 170. 

sclerosis of, 134. 

splenization of, 141. 
Lungs, syphilitic disease of, 171. 

morbid anatomy, 171. 

symptoms of, 171. 
Lumbago, 906. 
Luys, 1012, 1013. 1111. 
Lymphadenomata of the kidney, 635. 

of the heart, 536. 

Mackenzie, 1121. 
MaekriU, 703. 
Maclean, 887. 
Magnan, 1033. 
Mahomed, 553, 578, 948. 
Maier, 519. 

Malarial fever, continued. See Continued malarial 

fever, 867. 
.Malarial fever, introduction, 846-850. 
Malarial fever, pernicious. See Pernicious malarial 

fever, 877. 

Malarial infection, chronic. See Chronic malarial 

infection, 891. 
Malarial miasm, generation of, 847. 
Malassez, 220. 

Malignant jaundice. See Hepatitis, parenchymatous, 
389. 

Malignant pustule and gangrenous stomatitis, 239. 

Manassein, 780. 

Mania ephemera, 973. 

MannkopJ\ 721. 

Marantic thrombi, 533. 

Ma rch i a fa v a , 846 . 

Masked intermittent fever, 857. 

Maumene's test for sugar in the urine, 919. 

Maw-worm. See Intestinal parasites, 338. 

Mayer, 899, 973. 

Measles, complications, 827. 

differential diagnosis, 828. 

etiology, 823. 

morbid' anatomy, 822. 

prognosis, 829. 

sequelae, 828. 

■stages, 824. 

symptoms, 824. 

treatment, 830. 
Measles. German. See German measles, 831. 
Meckel, 475. 

Media for bacterial cultures, 25. 
Mediastinal tumors, etiology, 569, 

physical signs, 569. 

prognosis. 569. 

seat of, 509. 

symptoms. 569. 

treatment, 569. 

varieties of, 568. 
Megrim, 1094-5. 
Meigs, 842. 
Melaena, 320. 

Melanotic liver. See Liver, pigment degeneration 
of, 409. 

Melanotic tumors in the lungs, 170. 

Melasma suprarenalis. See Addison's disease, 937. 

Melier, 702. 

Mellituria. See Diabetes mellitus, 917. 
Membranous croup. See Laryngitis, acute croup- 
ous, 54. 

Membranous oesophagitis. See Oesophagitis, 252. 
Membranous pharyngitis, 251. 
Meniere's disease. See Vertigo, 1120. 
Meningeal delirium, 970. 

Meninges, hyperaemia of. See Spinal cord and 

meninges, hypersemia of, 1033. 
Meninges, tumors, etc. See Brain and meninges, 

tumors of, 1019. 
Meningitis, acute, differential diagnosis, 981. 
etiology, 978. 



Meningitis, acute, morbid anatomy, 977. 

prognosis, 981. 

stages, 979. 

symptoms, 979. 

treatment, 981. 
Meningitis, cerebro-spinal. See Cerebro-spinal men- 
ingitis, 712. 

Meningitis, chronic, differential diagnosis, 984. 

etiology, 984. 

morbid anatomy, 983. 

prognosis, 985. 

symptoms, 984. 

treatment, 985. 
Meningitis, epidemic cerebro-spinal. See Meningi- 
tis, epidemic, 712. 
Meningitis foudro\ r ante, 718. 
Meningitis, spinal, differential diagnosis, 1036. 

etiology, 1035. 

morbid anatomy, 1034. 

prognosis, 1036. 

symptoms, 1035. 

treatment, 1037. 
Meningitis, sub-acute, differential diagnosis, 983. 

etiology, 982. 

morbid anatomy, 982. 

prognosis, 983. 

symptoms, 982. 

treatment, 983. 
Meningitis, varieties, 977. 

Meningitis, tubercular, differential diagnosis, 989. 

etiology, 986. 

morbid anatomy, 985. 

prognosis, 989. 

stages, 987. 

symptoms, 986. 

treatment, 990. 
Menjaud, 1055. 

Mental disturbances in nervous diseases, 970. 

Mercurialism, chronic, 1081-2. 

Mercurial tremor. See Chronic mercurialism, 108 

Mercury in nephritis, 601, 616. 

Merkel, 713, 938. 

Meschede, 713. 

Meyer, 1049, 1051. 

Miasm, definition of, 648. 

Miasmatic contagious diseases, 648. 

Miasmatic diseases, 648. 

Michell, 699. 

Micrococci, definition, 29. 
Micrococci of diphtheria, 730, 733. 
Micrococci of endocarditis, 466. 
Micrococci of erysipelas, 745. 
Micrococci of pneumonia, 105. 
Micrococci of pyaemia, 725. 
Micrococci, pathogenic, 33. 
Migraine, 1090. 
Miliaria alba. 834. 

Miliary fever, differential diagnosis, 836. 

etiology, 834. 

morbid anatomy, 834. 

prognosis, 836. 

symptoms, 835. 

treatment, 837. 
Miliary tuberculosis, acute. See Tuberculosis, acute 

miliary, 750. 
Mitchell, 1029, 1068-1115. 

Mitral obstructions. See Mitral stenosis, 487. 
Mitral regurgitation, differential diagnosis, 495. 

etiology, 493. 

morbid anatomy. 491. 

physical signs, 494. 

symptomsr493. 
Mitral stenosis, differential diagnosis, 491. 

etiology, 489. 

morbid anatomy, 487. 

physical signs, 490. 

symptoms, 489. 
Montar/ue, Lady Mary, 799. 
Moore's test for sugar in the urine, 919. 
Morbus Addisonii." See Addison's disease, 937. 
Morbus maculosus Werlhofii. See Purpura, 945. 
Morphine in urcemia, 582. 
Moster, 942. 
Motor paralvsis, 965. 
Mouline, 1020. 
Mouth, diseases of, 236. 
i Movable or floating kidney. See Kidney, floating 
or movable, 638. 



INDEX. 



1139 



Moxon, 597, 1042. 

Mucous membrane, croupous inflammation of, 7. 
Mucous surfaces, inflammation of, 6. 
Mucous surfaces, ulceration of, 7. 
Mucus, 574. 

" Muguet." See Thrush, 241. 
Mulberry rash, 760. 
Multilocular hydatids, 424. 

Multilocular hydatids of liver. See Liver, multilocu- 
lar hydatids of, 424. 
Mummification, 20. 
Mumps. See Parotitis, 245. 
Murchison, 441, 442, 757, 769. 
Murmurs, cardiac, history of, 475. 

mechanism of, 475. 

post-diastolic, 485. 

theories of, 475. 
Murmurs, endocardial, characteristics of, 477. 

classification of, 478. 

combination of, 477. 

relative frequency of, 477. 

table of, 477. 

Muscular atrophy, progressive. See Progressive mus- 
cular atrophy, 1053. 
Muscular nutrition, 966. 

Muscular rheumatism. See Rheumatism, muscular, 
906. 

Myalgia. See Rheumatism, 906. 

"Mycosis endocardii." See Endocarditis, 467. 

Myelitis, acute, differential diagnosis, 1040. 

etiology, 1038. 

morbid anatomy, 1038. 

prognosis, 1040. 

symptoms, 1039. 

treatment, 1040. 

varieties of, 1037. 
Myelitis, chronic, differential diagnosis, 1042. 

etiology, 1041. 

morbid" anatomy, 1041. 

prognosis, 1042. 

symptoms, 1041. 

treatment, 1042. 
Myelogenic leukaemia. 933. 
Myelogenic pseudo-leukaemia, 928. 
Myocarditis, differential diaguosis, 524. 

etiology, 523. 

morbid anatomy, 522. 

prognosis, 524. 

symptoms, 523. 

treatment, 524. 

varieties of, 522. 
Myocarditis, chronic. See Fibroid diseases of the 

heart, 525. 
Myomata of the heart, 536. 
Myxcedema, differential diagnosis, 948. 

etiology, 948. 

morbid anatomy, 947. 

prognosis, 949. 

symptoms, 948. 

treatment, 949. 
Myxomata in lungs, 170. 

Myxomata of the brain. See Cerebral tumors, 1022. 

Nasal catarrh, atrophic, 39. 
Nasal catarrh, chronic. See Chronic coryza, 36. 
Nasal catarrh, dry. See Atrophic nasal catarrh, 
39. 

Nasal catarrh, fetid. See Ozpena, 41. 

Nasal catarrh, hypertrophic, 37. 

Nasal passages, classification of diseases of, 35. 

Nasal passages, diseases of, 35. 

Naso-pharyngeal catarrh, chronic. See Hypertrophic 

nasal catarrh, 37. 
Necrosis, 19. 
Necrosis, causes, 20. 

coagulation, 21. 

coagulation in phthisis, 202. 

terminations, 21. 

varieties, 20. 
Nephritic colic, 631. 
Nephritis, 591. 
Nephritis, acute, 592. 

differential diagnosis, 599. 

etiology, 594. 

morbid anatomy, 592. 

prognosis, 599. 

symptoms, 595. 

treatment, 600. 



Nephritis, acute interstitial, differential diagnosis, 
603. 

etiology, 603. 

morbid anatomy, 602. 

prognosis, 604. 

symptoms, 603. 

treatment, 604. 
Nephritis, amyloid, 617. See Kidney. 
Nephritis, catarrhal, 591. 
Nephritis, chronic interstitial, 610. 

differential diagnosis, 615. 

etiology, 612. 

morbid anatomy, 610. 

prognosis, 615. 

symptoms. 613. 

treatment, 615. 
Nephritis, chronic parenchymatous, differential diag- 
nosis, 607. 

etiology, 606. 
• morbid anatomy, 604. 

prognosis, 608. 

symptoms, 606. 

treatment, 609. 
Nephritis, desquamative, 593. 
Nephritis, diffuse, 602. 
Nephritis, glomerular, 593. 
Nephritis, parasitic, 603. 
Nephritis, strumous, 635. 
Nephritis, varieties, 591. 

Nervous cardiac palpitation. See Cardiac palpita- 
tion, nervous, 537. 

Nervous system, functional diseases of, 1096. 

Nervous system, general symptomatology of the 
diseases of, 965. 

Neuman, 933. 

Neuralgia, differential diagnosis, 1092. 

etiology, 1089. 

morbid anatomy, 1088. 

prognosis, 1093. 

symptoms, 1089. 

treatment, 1093. 

varieties, 1090. 
Neurasthenia, differential diagnosis, 1112. 

etiology, 1111. 

prognosis, 1112. 

symptoms, 1111. 

treatment, 1112. 
Neuritis nodosa, 1076. 
Neurotic nodes, 904. 
Neuroses of the heart, varieties of, 537. 
Neuroses of the larynx, 60. 

Neuroses of the stomach. See Stomach, neuroses of, 
281. 

New formations in the heart. See Heart, new forma- 
tions in, 536. 

New growths in the kidney. See Kidney, new 

growths in, 635. 
New Mexico, climate of, 235. 

Niemeijer, 134, 136, 205, 452, 468, 511, 899, 926, 928, 

952, 972, 990, 991, 999, 1009, 1017, 1021, 1032, 

1048, 1085. 
Nitro-glycerine in renal disease, 537. 
Nitro-glycerine in valvular disease, 5C6. 
Nodular infarction, pulmonary, 148. 
Nodular pulmonary apoplexy, 148. 
Noma. See Ulcerative stomatitis, 240. 
Non-inflammatory softening of the spinal cord. See 

Spinal cord, non-inflammatory softening of, 

1042. 

Non-malignant growths in the lungs, 170. 
Not/inagel, 972, 973, 976, 999, 1010, 1102, 1104. 
Nutrition, muscular, 966. 

Obermeier, 791, 1021, 1023. 
(Edema glottidis, 51. 

differential diagnosis of, 52. 

etiology of, 52. 

morbid anatomy of, 52. 

prognosis of, 53. 

symptoms of, 52. 

treatment, of, 53. 
(Edema of the larynx. 51. 
(Edema, pulmonary, differential diagnosis, 146. 

etiology, 145. 

morbid anatomy, 145. 

physical signs, 146. 

prognosis, 147. 

symptoms, 146. 



1140 



INDEX. 



(Edema, pulmonary, treatment, 147. 
(Edema. Vhchow's brown, 142. 
Oertel, 733, 84<). ' 

Oesophagitis, differential diagnosis, 254. 

etiology, 252. 

membranous, 252. 

morbid anatomy, 252. 

prognosis, 254. 

symptoms, 253. 

treatment. 254. 
(Esophagus, cancer of, differential diagnosis, 255. 

etiology, 254. 

morbid anatomy, 254. 

prognosis, 255. 

symptoms, 255. 

treatment, 255. 
(Esophagus, diseases of, 252. 
(Esophagus, stricture of, 253. 
Ogle, 1000. 

O'idium albicans. See Thrush, 241. 

Oligsemia, 923. 

OHivier, 1089. 

Oppolzpr, 1083. 

Ord, 947. 

Ormerod, 500. 

Osteomata in the lungs, 170. 

Osteomata of the brain. See Cerebral tumors, 1019. 
Otto, 992. 

Oxalate of lime in urine, 573. 
Oxyuris vermicularis, 341. 
Ozcena, 41. 

differential diagnosis, 42. 

etiology, 41. 

morbid anatomy, 41. 

prognosis, 42. 

symptoms, 41. 

treatment, 42. 

Pachymeningitis externa, differential diagnosis, 994. 

etiology, 993. 

morbid anatomy, 993. 

prognosis. 994. 

symptoms, 994. 

treatmi nt, 994. 
Pachymeningitis interna, differential diagnosis, 997. 

etiology, 995. 

morbid anatomy, 994. 

prognosis, 997. 

symptoms. 995. 

treatment, 997. 
Pachymeningitis spinalis, 1035. 
Paget, Mi. 

Palpitation of the heart, nervous. See Cardiac pal- 
pitation, nervous, 537. 
Pancreas, iitrophy of, 316. 
Pancreas, calculi of, morbid anatomy, 447. 

etiology, 447. 

symptoms, 447. 
Pancreas, cancer of, differential diagnosis, 446. 

etiology, 446. 

morbid anatomy, 445, 446. 

prognosis, 446. 

symptoms, 446. 
Pancreas, cysts of, et.i ology, 446. 

morbid anatomy, 446. 

symptoms, 446. 
Pancreas, diseases of, 444. 
Pancreas, fatty degeneration of, 445. 
Pancreas, round worms in, 447. 

small-celled sarcoma of, 446. 

s\ philitic gummata of, 446. 

tuberculosis of, 446. 

waxy degeneration of, 445. 
Pancreatitis, acute, differential diagnosis, 444. 

etiology, 444. 

morbid anatomy, 444. 

prognosis, 444. 

symptoms, 444. 

treatment, 444. 
Pancreatitis, chronic, etiology, 445. 

morbid anatomy, 445. 

symptoms, 445. 
Panum. 726. 

Papillomata of the brain. See Cerebral tumors, 1019. 

of the larynx, 65. 
Paralysis, acute ascending, differential diagnosis, 
1070. 

etiology, 1070. 



Paralysis, acute ascending, prognosis, 1071. 

symptoms, 1070. 

treatment, 1071. 
Paralysis, acute bulbar, etiology, 1043. 

morbid anatomy, 1043. 

prognosis, 1044. 

symptoms, 1043. 

treatment, 1044. 
Paralysis, acute spinal, of adults, differential diag- 
nosis, 1051. 

etiology, 1(151. 

prognosis, 1052. 

symptoms, 1051. 

treatment, 105-2. 
Paralysis agitans, differential diagnosis, 1084. 

etiology, 1083. 

morbid anatomy, 1083. 

prognosis, 1084. 

symptoms, 1083. 

treatment, 1084. 
Paralysis, Bell's. See Facial paralysis, 1084. 
Paralysis and spasm, localized. See Localized spasm 

and paralysis, 1078. 
Paralysis, chronic bulbar, differential diagnosis, 1047. 

etiology, 1046. 

morbid anaiomy, 1044. 

prognosis, 1047. 

symptoms, 1046. 

treatment, 1047. 
Paralysis, facial, differential diagnosis, 1084-5. 
Paralysis, general, 963, 

Paralysis, glosso labio-laryngeal. See Chronic bul- 
bar paralysis, 1044. 
Paralysis, infantile spinal, differential diagnosis, 
1050. 

etiology, 1049. 

morbid anatomy, 1048. 

prognosis, 1050. 

symptoms, 3049. 

treatment, 1051. 
Paralysis, lead. See Chronic lead-poisoning, 1083. 
Paralysis, motor, 965. 

Paralysis of the abductors of the vocal cords, 60. 

of the adductors of the vocal cords, 60. 

of the tensors of the vocal cords, 60. 
Paralysis, pseudo-hypertrophic. See Pseudo-hyper- 

trophic paralysis, 1068. 
Paralysis, recurrent laryngeal, 60. 
Paralysis, sensory, 969. 

Paralysis, spastic. See Amyotrophic lateral sclero- 
sis, li 67. 
Paraplegia, causes of, 968. 

definition of. 968. 
Parasites, intestinal. See Intestinal parasites, 338. 
Parasites in the heart, 536. 
Parasites in the kidney, 636. 
" Parasitic nephritis." See Nephritis, 603. 
Parchappe, 1030. 
Paresis, 965. 

Parenchymatous inflammation, 8. 
Parkes, 898. 

Parotitis, differential diagnosis, 247. 

etiology, 246. 

metastatic, 246. 

morbid anatomy, 245. 

prognosis, 247. 

symptoms, 246. 

treatment, 247. 

varieties of, 245. 
Parrot, 1107. 

Passive hyperemia of the liver. See Liver, passive 

hypersemia of, 371. 
Pasteur, 843, 844, 940. 
Peacock, 479. 
Peasoup discharges, 666. 
Penzoldt, 946. 
Pepper, 923. 

Periarteritis, etiology, 549. 

morbid anatomy, 549. 
Pericaecal abscess. See Perityphlitis, 313. 
Pericardial adhesions. 456. 

effusion, 456, 460. 

frictions, 460. 
Pericarditis, acute, differential diagnosis, 460. 

etiolouy, 456. 

morbid anatomy, 454. 

physical signs, 458. 

prognosis, 461. 



INDEX. 1141 



• Pericarditis, acute, symptoms, 457. 

treatment, 462. 

varieties of, 455. 
Pericarditis, chronic, differential diagnosis, 464. 

etiology, 463. 

morbid anatomy, 463. 

physical signs, 464. 

prognosis, 464. 

symptoms, 464. 

treatment, 464. 
Pericarditis, hemorrhagic, 455. 
Pericarditis, tubercular, 455. 
Pericardium, cancer of, 537. 

dropsy of. See Hydropericardium, 541. 

tuberculosis of, 537. 
Pereira, 1061. 

Perihepatitis, differential diagnosis, 395. 

etiology, 394. 
Perihepatitis, morbid anatomy, 394. 

prognosis. 395. 

symptoms, 394. 

treatment, 396. 

syphilitica, 394. 
Perineplrritic abscess. See Perinephritis, 637. 
Perinephritis, differential diagnosis, 638. 

etiology, 638. 

morbid anatomy, 637- 

physical signs, 638. 

prognosis, 638. 

symptoms. 638. 

treatment. 638. 
Peripheral neuritis, differential diagnosis, 1078. 

etiolog3 r , 1077. 

morbid anatomy, 1076. 

prognosis, 1078. 

symptoms, 1077. 

treatment, 1078. 
Periphlebitis, 554. 

Periproctitis, differential diagnosis, 336. 

etiology, 335. 

morbid anatomy, 335. 

prognosis, 336. 

symptoms, 336. 

treatment, 336. 
Peritonitis, 353. 

differential diagnosis, 361. 

etiology, 356. 

morbid anatomy, 353. 

prognosis, 362. 

symptoms, 358. 

treatment, 362. 
Peritonitis, cancerous, 356. 
Peritonitis, chronic, 355. 
Peritonitis, hemorrhagic, 355. 
Peritonitis, tubercular. 355. 
Peritonitis, varieties of, 353. 
Perityphlitis, differential diagnosis, 314. 

etiology, 313. 

morbid anatomy, 313. 

physical signs, 314. 

prognosis, 315. 

symptoms, 314. 

treatment, 315. 
Pernicious anaemia. See Progressive pernicious an- 
aemia, 928. 

Pernicious malarial fever, differential diagnosis, 
883. 

etiology, 878. 

morbid anatomy, 877. 

prognosis, 884. 

symptoms, 878. 

treatment, 855. 

varieties, 877. 
Pertussis. See Whooping-cough, 840. 
Petit mal, 1100. 
P/licger, 1046. 

Pharyngitis, catarrhal, morbid anatomy, 249. 
" etiology, 250. 

symptoms, 250. 

differential diagnosis, 250. 

prognosis, 250. 

treatment, 250. 
Pharyngitis, croupous, 251. 
Pharyngitis, diphtheritic, 251. 

Pharyngitis, follicular. See Catarrhal pharyngitis, 
249. 

Pharyngitis, membranous, 251. 

Pharyngitis, phlegmonous. See Quinsy, 247. 



Pharynx, classification of diseases of, 247. 

.diseases of, 247. 
Phenacetin, 654. 

Phlebitis, differential diagnosis, 555. 

etiology, 554. 

morbid anatomy, 554. 

prognosis, 555. 

symptoms, 555. 

treatment, 555. 
Phlegmonous gastritis. See Gastritis, phlegmonous, 
265. 

Phlegmonous pharyngitis. See Quinsy, 247. 
Phosphates in urine. 573. 
Phthisis. See Pulmonary tuberculosis, 199. 
Phthisis, catarrh of larynx, 49. 
cavities in, 211. 
classification of, 200. 
etiology of, 203, 206. 
pathology, 200. 
physical signs of, 207. 
prognosis, 209, 221. 
Phthisis, symptoms, 207, 215. 

cough, 217. 
emaciation, 219. 
haemoptysis, 218. 
pulse, 219. 
respirations, 220. 
sputa, 218. 
treatment, 256. 

antiseptic, 231. 
climatic, 232. 
hygienic, 232. 
medicinal, 227. 
prophylactic, 226. 
Phthisis, acute, 202. 

differential diagnosis, 209. 
etiology, 203. 
morbid anatomy, 202. 
physical signs, 207. 
prognosis, 209. 
symptoms, 207. 
treatment of, 209. 
Phthisis, chronic, 209. 
Phthisis, fibrous, 214. 

morbid anatomy, 216. 
Phthisis, hemorrhagic, 218. 
Phthisis, stonecutter's, 139. 
Pick, 1062, 1067. 
Piernet, 1063. 
Pietres, 1012. 

Pigment induration of lungs, 142. 
Pigment liver. See Liver, pigment degeneration of, 
409. 

Pigmentation, 17. 

Piles. See Hemorrhoids, 336. 

Piston pulse, 484. 

Plasmodium sanguinis malaria?, 846. 
Pleura, cancer of, etiology, 192. 

prognosis, 193. 

symptoms, 192. 

treatment, 193. 
Pleurisy, acute, 174. See Pleurisy, plastic. 
Pleurisy, adhesive, 191. See Pleurisy, interstitial. 
Pleurisy, dry, 174. 
Pleurisy, interstitial, 190. 

etiology, 191. 

morbid anatomy, 190. 

physical signs, 191. 

prognosis, 192. 

symptoms, 191. 
• treatment, 192. 
Pleurisy, plastic, 174. 

differential diagnosis, 177. 

etiology, 175. 

morbid anatomy, 174. 

physical signs, 176. 

prognosis, 178. 

symptoms, 175. 

treatment, 178. 
Pleurisy, sero-fibrinous, 179. 

differential diagnosis, 183. 

etiology, 180. 

morbid anatomy, 179. 

physical signs, 181. 

prognosis, 183. 

symptoms, 180. 

treatment, 184. 
Pleurisy, tubercular, 201. 



1142 



IKDEX. 



Pleurisy, varieties of, 174. 

Pleurisy, wit h a sero-fibrinous and purulent effusion. 

See Empyema, 186. 
Pleurisy, with effusion, 179. 
Pleurodynia, 906. 
Pneumatic cabinet, 231. 
Pneumonia, acute lobar, 96. 

bacillus of, 34. 

complications, 122. 

definition, 96. 

differential diagnosis, 119. 

etiology, 102. 

morbid anatomy, 96. 

physical signs, 115. 

prognosis, 121. 

rules for administration of quinine in, 126. 
rules for the use of cold baths in, 125- 
stages, 96, 98, 99. 
symptoms, 105. 
terminations, 100. 
treatment, 123. 
Pneumonia, bilious, 114. 

Pneumonia, broncho. See Pneumonia, lobular, 127. 
Pneumonia, catarrhal. See Pneumonia, lobular, 127. 
Pneumonia, chronic fibroid, 134. 
Pneumonia, chronic interstitial, 184. 
Pneumonia, chronic lobular, 131. 
Pneumonia, colloid caseous. See Chronic phthisis, 
211. 

Pneumonia, croupous, 96. 
Pneumonia, eclamptic, 112. 
Pneumonia, embolic, 148. 

fibroid, 134. 

hypostatic, 142. 
Pneumonia of heart disease, 142. 
Pneumonia, intermittent, 115. 
Pneumonia, interstitial, 134. 

differential diagnosis of, 137. 

etiology of, 136. 

morbid anatomy of, 134. 

physical signs of, 137. 

prognosis of, 138. 

symptoms of, 136. 

treatment of, 138. 
Pneumonia, interstitial tubercular, 214. 
Pneumonia, latent, 114. 

Pneumonia, lobular, differential diagnosis of, 132. 

etiology of, 129. 

morbid anatomy of, 127. 

physical signs of, 131. 

prognosis of, 133. 

symptoms of. 129. 

temperature in, 130. 

terminations of, 128. 

treatment of, 133. 
Pneumonia, " scooper's," 139. 
Pneumonia, syphilitic, of the new-born, 171. 
Pneumonia, tubercular, 200. 
Pneumonia, typhoid, 114. 
Pneumonic tuberculosis, 210. 

morbid anatomy, 210. 

symptoms, 215. 
Pneumono'koniosis, 139. 

differential diagnosis, 140. 

etiology, 139. 

morbid anatomy, 139. 

prognosis, 140. 

symptoms, 140. 

treatment, 140. 
Pneumopericardium, 542. 
Pneumorrhagia, 148. 
Pneumothorax, 193. 

differential diagnosis, 196. 

etiology, 1P3. 

morbid" anatomy, 193. 

physical signs, 195. 

prognosis, 196. 

symptoms, 194. 

treatment, 197. 
Poisoning, chronic lead. See Lead poisoning, 

chronic, 1080. 
Polio-myelitis, acute anterior. See Infantile pa- 
ralysis, 1048. 
Polio-mvelitis, chronic anterior, 1052-3. 
Pollock, 221. 
Polycholia, 389. 

Polydipsia. See Diabetes insipidus. 922. 
Polyuria. See Diabetes insipidus, 922. 



Pon, 996. 
Ponfick, 779, 928. 
Poore, 1078. 

" Portal thrombosis.'" See Pylephlebitis, 396. 
Powell, 144. 
Power, 597. 
Pribram, 973. 
Primavera, 921. 

Proctitis, differential diagnosis, 334. 

etiology, 334. 

morhid anatomy, 233. 

prognosis, 335. 

symptoms, 334. 

treatment, 335. 
Proctitis, chronic, 334. 

Prognosis in valvular disease of the heart, 501. 
Progressive muscular atrophy, differential diagnosis, 
1056. 

etiology, 1054. 

morbid anatomy, 1053. 

prognosis, 1056. 

symptoms, 1055. 

treatment, 1056. 
Progressive pernicious anaemia, differential diag- 
nosis s 930. 

etiology, 929. 

morbid anatomy, 928. 

prognosis, 930. 

symptoms, 929. 

treatment, 931." 
Psamommata of the brain. See Cerebral tumors, 1021. 
Pseudo-hypertrophic paralysis, etiology, 1068. 

morbid anatomy, 1068. 

prognosis, 1069. 

symptoms, 1069. 

treatment, 1069. 
Pseudo-leukaemia. See Hodgkin's disease, 935. 
Pseudo-membranes, 5. 
Ptomaines, 31. 

action of, 32. 

discovery, 31. 

in fever. 650. 

inoculation with, 32. 
Pulmonary anaemia, 157. 
Pulmonary apoplexy, diffuse, 152, 153. 
Pulmonary cancer, 168. 
Pulmonary collapse, 157. 
Pulmonary congestion, 141. 
Pulmonary emphysema, 159. 
Pulmonary gangrene, 153. 
Pulmonary infarction. See Infarction, 148. 
Pulmonary oedema. See (Edema, pulmonary, 145. 
Pulmonary tuberculosis, 199. 
Pulmonary tuberculosis, acute, 202. 

differential diagnosis, 209. 

etiology, 203. 

morbid anatomy, 202. 

physical signs, 207. 

prognosis, 209. 

symptoms, 207. 

treatment, 209. 
Pulmonary tuberculosis, chronic, 209. 

complications, 226. 

differential diagnosis, 224. 

etiolosry, 215. 

morbid anatomy, 210. 

physical signs, 221. 

prognosis, 225. 

symptoms, 215. 

treatment, 226. 

varieties, 209. 
Pulmonary tuberculosis, classification, 200. 
Pulmonary tuberculosis, pathology, 200. 
Pulmonic insufficiency. See Pulmonic regurgita- 
tion, 501. 

Pulmonic obstruction, differential diagnosis, 500. 

etiology, 500. 

morbid anatomy, 499. 

physical signs, 500. 

symptoms, 500. 
Pulmonic regurgitation, differential diagnosis, 501. 

morbid anatomy, 501. 

physical signs, 501. 
Pulmonic stenosis. See Pulmonic obstruction, 499. 
Pulse, Corrigan's, 484. 

water hammer, 484. 
Purpura, differential diagnosis, 947. 

etiology, 946. 



1143 



Purpura, morbid anatomy, 943. 

prognosis, 947. 

symptoms, 946. 

treatment, 947. 
Purpura hemorrhagica. See Purpura, 945. 
Purring thrill, 476, 490. 
Purulent infection. See Septicaemia, 722. 
Purulent inliltration, 100, 113. 
Pus, fate of, 9. 
Pus in urine. 575. 
Pus, theory of formation of. 4. 

Pustule, malignant, and gangrenous stomatitis, 239. 
Putrid fever. See Septicaemia, 722. 
Pyaemia, arterial, 469. 
Pyaemia, chronic, 728. 

differential diagnosis, 728 

etiology, 726. 

morbid' anatomy, 725. 

prognosis, 728. 

symptoms, 726. 

treatment, 728. 
Pyelitis, differential,diagnosis, 624. 

etiology, 622. 

morbid' anatomy, 621. 

prognosis, 625. 

symptoms, 623. 

treatment. 626. 
Pylephlebitis, adhesive, differential diagnosis, 397. 

etiology, 396. 

morbid anatomy. 396. 

physical signs, 397. 

prognosis, 397. 

symptoms. 397. 

treatment, 397. 
Pylephlebitis, suppurative, differential diagnosis, 
399 

etiology, 398. 

morbid" anatomy. 398. 

physical signs, 399. 

prognosis, 400. 

symptoms. 398. 

treatment, 400. 
Pyloric stenosis. 260. 
Pyonephrosis, 622. 
Pyopneumothorax, 193. 

differential diagnosis, 196. 

etiology, 193. 

morbid" anatomy, 193. 

physical signs, 195. 

prognosis, 196. 

symptoms. 194. 

treatment, 197. 
Pyrosis, 267. 

Quain, 508, 529. 541, 808, 876. 
" Quain's fattv heart," 526. 
Quincke, 791, 918. 928. 
Quinsy. See Tonsilitis, 247. 

Rabies. See Hydrophobia, 843. 
Rachitis. See Rickets, 951. 
Radclife, 1035. 
Rale, Laennec's, 165. 

pleuritic, in phthisis, 222. 

redux, 118, 119. 
Ralfe, 943. 

EamskiU, 979, 983, 997, 1003. 
Janvier, 507-521. 
Rawson. 903. 
Rayer, 923. 

Reaction of degeneration, 966. 
RecTclinghavsen, 725. 

Rectitis. See Enteritis, 287 ; Proctitis, 333. 
Reflex action, 965. 

Regurgitation at the aortic orifice. See Aortic re- 
gurgitation, 482. 

Regurgitation at the mitral orifice. See Mitral re- 
gurgitation, 491. 

Regurgitation at the pulmonary orifice. See Pul- 
monic regursitation, 501. 

Regurgitation at the' tricuspid orifice. See Tricus- 
pid resurcritation, 496. 

Bernhardt, 593. 

Reitz, 104. 

Relapsing fever, complications, 783. 
differential diagnosis, 784. 
etiology, 779. 
morbid anatomy, 778. 



Relapsing fever, prognosis, 784. 

symptoms, 781. 

synonyms, 778. 

treatment, 785. 
Bemak, 904, 1013, 1057. 
Remittent fever, infantile, 883. 

differential diagnosis, 863. 

etiology, 859. 

morbid" anatomy, 858. 

prognosis, 864. 

symptoms, 860. 

treatment, 864. 

varieties, 862. 
Remitto-typhus, 866. 

Renal calculi, differential diagnosis, 632. 

etiology, 630. 

morbid anatomy, 629. 

prognosis, 632. 

symptoms, 631. 

treatment, 632. 
Renal cancer, differential diagnosis, 634. 

etiolosry, 633. 

morbid anatomy, 633. 

prognosis, 634. 

symptoms, 634. 

treatment. 634. 
Renal colic, 631. 

Renal hemorrhage, etiology, 589. 

morbid anatomy, 588. 

prognosis, 590. 

symptoms, 589. 

treatment, 590. 
Renal hyperemia, differential diagnosis, 586. 

etiology, 585. 

morbid anatomy, 583. 

prognosis, 586. 

symptoms, 585. 

treatment, 587. 

varieties, 583. 
Renan, 3S1. 

Resolution, inflammatory, 4. 
Respiratory organs, diseases of, 35. 
Retropharyngeal abscess, differential diagnosis, 252. 

etiology, 251. 

morbid" anatomy, 251. 

prognosis, 252. 

symptoms, 251. 

treatment, 252. 
Reynolds. 1004, 1006,1078, 1096. 1098. 110-2, 1103,1104, 
1108. 

Rheumatic fever. See Rheumatism, acute articular, 
896. 

Rheumatism, acute articular, differential diagnosis, 
898. 

etiology, .896. 

morbid anatomy, 895. 

prognosis, 898. 

symptoms, 896. 

treatment, 899. 
Rheumatism, chronic articular, differential diag- 
nosis, 902. 

etiolosry, 901. 

morbid anatomy, 901. 

prognosis, 902. 

svmptoms, 901. 

treatment. 902. 
Rheumatism, muscular, differential diagnosis, 907. 

etiology, 906. 

morbid anatomy, 906. 

prognosis, 907. 

symptoms, 906. 

treatment, 907. 

sub-acute, 901. 

varieties of, 895. 
Rheumatism, sub-acute, 901. 

Rheumatoid arthritis. See Arthritis deformans, 903. 
Richardson, 896. 

Rickets, differential diagnosis, 953. 

etiology. 952. 

morbid" anatomy, 951. 

prognosis, 953. 

symptoms, 952. 

treatment, 953. 
RUlier, 713. 
RiUiet. 730, 991. 

Rinfleisch, 128. 212, 213, 472, 529, 1017, 1021. 
Ringer, 126, 923. 
Roberts, 463, 1056. 



1144 



INDEX. 



Rohre, 633. 

Rokitansky, 136, 149, 150, 451, 994, 1007, 1017. 
Rose fever, 89. 
Rosen stein, 940. 

Rosenthal, 1004, 1012, 1013, 1033, 1044, 1067, 1083, 

1104, 1111. 
Roseola, See German measles, S31. 
Rostan, 446. 

Rotheln. See German measles, 831. 
Round worm. See Intestinal parasites, 338. 
Rubeola. See Measles, 822. 
Ruhle, 526. 
Rullier, 1108. 
Runeberg, 594, 597. 

Rupture of the heart. See Heart, rupture of, 532. 
Russell, 105. 
Rutherford, 443. 
Rutty, 778, 785. 

Sabourin, 382. 

bago-spleen. See Spleen, waxy degeneration of, 
451. 

" St. Vitus'' dance." See Chorea, 1112. 

Salol as antipyretic, 654. 

Salter, 526. 

Sanderson, 722, 726. 

Sarcinie ventriculi, 262. 

Sarcomata in lungs, 170. 

Sarcomata of the brain. See Cerebral tumors. 1019. 
Sarcomata of the heart, 536. 
Sarcomata of the kidney, 635. 
Sarcomata of the mediastinum, 568. 
Saturnismus. See Lead poisoning, 1080. 
scarlatina. See Scarlet fever, 805. 
Scarlet fever, complications, 806, 814. 

differential diagnosis, 816. 

etiology, 807. 

irregularities, 812. 

morbid anatomy, 805. 

prognosis, 818. 

sequelae, 814. 

stages, 805. 

symptoms, 809. 

treatment, 819. 

varieties, 805. 
Schloz, 1018. 
Schmidt, 533. 
Schneemann, 1055. 
Schilppel, 949, 1074. 

Sclerosis, amyotrophic lateral. See Amyotrophic 
lateral sclerosis, 1067. 

Sclerosis, cerebro-spinal. See Cerebro-spinal sclero- 
sis, 1057. 

Sclerosis of arteries, 548. 

Sclerosis of the brain, differential diagnosis, 1029. 

etiology, 1028. 

morbid anatomy, 1027. 

prognosis, 1029. 

symptoms, 1028. 

treatment, 1029. 
Sciatica, 1090. 

Scorbutus. See Scurvy, 943. 

Scrivener's palsy. See Localized spasm and paraly- 
sis, 1078. 

Scrofula, differential diagnosis, 951. 

etiology, 949. 

morbid anatomy, 949. 

prognosis, 951. 

symptoms, 950. 

treatment, 951. 
" Scrofulosis." See Scrofula, 949. 
Scurvy, morbid anatomy, 943. 

differential diagnosis, 944. 

etiology, 944. 

prognosis, 945. 

symptoms, 944. 
Scurvy, treatment, 945. 
Seasickness, differential diagnosis, 1123. 

etiology, 1122. 

morbid anatomy, 1122. 

prognosis, 1124. 

symptoms, 1123. 

treatment, 1124. 
Seat-worm. See Intestinal parasites, 338. 
Seeligmuller, 1051. 
Sensory paralysis, 969. 
Sepsin, 722. 

Septicaemia, differential diagnosis, 724. 



Septicaemia, etiology, 722. 

morbid anatomy, 722. 

prognosis, 724. 

symptoms, 723. 

treatment, 724. 
Septic endocarditis, 467. 
Serous membranes, inflammation of, 5. 
Shaking palsy, 1083. 
Shand, 947. 
Shattuck, 843. 
Sibson, 554. 

Sick-headache. See Megrim, 1094. 
Siderosis, 139. 
Skcda, 494, 495, 1083. 
Sloughing, 4. 

Small granular fatty kidney. See Nephritis, chronic 

parenchymatous, 604. 
Small-pox complications, 786, 790. 

differential diagnosis, 794. 

etiology, 787. 

morbid anatomy, 786. 

prognosis, 795. 

symptoms, 789. 

treatment, 797. 

Varieties, 785. 
Softening of the brain. See Cerebral softening, 1001. 
Southey, 598, 616. 
Spanaemia. See Anaemia, 923. 

Spasm and paralysis, localized. See Localized spasm 

and paralysis, 1078. 
Spasmodic tabes dorsalis, differential diagnosis, 1066. 

etiology, 1065. 

morbid anatomy, 1065. 

prognosis, 1067. 

symptoms, 1066. 

treatment, 1067. 
Spasms, 969. 

Spastic paralysis. See Amyotrophic lateral sclerosis, 
1067. 

Spermatozoa in urine, 577. 
Spina-bifida, 1075. 

Spinal apoplexy, differential diagnosis, 1073. 

etiology, 1072. 

morbid anatomy, 1071. 

prognosis, 1073. 

symptoms, 1072, 

treatment, 1073. 
Spinal cord and meninges, hyperaemia of, differential 
diagnosis, 1034. 

etiology, 1033. 

morbid anatomy, 1033. 

prognosis, 1034. 

symptoms, 1033. 

treatment, 1034. 

varieties, 1033. 
Spinal cord, diseases of, 1C32. 
Spinal cord, classification of diseases of, 1032. 
Spinal cord, hyperaemia of. See Spinal cord and 

meninges, hyperaemia of, 10i3. 
Spinal cord, non-inflammatory softening of, differ- 
ential diagnosis, 1043. 

etiology, 1042. 

morbid anatomy, 1042. 

prognosis, 1043. . 

symptoms, 1042. 

treatment, 1043. 
Spinal cord, tumors of, differential diagnosis, 1074. 

prognosis, 1074. 

symptoms, 1073. 

treatment, 1074. 
Spinal irritation, differential diagnosis, 1119. 

etiology, 1117. 

prognosis, 1119. 

symptoms, 1118. 

treatment, 1119. 
Spinal meningitis. See Meningitis, spinal, 1034. 

paralysis, infantile. See Paralysis, infantile 
spinal, 1048. 

Spinal paralysis of adults, acute. See Paralysis, acute 

spinal, of adults, 1051. 
Spirillum cholerse, 33. 
Spirochaete Obermaieri, 34, 779. 
Spleen, amyloid, 451. 
Spleen, cancer of, 452. 
Spleen, cysts of, 452. 
Spleen, diseases of, 447. 

Spleen, enlarged. See Spleen, hypertrophy of, 450. 
Spleen, gummata of, 452. 



IKDEX. 



1145 



Spleen, hydatids of, 452. 

Spleen, hy perse mi a of, etiology, 447. 

morbid anatomy, 447. 

prognosis, 4-18. 

symptoms, 447. 

treatment, 448*. 
Spleen, hypertrophy of, etiology, 451. 

morbid anatomy, 450. 

symptoms, 451. 

treatment, 451. 

varieties. 451. 
Spleen, infarction of, 448. 

Spleen, inflammation of, differential diagnosis, 448. 

etiology, 448. 

morbid anatomy, 448. 

physical signs, 448. 

prognosis, 449. 

symptoms, 448. 

treatment, 449. 
Spleen, morbid growths in, 452. 
Spleen, the sago. See Spleen, waxy degeneration of, 
451. 

Spleen, tubercles in. 452. 

Spleen, waxy degeneration of, etiology, 451. 

morbid anatomy, 451. 

symptoms, 452. 

treatment, 452. 
Splenitis. See Spleen, inflammation of, 448. 
Splenization of the lungs, 142. 
Sporadic cholera. See Cholera morbus, 296. 
Spotted fever. See Cerebro-spinal meningitis, 712. 
" Sprue. 1 ' See Thrush, 241. 
Staphylococcus pyogenes albus, 33. 
Staphylococcus pyogenes aureus, 33. 
Staphylococcus pyogenes citreus, 33. 
Staining of bacteria, 26. 
Stasis, inflammatory, 2. 
Sleiner, 1033. 
Stewart, 638. 

Stiemer, 797. % 
Stokes, 484, 657. 

Stomach, acidity of, from hypersecretion, and from 

fermentation. 269. 
Stomach, cancer of, 269. 

differential diagnosis, 273. 

etiology, 272. 

morbid anatomy, 270. 

physical signs, 273. 

prognosis, 274. 

symptoms, 272. 

treatment. 275. 

varieties. 269. 
Stomach, dilatation of, differential diagnosis, 285.- 

etiology. 283. 

morbid anatomy. 283. 

physical signs, 285. 

prognosis, 285. 

symptoms, 2S4. 

treatment, 285. 
Stomach, diseases of, 256. 

Stomach, erythism of. See Stomach, neurosis of, 
281. 

Stomach, hemorrhagic erosion in, 262. 
Stomacb, morbid sensibility of. See Chronic gastri- 
tis, 259. 

Stomach, neuroses of, differential diagnosis, 281. 

etiology, 281. 

prognosis, 281. 

symptoms, 281. 

treatment, 282. 
Stomach, ulcer of. differential diagnosis, 279. 

etiology, 277. 

morbid anatomy, 275. 

prognosis, 279. 

symptoms. 277. 

treatment, 280. 

varieties, 275. 
Stomatitis, aphthous. See Follicular stomatitis, 238. 
Stomatitis, catarrhal. 236. 

differential diagnosis, 237. 

etiolosry, 236. 

morbid anatomy, 236. 

prognosis, 237. 

symptoms, 237. 

treatment, 237. 
Stomatitis, croupous. See Follicular stomatitis, 238. 
Stomatitis, follicular. 238. 
Stomatitis, gangrenous, 239. 



Stomatitis, ulcerative, differential diagnosis, 240. 

etiology, 240. 

morbid anatomy, 240. 

prognosis, 241. 

symptoms, 240. 

treatment, 241. 
Stone-cutter's phthisis, 139. 
" Stony kidney." See Renal hyperaemia, 583. 
Sfrackins, 105. 

Streptococcus erysipelatis, 745. 

Streptococcus pyogenes, 33. 

Strieker, 914. 977. 

Stricture of the oesophagus, 253. 

Strophanthus in valvular disease. 506. 

Strophanthus in cardiac dilatation, 521. 

Strumous enteritis. See Intestinal ulcers, 317. 

Strumous nephritis, 635. 

Stumpett, 1066. 

Sturges, 104^ 

Sub-acute meningitis. ^Meningitis, sub-acute, 982. 

rheumatism. See Rheumatism, sub-acute, 901. 
Sudamina, 834. 

Sunstroke, differential diagnosis, 1117. 

etiology, 1116. 

morbid" anatomy, 1115. 

prognosis, 1117. 

symptoms, 1116. 

treatment, 1117. 
Suppuration, 4." 

Suppurative hepatitis, circumscribed. See Hepatitis, 

suppurative, 383. 
Suppurative lenitis, 265. 

pylephlebitis. See Pylephlebitis, suppurative, 
"398. 

Surgical fever. See Septicaemia,' 722. 

kidney. See Acute interstitial nephritis, 602. 
Sutton, 509. 
Swine-pox, 803. 
Syncopal typhus, 712. 
Syphilis, differential diagnosis, 963. 

etiology. 960. 

inherited, 962. 

morbid anatomy, 959. 

prognosis, 963. 

symptoms, primary, 960. 

secondary, 961. 
tertiary, 962. 

treatment, 963. 
Syphilis of the dura mater, differential diagnosis, 
998. 

morbid anatomy, 997. 
prognosis, 998. 
symptoms, 998. 
treatment, 998. 

of the heart. See Heart, svphilitic disease of, 
543. 

of the liver. See Liver, gummata of, 417. 
of the lung, 171. 
gummata of the kidney, 635. 
pneumonia of the new-born. 111. 
Syphilitic disease of arteries, 549. 

Tabacosis, 139. 

Tabes dorsalis. See Locomotor ataxia, 1060. 
Tabes dorsalis, spasmodic. See Spasmodic tabes 

dorsalis, 1065. 
Tabes mesenterica. See Intestinal ulcers, 318. 
Taenia mediocancellata, 339. 
Taenia saginata. 339. 
Taenia solium, 339. 
Tanner, 991. 

Tape-worm. See Intestinal parasites, 339. 

Teale, 729. 

Tendon, reflex, 965. 

Tests lor saccharine urine, 919. 

Tetanus, differential diagnosis, 1088. 

etiology, 1087. 

morbid" anatomy, 1087. 

prognosis, 1088. 

svmptoms. 1087. 

treatment, 1088. 
Tetany, 1119. 
Thaon, 211. 

The germ theory of disease, 648. 
Theory of organisms of disease, 648. 
Thermic fever, 1116. 
Thermogenic centers, 650. 
Thomas, 809, 888, 890. 



1146 



INDEX. 



Thoracic aneurism, differential diagnosis, 564. 

definition, 559. 

etiology, 5G0. 

morbid anatomy, 559. 

physical signs, 563. 

prognosis, 565. 

symptoms, 561 . 

treatment, medical, 566. 

surgical, 567. 

varieties, 559. 
Thread-worm. See Intestinal parasites, 341. 
Thrombi in the heart. See Cardiac thrombosis, 532. 
Thrombosis, etiology, 557. 

morbid anatomy, 556. 

symptoms, 557. 
Thrombosis of the brain. See Cerebral thrombosis 

and embolism, 998. 
Thrush, 241. 

differentia] diagnosis, 242. 

etiology, 242. 

morbid anatomy, 241. 

prognosis, 242. 

symptoms, 242. 

treatment, 242. 
Tic douloureux, 1096. 
Todd, 912. 

Tongue, cancer of, differential diagnosis, 245. 

etiology, 244. 

morbid anatomy, 244. 

prognosis, 245. 

symptoms, 244. 

treatment, 245. 
Tonsilitis, differential diagnosis, 248. 

etiology, 248. 

morbid anatomy, 247. 

prognosis, 248. 

symptoms, 248. 

treatment, 249. 
Tophi, 909. 

Torpid liver. See Liver, functional derangements 
of, 440. 

Torticollis. See Wry-neck, 906. 

Toxic gastritis. See Gastritis, acute, 256. 

Traube, 116, 156, 546, 592, 1044. 

Traumatic fever. See Septicaemia, 722. 

Tremor, mercurial. See Chronic mercurialism, 1081. 

Trichina spiralis, 341. 

Trichinosis, differential diagnosis, 959. 

etiology, 958. 

morbid anatomy, 957. 

prognosis, 959. 

symptoms, 958. 

treatment, 959. 
Trichocephalus crenatus, 341. 
Tricocephalus dispar, 341. 

Tricuspid regurgitation, differential diagnosis, 499. 

etiology, 497. 

morbid anatomy, 496. 

physical signs, 49S. 

symptoms, 49S. 
Tricuspid stenosis, 496. 
Trismus nascentium, 1087. 
Trojanowsky, 809. 

Trommer's test for sugar in the urine, 919. 
Trophic changes in nervous diseases, 971. 
Tropical typhoid, 877. 

Trousseau, 90, 442, 539, 545, 730, 733, 793, 923, 973, 

990. 1009, 1010, 1060, 1103, 1115, 1119. 
Tubercle, 21. 
Tubercle, changes in, 22. 
Tubercle bacilli, 23, 33. 
Tubercle bacilli in phthisis, 200, 201. 
Tubercle bacilli in pleurisy, 175, 180. 
Tubercles in spleen, 452. 
Tubercles in the heart, 536. 

Tubercular disease of the kidney. See Kidney tuber- 
culosis of, 635. 

Tubercular infection, methods of, 23. 

Tubercular meningitis. See Meningitis, tubercular, 
985. 

Tuberculosis, 23. 

Tuberculosis, acute miliary, development, 23. 
differential diagnosis, 751. 
etiology, 750. 
morbid anatomy, 750. 
physical signs, 751. 
prognosis, 752. 
symptoms, 750. 



Tuberculosis, acute miliary, treatment, 752. 
Tuberculosis, disseminated, 210. 

differential diagnosis, 212. 

morbid anatomy, 212. 

symptoms, 216. 
Tuberculosis, heredity of, 24. 

Tuberculosis of the liver. See Liver, tuberculosis 
of, 426. 

Tuberculosis of the pericardium, 536. 

Tuberculosis, pulmonary'. See Pulmonary tubercu- 
losis, 199. 

Tuberculous granules in arteries, 549. 

Tuberculous ulcers of the intestines. See Intestinal 
ulcers, 316. 

Tufnett, 566. 

Tumor albus, 950. 

Tumors of the brain and meninges. See Brain and 

meninges, tumors of, 1QJ9. 
Tumors of the spinal cord. See Spinal cord, tumors 

of, 1073. 
Turck, 1011. 

Tiirck, degeneration of, 1067. 

TyndalPs experiments concerning vegetable organ- 
isms. See Phthisis, 233. 
Typhlitis, differential diagnosis, 310. 

etiology, 309. 

morbid anatomy, 309. 

physical signs, 310. 

prognosis, 310. 

symptoms, 309. 

treatment, 311. 
Typho-malarial fever. See Continued malarial fever, 
866. 

Typhoid fever, abortive form, 674. 

causes of death, C80. 

complications, 678. 

critical period, 680. 

differential diagnosis, 674. 

eruption of, 672. 

etiology, 662. 

incubation, 663. 

morbid anatomy, 655-661. 

prognosis, 676. 

relapses, 681. 

symptoms, 664-672. 

synonyms, 655. 

temperature in, 664. 

treatment, 681. 

use of cold baths in, 682. 

use of antipyretics in, 6S4. 

varieties, 673. 
Typhus fever, complications, 754. 

differential diagnosis, 765. 

etiology, 756. 

morbid anatomy, 752. 

prognosis, 769. 

symptoms, 758. 

synonyms, 752. 

treatment, 773. 
Typhus siderans, 772. 
Tyrosin in urine, 571. 

Ulceration, 4. 

Ulceration of mucous surfaces, 8. 
Ulcerative stomatitis. See Stomatitis, ulcerative, 
240. 

Ulcer of stomach, 275. 

classification, 275. 

differential diagnosis, 279. 

etiology, 277. 

morbid anatom}', 275. 

pathogenesis, 277. 

prognosis, 279. 

symptoms, 277. 

treatment, 280. 
Ulcers of the bowel. See Intestinal ulcers, 315. 
Ulcers of the intestine. See Intestinal ulcers, 315. 
Uraemia, differential diagnosis, 579. 

etiology r , 578. 

prognosis, 580. 

symptoms, 579. 

theories oi, 578. 

treatment, 581. 
Uraemic coma, 575. 
Uraamic convulsion, 579. 
Urates. 572. 
Urea, 569. 
Uric acid, 570, 572. 



INDEX. 



1147 



Urinary casts, varieties of, 575. 

Urinary sediments, 572. 

Urine, animal organisms in, 577. 

bile in, 5T1. 

blood in, 574. 

casts in. 575. 

inorganic constituents of, 570. 
normal constituents of, 569. 
pus in, 575. 
sediments in, 572. 
tests for sugar in, 919. 
vegetable organisms in, 577. 
Urine of "acute nephritis, 597. 
amyloid nephritis, 619. 
cholera, 708. 

chronic nephritis, 607, 613. 
diabetes, 922. 
rheumatism, 897. 
typhoid fever.' 663. 
typhus fever, 765. 
yellow fever, 700. 

Vaccination, 799. 
Vaccinia, 800-802. 
Vallender, 1104. 
Valvular aneurisms, 468, 474. 

Valvular diseases of the heart, and cardiac murmurs, 
475. 

Valvular diseases of the heart, prognosis in, 501. 

Valvular diseases of the heart, treatment of, 504. 

Varicella, differential diagnosis, 804. 

Variola conflnens, 792. 

Variola discreta, 789. 

Variola hemorrhagica, 787, 793. 

Variola. See Small-pox, 785. 

Varioloid, morbid anatomy, 802. 

prognosis, b04. 

symptoms, 802. 

treatment, 804. 
Varix, morbid anatomy, 555. 
Veins, diseases of, 547. 
VerdeU, 108. 

Vertigo, differential diagnosis, 1121. 

etiology, 1120. 

morbid anatomy, 1120. 

prognosis, 1121. 

symptoms, 1120. 

treatment, 1121. 

varieties, 1120. 
Vertigo, stomachic and cerebral, 267. 
Vesicular bronchitis, 157. 
Vesicular emphysema, 159. 
Vesicular measles, 823. 
Vieussens, 475. 
' Vigla, 980. 

Virchaw, 142, 143, 148. 483, 730, 926, 932. 949, 950. 

984. 994, 1021, 1022, 1029, 1054. 
Virchow's brown oedema of lungs, 142. 
Vocal cords, paralysis of. See Neuroses of the 

larynx, 60. 
Vogel, 102. 



Voison, 1055. 

Volvulus. See Intestinal obstruction, 323. 
Von Graefe, 546. 
Von Brithn, 962. 
Vulpian, 497, 1029. 

Wagner, 928, 952, 1021. 
"Walking typhus," 772. 
Walshe, 121, 502. 
Warburg's tincture, 886. 
Warfynge, 937. 

Warren's test for sugar in the urine, 919. 

Waierhoiise, 799. 
Watson, 972, 991. 

Waxy degeneration of the heart. See Heart, amy- 
loid degeneration of, 529. 

Waxy degeneration of the intestines. See Intes- 
tines, waxy degeneration of, 329. 

Waxy degeneration of the pancreas. See Pancreas, 
waxy degeneration of. 445. 

Waxy kidney. See Kidney, 617. 

Waxy liver. See Liver, amyloid degeneration of, 
400. 

Weigert, 729, 786, 788. 

Weigert's method of staining, 27, 149. 

Weldon, 931. 

Werlhof, 948. 

Westphal, 1021, 1098. 

Whip-worm. See Intestinal parasites, 341. 
White flux, 295. 

Whoopino;-cou2:h, differential diagnosis, 841. 

etiology, 840. 

morbid anatomy, 840. 

prognosis, 841. 

sjmptoms, 840. 

treatment, 842. 
Wlckes, 469. 
Wilts, 928, 1010. 
Williams. 205, 235. 
Wilson, 775. 
Woakes, 1121. 
Wood, 866, 867, 876. 

Worms. See Intestinal parasites, 338. 
Wry neck, 906. 
Wunderlich, 468, 899, 1108. 

Yellow fever, differential diagnosis, 701. 

etiology, 695. 

morbid anatomy, 693. 

prognosis, 702. 

symptoms, 697. 

synonyms, 693. 

treatment. 702. 
"Yellow tubercle, " 210. 

Zalin, 731. 
Zenker: 753. 

Zenker's vitreous degeneration, 753. 
Ziemssen, 121. 136. 
Zidzer, 793, 797. 



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